The DOI matches its Crossref record; 134 of the 136 references it cites were found in a registry or an index, and 1 are not checked yet; 3 of the 142 sources its claims cite were checked for support.
Influence of Metabolism on Epigenetics and Disease
Open accessAbstract
Chemical modifications of histones and DNA, such as histone methylation, histone acetylation, and DNA methylation, play critical roles in epigenetic gene regulation. Many of the enzymes that add or remove such chemical modifications are known, or might be suspected, to be sensitive to changes in intracellular metabolism. This knowledge provides a conceptual foundation for understanding how mutations in the metabolic enzymes SDH, FH, and IDH can result in cancer and, more broadly, for how alterations in metabolism and nutrition might contribute to disease. Here, we review literature pertinent to hypothetical connections between metabolic and epigenetic states in eukaryotic cells.
Verified 2026-10-06 · 1 reference not checked yet
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
83 Not checked yet · 22 No basis given · 19 Own interpretation · 2 Partly supported · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Undifferentiated ESCs contain significantly higher levels of acetyl-CoA than the embryoid body (EB) cells induced to differentiate by the combined withdrawal of leukemia-inhibitory factor (LIF) and application of retinoic acid (RA)”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Acetyl-CoA Fluctuation
What the sources say
- Not checked yetcites Wang et al., 2009a
- Partly supportedcites Wang et al., 2011 sourceExperimental — accuracy not yet measured
The paper states that acetyl-CoA levels drop as mouse ES cells differentiate, and its metabolite survey compares undifferentiated cells with embryoid bodies produced by LIF withdrawal and retinoic acid (section labeled Abstract; page unavailable). Figure 1’s caption describes triplicate measurements, but the available text does not establish that the acetyl-CoA difference was statistically significant. (LLM, conf=0.84)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“When undifferentiated ESCs are exposed to a specific chemical inhibitor of the TDH enzyme, intracellular levels of acetyl-CoA drop precipitously”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Acetyl-CoA Fluctuation
What the sources say
- Not checked yetcites Alexander et al., 2011 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“numerous acetylation marks on the K9, K14, K23, and K27 residues of histone H3 and the K5, K8, and K12 residues on histone H4 only appear over a 30–45 min window corresponding exactly with the Ox/RB boundary that is coincident with the peak abundance of intracellular acetyl-CoA.”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Control of Gene Expression by Acetyl-CoA
What the sources say
- Not checked yetcites Cai et al., 2011
- Not checked yetcites Cai and Tu, 2011
- Not checked yetcites Cai and Tu, 2012 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Studies of two different eukaryotic cells have indeed given evidence of significant fluctuation in acetyl-CoA.”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Acetyl-CoA Fluctuation
What the sources say
- Not checked yetcites Klevecz et al., 2004 source
- Not checked yetcites Tu et al., 2005
- Not checked yetcites Tu and McKnight, 2006
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“the off-rate of acetyl-CoA binding to the yeast GCN5 enzyme is more than an order of magnitude more rapid than that of human p300/CBP HAT enzyme, human GCN5, or Tetrahymena GCN5”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Acetyl-CoA and Histone Acetyltransferase Enzymes
What the sources say
- Not checked yetcites Langer et al., 2002 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Acetyl-CoA levels peak at a 6-fold-higher level at the transition of the oxidative (Ox) phase to the reductive building (RB) phase relative to the metabolically quiescent, reductive charging (RC) phase of the YMC”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Acetyl-CoA Fluctuation
What the sources say
- Not checked yetcites Cai et al., 2011
- Not checked yetcites Tu et al., 2007
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The GCN5 histone acetylase enzyme of the SAGA complex has been identified as the critical enzyme responsible for transient acetylation of growth genes at the Ox/RB boundary”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Acetyl-CoA and Histone Acetyltransferase Enzymes
What the sources say
- Not checked yetcites Cai et al., 2011
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Further DNA microarray and ChIP-seq experiments led to the identification of roughly 1,000 growth genes selectively acetylated and activated only when intracellular levels of acetyl-CoA peak”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Control of Gene Expression by Acetyl-CoA
What the sources say
- Not checked yetcites Cai et al., 2011
- Not checked yetcites Tu et al., 2005
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“catalytically active GCN5 is critically required for YMC oscillation”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Acetyl-CoA and Histone Acetyltransferase Enzymes
What the sources say
- Not checked yetcites Cai et al., 2011
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“when NAD+ levels were measured as a function of the YMC, which is far more robust in amplitude than metabolic fluctuation taking place as a function of the circadian cycle, no changes in NAD+ levels were observed”
§ Influence of Metabolism on Epigenetics and Disease > NAD+ and Deacetylation > NAD+ and Sirtuin Deacetylases
What the sources say
- Not checked yetcites Tu et al., 2007
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 28
- Probably not a substantial claim. 9
- The quote only partly states this claim. 1
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“the genes encoding SIRT3 and SIRT6 are tumor suppressors”
§ Influence of Metabolism on Epigenetics and Disease > NAD+ and Deacetylation > NAD+ and Sirtuin Deacetylases
What the sources say
- Partly supportedcites Kim et al., 2010 sourceExperimental — accuracy not yet measured
The Results section identifies SIRT3 as a tumor suppressor, reporting mammary tumors in SIRT3-knockout mice but none in wild-type controls. The Introduction mentions SIRT6 only as a member of the sirtuin family; our copy does not establish tumor-suppressor activity for SIRT6. (LLM, conf=0.90)
- Supportedcites Sebastián et al., 2012 source
The Discussion describes SIRT3 as having tumor-suppressive activity and states that this study shows SIRT6 functions as a tumor suppressor. It distinguishes their contexts—SIRT3’s reported effect is in already transformed cells, whereas SIRT6 can suppress tumor initiation—but supports the claim about both genes. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
None of the sources cited for this claim have been checked yet.
In the paper
“Undifferentiated mouse ESCs express levels of TDH upward of 1,000-fold higher relative to any other source of mouse cells or tissues, and the gene encoding TDH is stringently repressed immediately upon induction of ESC differentiation”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Acetyl-CoA Fluctuation
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“When NAD+ levels were measured in liver tissue of wild-type mice, two ultradian sets of peaks and troughs of NAD+ abundance were observed per 24 hr cycle (Ramsey et al., 2009). The peak-to-trough fluctuation in NAD+ abundance varied by 20%–30%, as reported in the latter study.”
§ Influence of Metabolism on Epigenetics and Disease > NAD+ and Deacetylation > NAD+ and Sirtuin Deacetylases
What the sources say
- Not checked yetcites Ramsey et al., 2009 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“By administering β-hydroxybutyrate to laboratory mice via an intraperitoneal pump, Shimazu and colleagues were able to demonstrate enhancement of H3K9 and H3K14 acetylation, induced expression of FOXO3A–regulated genes, and resistance to oxidative stress.”
§ Influence of Metabolism on Epigenetics and Disease > NAD+ and Deacetylation > NAD+ Independent Histone Deacetylases
What the sources say
- Not checked yetcites Shimazu et al., 2013 source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Acetyl-CoA can also be produced catabolically from threonine via a mitochondrial threonine dehydrogenase enzyme uniquely expressed in mouse embryonic stem cells”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Acetyl-CoA Generation
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Acetyl-CoA can be produced through a variety of metabolic pathways, both catabolic and anabolic”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Acetyl-CoA Generation
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“This yeast growth gene battery matches closely with the genes induced by the c-Myc oncoprotein in mammalian cells”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Cancer Connection
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“metazoan cells have evolved the malate-citrate antiporter system to move mitochondrial citrate to the cytoplasm, where it can combine with ATP and CoA to be converted to acetyl-CoA and oxaloacetate via the ATP citrate lyase enzyme, thereby affording a cytoplasmic pool of acetyl-CoA for lipid biosynthesis.”
§ Influence of Metabolism on Epigenetics and Disease > Acetyl-CoA: “Activated Acetate” and Histone Acetylation > Acetyl-CoA Generation
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“S-adenosylmethionine (SAM) contains the active methyl donor group utilized by most methyltransferase enzymes”
§ Influence of Metabolism on Epigenetics and Disease > Methylation of DNA and Histones: SAM and the “Activated Methyl Cycle“
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“NAD+ levels fluctuate as a function of the circadian cycle, thereby instructing nuclear sirtuin enzymes to control the epigenetic state of chromatin in an NAD+-regulated manner.”
§ Influence of Metabolism on Epigenetics and Disease > NAD+ and Deacetylation > NAD+ and Sirtuin Deacetylases
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“sirtuin enzymes sit in diametric opposition to protein acetylating and that protein acetylation can be influenced by intracellular levels of acetyl-CoA.”
§ Influence of Metabolism on Epigenetics and Disease > NAD+ and Deacetylation > NAD+ and Sirtuin Deacetylases
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Histone and DNA chemical modifications are central to epigenetic control of gene expression.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The activated methyl cycle can then be looped back via the transfer of a methyl group from N5-MTHF to homocysteine, regenerating methionine.”
§ Influence of Metabolism on Epigenetics and Disease > Methylation of DNA and Histones: SAM and the “Activated Methyl Cycle“
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“those that are NAD+-dependent, yielding O-acetyl-ADP-ribose, the deacetylated substrate, and nicotinamide as products”
§ Influence of Metabolism on Epigenetics and Disease > NAD+ and Deacetylation
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“These data provide evidence that a distinct metabolite, β-hydroxybutyrate, is able not only to fuel metabolic adaptation to starvation but also to help sustain a protective epigenetic state by inhibiting the activities of NAD+-independent histone deacetylase enzymes.”
§ Influence of Metabolism on Epigenetics and Disease > NAD+ and Deacetylation > NAD+ Independent Histone Deacetylases
What the sources say
- Not checked yetcites Shimazu et al., 2013 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Histone and DNA chemical modifications are central to epigenetic control of gene expression.
None of the sources cited for this claim have been checked yet.
In the paper
“AceCS2 is acetylated on a specific lysine residue that inhibits the ability of the enzyme to convert acetate into acetyl-CoA, a regulatory scheme conserved from Salmonella to mammals”
§ Influence of Metabolism on Epigenetics and Disease > NAD+ and Deacetylation > NAD+ and Sirtuin Deacetylases
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“SAM is produced by the condensation of methionine and ATP during the first of nine steps required for the conversion of methionine to succinyl-CoA.”
§ Influence of Metabolism on Epigenetics and Disease > Methylation of DNA and Histones: SAM and the “Activated Methyl Cycle“
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“access to ample nutrients can simplistically be understood to inhibit the activities of the two proteins via acetyl-CoA-mediated acetylation. This inhibition, in turn, can be respectively counterbalanced by the mitochondrial SIRT3 and nuclear SIRT1 enzymes.”
§ Influence of Metabolism on Epigenetics and Disease > NAD+ and Deacetylation > NAD+ and Sirtuin Deacetylases
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Enzyme-catalyzed donation of the methyl group of SAM to an acceptor macromolecule yields S-adenosylhomocysteine (SAH), which, in turn, is hydrolyzed to homocysteine and adenosine.”
§ Influence of Metabolism on Epigenetics and Disease > Methylation of DNA and Histones: SAM and the “Activated Methyl Cycle“
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Simultaneous increases in the intracellular abundance of threonine and 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) were observed upon TDH inhibition in ESCs.”
§ Influence of Metabolism on Epigenetics and Disease > Methylation of DNA and Histones: SAM and the “Activated Methyl Cycle“ > Threonine Dehydrogenase and SAM
What the sources say
- Not checked yetcites Alexander et al., 2011 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“These impediments were selective; threonine deprivation had no effect on the deposition of H3K4me1, H3K9me3, H3K27me3, H3K36me3, or H3K79me3 marks on histone tails.”
§ Influence of Metabolism on Epigenetics and Disease > Methylation of DNA and Histones: SAM and the “Activated Methyl Cycle“ > Threonine Dehydrogenase and SAM
What the sources say
- Not checked yetcites Shyh-Chang et al., 2013 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one. The quote only partly states this claim.
In the paper
“In a landmark paper, Yang Shi and coworkers showed that LSD1 (also called KDM1A or AOF2) is a nuclear FAD-dependent enzyme capable of demethylating methylated H3K4 both in vitro and in vivo, thereby establishing that histone methylation is a dynamic, reversible process (Shi et al., 2004).”
§ Influence of Metabolism on Epigenetics and Disease > FAD and Histone Demethylation
What the sources say
- Not checked yetcites Shi et al., 2004 source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: FAD is derived from riboflavin and functions as a prosthetic group for certain oxidation-reduction enzymes.
None of the sources cited for this claim have been checked yet.
In the paper
“The latter protein is a small bZip transcription factor that, depending upon its heterodimeric partner, can either repress or activate gene expression (Hintze et al., 2007; Igarashi and Sun, 2006; Muto et al., 1998; Ochiai et al., 2006; Zhang et al., 2006).”
§ Influence of Metabolism on Epigenetics and Disease > Methylation of DNA and Histones: SAM and the “Activated Methyl Cycle“ > SAM and Histone/DNA Methylation
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“LSD1, in turn, regulates mitochondrial respiration and energy expenditure.”
§ Influence of Metabolism on Epigenetics and Disease > FAD and Histone Demethylation
What the sources say
- Not checked yetcites Hino et al., 2012 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In this regard, intracellular fumarate and succinate concentrations are estimated to be in the high micromolar and low millimolar range, respectively (Johnson et al., 2008).”
§ Influence of Metabolism on Epigenetics and Disease > 2-Oxoglutarate-Dependent Dioxygenases > 2-Oxoglutarate
What the sources say
- Not checked yetcites Johnson et al., 2008 source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This presumably allows such enzymes to respond to changes in the concentrations of available agonists and antagonists.”
§ Influence of Metabolism on Epigenetics and Disease > 2-Oxoglutarate-Dependent Dioxygenases > 2-Oxoglutarate
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“By contrast, the collagen prolyl hydroxylases have very low O2 Km, presumably so that they can function in environments such as poorly vascularized wounds (Hirsilä et al., 2003).”
§ Influence of Metabolism on Epigenetics and Disease > 2-Oxoglutarate-Dependent Dioxygenases > Iron and Oxygen
What the sources say
- Not checked yetcites Hirsilä et al., 2003 source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“5hmC in the nervous system is associated with actively transcribed genes and is recognized by the histone-reader protein MeCP2, which is mutationally inactivated in the neurological disorder of Rett syndrome (Mellén et al., 2012).”
§ Influence of Metabolism on Epigenetics and Disease > 2-Oxoglutarate-Dependent Dioxygenases > JmjC and TET Demethylases
What the sources say
- Not checked yetcites Mellén et al., 2012 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This suggests either that these phenotypes are not due to epigenetic targets of R-2HG or that R-2HG-induced epigenetic changes are surprisingly dynamic.”
§ Influence of Metabolism on Epigenetics and Disease > SDH, FH, and IDH Mutations and Cancer
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These metabolites appear to cause cancer by affecting the behavior of various 2-oxoglutarate-dependent dioxygenases, including dioxygenases linked to DNA and histone methylation, and therefore have the potential to alter the epigenome.”
§ Influence of Metabolism on Epigenetics and Disease > SDH, FH, and IDH Mutations and Cancer
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In addition, TET2 inactivation is sufficient to promote hematopoietic stem cell self-renewal and to block differentiation (Figueroa et al., 2010; Li et al., 2011; Moran-Crusio et al., 2011; Noushmehr et al., 2010; Turcan et al., 2012; Losman et al., 2013).”
§ Influence of Metabolism on Epigenetics and Disease > SDH, FH, and IDH Mutations and Cancer
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In summary, SDH, FH, and IDH mutations cause the accumulation of succinate, fumarate, and R-2HG, respectively.”
§ Influence of Metabolism on Epigenetics and Disease > SDH, FH, and IDH Mutations and Cancer
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Deletion of HIF1α, however, worsened the pathological changes observed in mice engineered to lack FH, suggesting that it normally constrains, rather than promotes, the emergence of FH-defective tumors (Adam et al., 2011).”
§ Influence of Metabolism on Epigenetics and Disease > SDH, FH, and IDH Mutations and Cancer
What the sources say
- Not checked yetcites Adam et al., 2011 source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In this regard, TET2 and IDH mutations are both found in acute myelogenous leukemia and are mutually exclusive, consistent with the idea that R-2HG produced by mutant IDH provides an alterative means of inactivating TET2 (Figueroa et al., 2010).”
§ Influence of Metabolism on Epigenetics and Disease > SDH, FH, and IDH Mutations and Cancer
What the sources say
- Not checked yetcites Figueroa et al., 2010 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This might suggest that folate deficiency correlates with, but does not cause, cancer or that folate is important during an early time window, perhaps occurring at an early age and prior to or during tumor initiation, but not thereafter.”
§ Influence of Metabolism on Epigenetics and Disease > Nutrition, Epigenetics, and Disease
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“There is increasing evidence that early exposures, including intrauterine exposures, can lead to lasting epigenetic changes and that epigenetic differences can influence many phenotypes, including the risk of disease.”
§ Influence of Metabolism on Epigenetics and Disease > Conclusions and Future Questions
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Interestingly, R-2HG is sufficient to promote cytokine independence and block differentiation of hematopoietic cells in vitro and these effects are fairly rapidly reversed upon R-2HG withdrawal (Losman et al., 2013; K. Yen, personal communication).”
§ Influence of Metabolism on Epigenetics and Disease > SDH, FH, and IDH Mutations and Cancer
What the sources say
- Not checked yetcites Losman et al., 2013 source
- Not checked yetcites K. Yen, personal communication
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Histone and DNA chemical modifications are central to epigenetic control of gene expression.
“Chemical modifications of histones and DNA, such as histone methylation, histone acetylation, and DNA methylation, play critical roles in epigenetic gene regulation.”
The paper relies on this without support.
Cancer can arise from mutations in the metabolic enzymes SDH, FH, and IDH.
“This knowledge provides a conceptual foundation for understanding how mutations in the metabolic enzymes SDH, FH, and IDH can result in cancer”
The paper relies on this without support.
Both histone and DNA methylation require SAM as the high-energy methyl donor.
“Both histone and DNA methylation require SAM as the high-energy methyl donor (Figure 3).”
The paper relies on this without support.
FAD is derived from riboflavin and functions as a prosthetic group for certain oxidation-reduction enzymes.
“Flavin adenine dinucleotide (FAD) is derived from the vitamin riboflavin (vitamin B2) and functions as the prosthetic group for certain oxidation-reduction enzymes.”
The paper relies on this without support.
Riboflavin is phosphorylated by riboflavin kinase to FMN, which is converted to FAD by FAD synthetase.
“Riboflavin is phosphorylated by riboflavin kinase to generate riboflavin 5′-phosphate (sometimes called flavin monucleotide or FMN), which is then converted to FAD by FAD synthetase (also called FMN adenyl-transferase).”
The paper relies on this without support.
Riboflavin kinase appears rate limiting for FAD production.
“The former enzyme appears to be rate limiting for FAD production.”
The paper relies on this without support.
FAD is produced in mitochondria.
“FAD is produced in mitochondria.”
The paper relies on this without support.
2-oxoglutarate-dependent dioxygenases require oxygen and Fe(II) in addition to 2-oxoglutarate.
“2-oxoglutarate-dependent dioxygenases require oxygen and Fe (II) in addition to 2-oxoglutarate (also called α-ketoglutarate).”
The paper relies on this without support.
2-oxoglutarate is decarboxylated to succinate during the oxidation reaction.
“The latter metabolite is decarboxylated to succinate during the oxidation reaction (Figure 5).”
The paper relies on this without support.
These enzymes are sensitive to reactive oxygen species and their activity is enhanced by ascorbic acid.
“These enzymes are also sensitive to reactive oxygen species and their activity is enhanced in the presence of ascorbic acid.”
The paper relies on this without support.
HIF synthesis is influenced by the PI3K-AKT-mTOR pathway sensing nutrients, while its degradation is controlled by EglN prolyl hydroxylases responding to oxygen and Krebs cycle intermediates.
“HIF synthesis is influenced by the PI3K-AKT-mTOR pathway, which senses nutrients such as glucose and amino acids, while its degradation is under the control of the EglN prolyl hydroxylases, which respond to changes in oxygen and different Krebs cycle intermediates (Figure 6A).”
The paper relies on this without support.
2-oxoglutarate is produced from isocitrate in mitochondria by IDH2 and IDH3 in the TCA cycle and can also be generated from several amino acids including arginine, proline, histidine, and glutamine.
“2-oxoglutarate is produced from isocitrate in the mitochondria by the action of isocitrate dehydrogenases 2 and 3 (IDH2 and IDH3) in the TCA cycle and can also be generated from several amino acids including arginine, proline, histidine, and glutamine, which can be converted to glutamic acid and transaminated to produce 2-oxoglutarate.”
The paper relies on this without support.
2-oxoglutarate generated in the TCA cycle is converted to succinyl CoA by the 2-oxoglutarate dehydrogenase complex and is consumed during conversion of cysteine and lysine to pyruvate and acetyl-CoA.
“2-oxoglutarate generated in the course of the TCA cycle is converted to succinyl CoA by the action of the 2-oxoglutarate dehydrogenase complex and is also consumed during the conversion of cysteine and lysine to pyruvate and acetyl-CoA, respectively.”
The paper relies on this without support.
2-oxoglutarate generated in mitochondria can enter the cytosol via specific transporters such as the malate-2-oxoglutarate antiporter.
“2-oxoglutarate generated in the mitochondria can enter the cytosol, either as 2-oxoglutarate or after transamination to produce glutamic acid, via specific transporter proteins such as the malate-2-oxoglutarate antiporter, which participates in the malate-aspartate shuttle.”
The paper relies on this without support.
IDH1 resides in the cytosol and peroxisomes and provides an alternative source for nonmitochondrial 2-oxoglutarate.
“A third IDH paralog, IDH1, resides in the cytosol and peroxisomes and provides an alternative source for nonmitochondrial 2-oxoglutarate.”
The paper relies on this without support.
Altered epigenetics is believed to play a part in diseases including diabetes, obesity, dyslipidemia, hypertension, and neurodegeneration.
“Altered epigenetics is believed to play a part in a variety of diseases in addition to cancer, including diabetes, obesity, dyslipidemia, hypertension, and neurodegeneration.”
The paper relies on this without support.
Diet influences one-carbon metabolism, which plays an important role in DNA and histone methylation and in disease risk.
“In this regard, particular attention has been paid to the influence of diet on one-carbon metabolism, which plays an important role in DNA and histone methylation and in risk of disease.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“metabolic intermediates of the TCA cycle affect epigenetic-mediated control of gene expression through regulating the modification of histones and DNA 137,138”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [137]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Influence of Metabolism on Epigenetics and Disease > Methylation of DNA and Histones: SAM and the “Activated Methyl Cycle“ > Threonine Dehydrogenase and SAM
“The H3K4me2 and H3K3me3 marks that disappear when mouse ESCs are deprived of threonine”
§ Influence of Metabolism on Epigenetics and Disease > Methylation of DNA and Histones: SAM and the “Activated Methyl Cycle“ > Threonine Dehydrogenase and SAM
“Intriguingly, threonine restriction was observed to dramatically impede deposition of the H3K4me2 and H3K4me3 marks on chromatin.”
Citations
Cites
DNA methylation patterns and epigenetic memory
Bird, A. (2002) · Genes & Development · doi:10.1101/gad.947102 · Cited by 7,124
Conversion of 5-Methylcytosine to 5-Hydroxymethylcytosine in Mammalian DNA by MLL Partner TET1
Tahiliani, M., Koh, K. P., Shen, Y., Pastor, W. A., Bandukwala, H., Brudno, Y., Agarwal, S., Iyer, L. M., Liu, D. R., Aravind, L., et al. (2009) · Science · doi:10.1126/science.1170116 · Cited by 5,836
A bivalent chromatin structure marks key developmental genes in embryonic stem cells
Bernstein, B. E., Mikkelsen, T. S., Xie, X., Kamal, M., Huebert, D. J., Cuff, J., Fry, B., Meissner, A., Wernig, M., Plath, K., et al. (2006) · Cell · doi:10.1016/j.cell.2006.02.041 · Cited by 5,361
Cancer-associated IDH1 mutations produce 2-hydroxyglutarate
Dang, L., White, D. W., Gross, S., Bennett, B. D., Bittinger, M. A., Driggers, E. M., Fantin, V. R., Jang, H. G., Jin, S., Keenan, M. C., et al. (2009) · Nature · doi:10.1038/nature08617 · Cited by 4,154
Histone demethylation mediated by the nuclear amine oxidase homolog LSD1
Shi, Y., Lan, F., Matson, C., Mulligan, P., Whetstine, J. R., Cole, P. A., Casero, R. A., & Shi, Y. (2004) · Cell · doi:10.1016/j.cell.2004.12.012 · Cited by 4,051
Tet proteins can convert 5-methylcytosine to 5-formylcytosine and 5-carboxylcytosine
Ito, S., Shen, L., Dai, Q., Wu, S. C., Collins, L. B., Swenberg, J. A., He, C., & Zhang, Y. (2011) · Science · doi:10.1126/science.1210597 · Cited by 3,451
Cancer epigenetics: from mechanism to therapy
Dawson, M. A., & Kouzarides, T. (2012) · Cell · doi:10.1016/j.cell.2012.06.013 · Cited by 3,203
Nutrient control of glucose homeostasis through a complex of PGC-1α and SIRT1
Rodgers, J. T., Lerin, C., Haas, W., Gygi, S. P., Spiegelman, B. M., & Puigserver, P. (2005) · Nature · doi:10.1038/nature03354 · Cited by 3,160
Xu, W., Yang, H., Liu, Y., Yang, Y., Wang, P., Kim, S.-H., Ito, S., Yang, C., Wang, P., Xiao, M.-T., et al. (2011) · Cancer Cell · doi:10.1016/j.ccr.2010.12.014 · Cited by 2,875
Tet-Mediated Formation of 5-Carboxylcytosine and Its Excision by TDG in Mammalian DNA
He, Y., Li, B.-Z., Li, Z., Liu, P., Wang, Y., Tang, Q., Ding, J., Jia, Y., Chen, Z., Li, L., et al. (2011) · Science · doi:10.1126/science.1210944 · Cited by 2,776
Cited by
Sorted by citations
Items 801–900 of 925
studiesselection heuristic algorithm for nutrigenomics
Valour, D., Hue, I., Grimard, B., & Valour, B. (2013)
Mechanisms of communication from mitochondria to lysosomes
Fernández-Mosquera, L. (2017) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-6214
Monitoring intracellular redox metabolism with genetically encoded fluorescent sensors
Zhao, Y., Yi, Y. A. N. G., & Zhang, Z. (2017) · Scientia Sinica Vitae · doi:10.1360/n052017-00086
Energy Metabolism and Epigenetics
Bultman, S. J. (2017) · Springer eBooks · doi:10.1007/978-3-319-31143-2_87-1 · Cited by 1
Wetmore, B. A. (2017) · John Wiley & Sons, Inc. eBooks · doi:10.1002/9781119023647.ch17
The Effects of Exercise on LINE-1 Regulation
Romero, M. A. (2019)
Talwin drug warning from Winthrop Laboratories.
Zander, E. (1969) · PubMed Central
Fetal and Placental Growth Physiology and Pathophysiology
Han, V. K. M., Radford, B. N., & Awamleh, Z. (2019) · Elsevier eBooks · doi:10.1016/b978-0-12-814823-5.00040-4
Nutrition, Epigenetics and Cancer Prevention
de Conti, A., Pogribny, I. P., & Ross, S. A. (2019) · Royal Society of Chemistry eBooks · doi:10.1039/9781788016506-00183
A Roadmap to Immunotherapy: Lesson from the Hallmarks and Signaling Pathways of CancerPreprint
Derakhshani, A., Rostami, Z., Safarpour, H., Taefehshokr, S., Tabrizi, N. J., Shadbad, M. A., Kooshkaki, O., Astamal, R. V., Argentiero, A., Singh, P. K., et al. (2020) · Preprints.org · doi:10.20944/preprints202011.0034.v1
Modeling Functional Modules Using Statistical and Machine Learning Methods
Çubuk, C. (2020) · RiuNet (Universitat Politècnica de València) · doi:10.4995/thesis/10251/156175
Minh, G. L., & Reginato, M. J. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-820472-6.00038-4
Nükleobazların Demetilasyonu ve Güncel Gelişmeler
KARTLAŞMIŞ, K., & Dikmen, N. (2021) · Arşiv Kaynak Tarama Dergisi · doi:10.17827/aktd.906243
Epigenetics of pulmonary diseases
Thoutam, A., & Kolliputi, N. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-823928-5.00006-2
7267 函館市西部地区の町並み景観の変貌とその要因に関する研究 : -経年的追跡調査による- 2. 変貌の要因と景観誘導の可能性
森下, 満., 足達, 富., 野口, 孝., & 山下, 圭. (1992) · 学術講演梗概集. F, 都市計画, 建築経済・住宅問題, 建築歴史・意匠
Manipulating Histone Acetylation Leads to Adverse Effects in Hemangiosarcoma CellsPreprint
Suzuki, T., Aoshima, K., Yamazaki, J., Kobayashi, A., & Kimura, T. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.12.10.472173
Waye, M. M. Y. (2021) · Springer eBooks · doi:10.1007/978-3-030-22009-9_966
Metabolism in Human Pluripotent Stem Cells and Cardiomyocytes for Regenerative Therapy
Umei, T. C., & Tohyama, S. (2022) · The Keio Journal of Medicine · doi:10.2302/kjm.2021-0015-ir
Faculty Opinions recommendation of Control of endothelial quiescence by FOXO-regulated metabolites.
Chandel, N. S. (2021) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.739855328.793585428
Energy Metabolism and Epigenetics
Bultman, S. J. (2019) · Springer eBooks · doi:10.1007/978-3-319-55530-0_87
Shankaraiah, R. C., Masatti, L., Samuel, A., & Negrini, M. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-822287-4.00006-2
Faculty Opinions recommendation of Metabolic regulation of gene expression by histone lactylation.
Mansuy, I. M. (2019) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.736798401.793568042
Carlberg, C., Ulven, S. M., & Molnár, F. (2016) · Springer eBooks · doi:10.1007/978-3-319-30415-1_5
Treviño, L. S., & Walker, C. L. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-801238-3.95610-1
Fém nanorészecskék és hiszton-deacetiláz inhibitorok tumorellenes hatásának vizsgálata
Igaz, N. (2021) · SZTE Repository of Dissertations (University of Szeged) · doi:10.14232/phd.10766
Takaya, J. (2019) · Springer eBooks · doi:10.1007/978-3-319-55530-0_61
Dietary and Metabolic Compounds Affecting Covalent Histone Modifications
Davison, G. W. (2022) · Elsevier eBooks · doi:10.1016/b978-0-323-91909-8.00024-4
DNA damage, metabolism, and epigenetic regulation
Ganguly, S., Ghanem, A., & Mian, O. Y. (2022) · Elsevier eBooks · doi:10.1016/b978-0-323-91081-1.00001-7
Mitochondrion at the crossroads between nutrients and the epigenome
Bordoni, L., & Sergi, D. (2022) · Elsevier eBooks · doi:10.1016/b978-0-323-90256-4.00015-1
Epigenetic mechanisms in cardiovascular diseases
Varadarajan, S., Ushio‐Fukai, M., & Fukai, T. (2023) · Elsevier eBooks · doi:10.1016/b978-0-12-823931-5.00020-7
Colcerasa, A., Friedrich, F., Melesina, J., Moser, P., Vogelmann, A., Tzortzoglou, P., Neuwirt, E., Sum, M., Zhang, L., Ramos‐Morales, E., et al. (2023) · ChemRxiv · doi:10.26434/chemrxiv-2023-7x8pz-v2
Eine Einführung in menschliche Krebserkrankungen
Schulz, W. A. (2024) · Springer eBooks · doi:10.1007/978-3-031-42806-7_1
Additional file 3 of Prognostic value and co-expression patterns of metabolic pathways in cancers
Zhang, D., Guo, Y. P., & Xie, N. (2020) · Figshare · doi:10.6084/m9.figshare.13502146
Additional file 4 of Prognostic value and co-expression patterns of metabolic pathways in cancers
Zhang, D., Guo, Y. P., & Xie, N. (2020) · Figshare · doi:10.6084/m9.figshare.13502149
Additional file 1 of Prognostic value and co-expression patterns of metabolic pathways in cancers
Zhang, D., Guo, Y. P., & Xie, N. (2020) · Figshare · doi:10.6084/m9.figshare.13502140
Additional file 5 of Prognostic value and co-expression patterns of metabolic pathways in cancers
Zhang, D., Guo, Y. P., & Xie, N. (2020) · Figshare · doi:10.6084/m9.figshare.13502152
Additional file 2 of Prognostic value and co-expression patterns of metabolic pathways in cancers
Zhang, D., Guo, Y. P., & Xie, N. (2020) · Figshare · doi:10.6084/m9.figshare.13502143
Kuwabara, S., Mizoguchi, T., Ma, J., Kanoh, T., Ohta, Y., & Itoh, M. (2024) · Genes to Cells · doi:10.1111/gtc.13176
Razzaq, A., Ali, N., Iftikhar, M., Shah, A. A., Nisa, Z. U., Ashraf, M. Y., Fatima, T., Raja, V., & El‐Sheikh, M. A. (2024) · Research Square · doi:10.21203/rs.3.rs-5356796/v1
Filipowicz, A. R., Chen, Q., & Allard, P. (2024) · Elsevier eBooks · doi:10.1016/b978-0-323-95488-4.00139-x
Itami, N., & Hirao, Y. (2024) · Journal of Reproduction and Development · doi:10.1262/jrd.2024-090
A transcriptional biosensor reveals mechanisms of α-ketoglutarate signaling to chromatin
Sternisha, A. C., Li, H., Gajendra, K., Xiao, Y., Zhao, X., Traylor, J. I., Guo, L., Jun, J. H., Fleishman, M., Shipman, T., et al. (2026) · Science · doi:10.1126/science.adx8675
Yang, X., Gan, H., Bai, Y., Yu, T., Zhou, D., Wang, Y., Jia, R., Wei, C., Lu, M., & Lu, F. (2025) · Theriogenology · doi:10.1016/j.theriogenology.2025.117602
Epigenetics in doxorubicin cardiotoxicity
Ferreira, L. L., da Silveira, R. G., Oliveira, P. J., & Cunha‐Oliveira, T. (2025) · Elsevier eBooks · doi:10.1016/b978-0-443-18722-3.00035-9
Epigenetics, the vascular wall and atherosclerosis
Lund, G., & Zaina, S. (2025) · Elsevier eBooks · doi:10.1016/b978-0-443-13825-6.00302-2
Fetal and Placental Growth Physiology and Pathophysiology
Han, V. K. M., Radford, B. N., Awamleh, Z., Jang, C. E., Kakadia, J. H., Matusa, A. M., & Iosef, C. (2020) · Elsevier eBooks · doi:10.1016/b978-0-443-23940-3.00019-3
Differential Flux-Balance Analysis Infers Metabolic Mutations Associated with Cancer
Pagliarini, R. (2025) · Lecture notes in computer science · doi:10.1007/978-3-032-08452-1_13
SIRT6–GLUL axis: rewiring nitrogen metabolism in intrahepatic cholangiocarcinoma
Zhou, H., Li, H., Wu, N., & Calvisi, D. F. (2025) · Gut · doi:10.1136/gutjnl-2025-337554
Fehlende Erblichkeit bei genetisch komplexen Erkrankungen
Neubauer, B. A., & Klein, K. M. (2014) · Clinical Epileptology · doi:10.1007/s10309-013-0351-1
Yan, E., Tan, M., Jiao, N., He, L., Wan, B., Zhang, X., & Yin, J. (2024) · Figshare · doi:10.6084/m9.figshare.26743253
Yan, E., Tan, M., Jiao, N., He, L., Wan, B., Zhang, X., & Yin, J. (2024) · Figshare · doi:10.6084/m9.figshare.26743250
Yan, E., Tan, M., Jiao, N., He, L., Wan, B., Zhang, X., & Yin, J. (2024) · Figshare · doi:10.6084/m9.figshare.26743247
Yan, E., Tan, M., Jiao, N., He, L., Wan, B., Zhang, X., & Yin, J. (2024) · Figshare · doi:10.6084/m9.figshare.26743244
Integrating Artificial Intelligence into metabolomics for predicting diseases
Kumar, D., Siddique, K. R., Trivedi, R., & Gupta, S. K. (2026) · Progress in molecular biology and translational science · doi:10.1016/bs.pmbts.2026.01.010
From cellular cognition to psychopathology: a three-level framework of biological decision-making
Guerrero, G. L. N. (2026) · Medical Hypotheses · doi:10.1016/j.mehy.2026.111914
Panchenko, P. E. (2015) · theses.fr (ABES) · doi:10.70675/1c8455acza5c1z427fzb7c6z5b17ad36641e
Becker, P. N., Kulow, V. A., Czopek, C. S., Roegner, K., Ter‐Avetisyan, G., Loth, A., Nitzsche, B., Erdogan, C., Schreiber, A., Höpfner, M., et al. (2026) · Cells · doi:10.3390/cells15070633
Nicoletti, S. (2017) · theses.fr (ABES) · doi:10.70675/89efde8dzf329z4c08zad57z08ffd23d7992
Lecoutre, S. (2017) · theses.fr (ABES) · doi:10.70675/65a35937ze6d1z436ezb142z7812e3f38007
Carence précoce en donneurs de méthyles dans le cervelet : mécanismes moléculaires et épigénétiques
Willekens, J. (2017) · theses.fr (ABES) · doi:10.70675/66d487f0z6da0z4367zafc6z07b11690c9cb
Dynamics of histone modification in integration of metabolic activity and stress response
Cui, X. (2019) · theses.fr (ABES) · doi:10.70675/32bafdbez364az45d9za79fz8caef581c172
Jeljeli, M. M. (2020) · theses.fr (ABES) · doi:10.70675/dfc4dd10z9fb4z4e16z836dz778a7ef9d1c1
Targeting the metabolic environment to modulate T cell effector function
Matias, M. I. (2019) · theses.fr (ABES) · doi:10.70675/0582ddaaze61dz4707z9cb1zdb8fe1d82653
Koźlak, M. (2019) · theses.fr (ABES) · doi:10.70675/0fd942ebz4198z4499za7eazb6a4014d0e09
À la rencontre des "readers" de l'ADN méthylé
Erdmann, D. (2021) · theses.fr (ABES) · doi:10.70675/f2b76a23z3f81z46f4z85a7z4abc4c194eae
Zhou, Y., Xu, S., Liu, Y., Xie, C., Li, C., Liu, L., Liao, G., Liu, X., & Li, J. (2026) · Analytical Chemistry · doi:10.1021/acs.analchem.6c00699
Inflammaging: Immune–Metabolic Crosstalk Between the Prostate–Testis and Musculoskeletal System
Bossio, S., Russa, D. L., Rago, V., Dio, M. D., Aversa, A., & Perri, A. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27083612 · Cited by 1
Design and Discovery of Pyridazinone-Based MAT2A Inhibitors Targeting MTAP-Deficient Cancers
Zhang, Y., Wang, P., Xie, Z., Huang, Y., Ding, Y., Liu, J., Chen, Y., & Hu, Y. (2026) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.5c03074
Cellular reprogramming for reverse aging
Mishra, P. K., Ghosh, S., Singh, D. K. K., & Sinha, J. K. (2026) · Elsevier eBooks · doi:10.1016/b978-0-443-33159-6.00001-1
Tumor cell intrinsic mechanisms of immune escape
Sriram, G., Aquib, A., Glassman, R., & Birge, R. B. (2026) · Cell Communication and Signaling · doi:10.1186/s12964-026-02891-3
Physicochemical approach to investigating epigenetic mutations in DNA structures
Александровна, А. Д., Passarelli, A., Porzio, A. D., D’Aria, F., & Giancola, C. (2026) · Journal of Thermal Analysis and Calorimetry · doi:10.1007/s10973-026-15513-4
Proteomic and Metabolomic Analysis of PCK2-Dependent Alterations in Group 3 Medulloblastoma Cells
Pai, M. G. J., Patra, S., Bharambe, H. S., Shirsat, N. V., & Srivastava, S. (2026) · Journal of Proteome Research · doi:10.1021/acs.jproteome.5c01150
Diet, Food, Supplements, and Depression
Sunzeri, F. (2026) · Springer eBooks · doi:10.1007/978-3-032-14465-2_20
He, J., Bao, J., Deng, S., Zang, W., Yan, H., Zhao, Z., Zhang, G., Liu, R., Chen, J.-X., Hu, Y., et al. (2026) · Advanced Science · doi:10.1002/advs.202521445
Al-Ewaidat, O. A., & Naffaa, M. M. (2026) · Exploration of Immunology · doi:10.37349/ei.2026.1003255
Advances in Visualizing Cytosine Methylation and Allele‐Specific Epigenetic States in Tissue Context
Kitazawa, S., Haraguchi, R., & Kitazawa, R. (2026) · Pathology International · doi:10.1111/pin.70133
Photo-downregulation of SIRT4 mitigates aging in mice by enhancing H3K9ac via fatty acid metabolismPreprint
Deng, F., Yang, R., Niu, J., Wang, M., Liu, Y., Li, X., Gao, Z., Yang, L., Liu, H., Yang, Y. Q., et al. (2026) · eLife · doi:10.7554/elife.111498
Photo-downregulation of SIRT4 mitigates aging in mice by enhancing H3K9ac via fatty acid metabolismPreprint
Deng, F., Yang, R., Li, X., Niu, J., Gao, Z., Wang, M., Liu, Y., Yang, L., Liu, H., Yang, Y. Q., et al. (2026) · eLife · doi:10.7554/elife.111498.1
González‐Nieto, D., Pérez‐Rigueiro, J., Rojo, F. J., Panetsos, F., & Guinea, G. V. (2026) · Gels · doi:10.3390/gels12060486
Zhang, L., Liu, L., Wang, Y., Wang, A., Tang, W., Song, Y., Zhang, Z., Chen, Y., Liao, D., Liang, H., et al. (2026) · 中国科学通报：英文版 · doi:10.1016/j.scib.2026.06.007
Conclusion and future perspectives in epigenetic phytotherapy for lung cancer
Charan, S., Masih, G. D., Singh, R. S., Singh, A. K., Soroy, B., Kumar, U., Pal, D., & Medhi, B. (2026) · Elsevier eBooks · doi:10.1016/b978-0-443-45146-1.00006-0
Bagge, E. K., Kubota‐Sakashita, M., Fujimori-Tonou, N., Kasahara, T., & Kato, T. (2026) · Neuroscience Research · doi:10.1016/j.neures.2026.105089
Jin, F., Wu, W., Yang, X. L., Fan, X. H., Zhao, X., Liu, W., & Fan, X. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27136057
Salminen, A., Kaarniranta, K., & Kauppinen, A. (2026) · Biogerontology · doi:10.1007/s10522-026-10470-9
Okashita, N., & Tachibana, M. (2026) · Advances in experimental medicine and biology · doi:10.1007/978-981-92-1439-6_3
Feeding the epigenome: EZH2 as a metabolic integrator of cell fate in development and cancer
Ansari, S. A., & Emerald, B. S. (2026) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2026.101499 · Cited by 1
Cai, M., Liao, Y., Lin, J., Chen, X., Wang, J., Li, Z., Yang, Z., & Cai, D. (2026) · Clinical and Translational Discovery · doi:10.1002/ctd2.70178
Metabolites with a message: impacts on epigenetics and implications for epimetabopathies
Banerjee, I., Mondal, A., Kamat, S. S., & Das, C. (2026) · EMBO Reports · doi:10.1038/s44319-026-00891-5
Malikov, N., & Cherepnev, G. (2026) · doi:10.24108/preprints-3116008
Chen, S., Wang, X., Xuan, Q., Liu, C., Su, Y., Liu, Z., Jia, L., Ren, Y., Cui, W., Fan, X., et al. (2026) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2026.08.007
Casotti, M. C., Ferreira, B. C., Campanharo, B. P., Campanharo, C. V., Delfino, C. D. S. C., Teixeira, C. A. F., Pesente, F., Pavan, I. P., Machado, J. D. O., Maurício, L. S. R., et al. (2026) · Biosystems · doi:10.1016/j.biosystems.2026.105923
Khatun, M. M., Sarker, M. A., Podder, M. K., Biswas, M. S., Hasan, M. M., Tamannaa, Z., Hossain, M. N., Badhon, R. S., & Akter, M. A. (2026) · Health Science Reports · doi:10.1002/hsr2.73070
Gáll, T., Pethő, D., Póliska, S., Balla, J., & Balla, G. (2026) · Pharmaceuticals · doi:10.3390/ph19091355
Swietach, P., Gill, E. K., & Holzner, L. M. W. (2026) · Biochemical Society Transactions · doi:10.1042/bst20260178
Metadata
- Authors
- Kaelin, W. G., & McKnight, S. L.
- Affiliations
- Brigham and Women's Hospital (US)
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Kaelin, William G.
- McKnight, Steven L.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2013-03
- Volume
- 153
- Issue
- 1
- Pages
- 56-69
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3775362
- OpenAlex
- W2035010201
- Semantic Scholar
- 732b8265382027a841509c4b7ef3185231cba71c
- Cited by
- 920
- References
- 136
- Citations by year
- 2026: 89 · 2025: 41 · 2024: 52 · 2023: 49 · 2022: 57 · 2021: 85 · 2020: 74 · 2019: 84 · 2018: 58 · 2017: 70 · 2016: 73 · 2015: 82 · 2014: 71 · 2013: 32
- FWCI
- 8.09
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Cancer Institute (R01CA068490, R01CA076120)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- metabolism, epigenetics, histone methylation, histone acetylation, DNA methylation, epigenetic regulation, succinate dehydrogenase, fumarase, isocitrate dehydrogenase, cancer, nutrition and disease
- MeSH terms
- Acetylation, Animals, Disease, Histones, Humans, Metabolism, Methylation, DNA Methylation, Epigenesis, Genetic
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-06, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-06 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
