Mechanisms of DNA damage, repair, and mutagenesis

In the paper

“Such inherently predisposed reactions of DNA with molecules from its immediate surroundings fuel the development of hereditary diseases and sporadic cancers [Visconti and Grieco, 2009; Reuter et al., 2010; Perrone et al., 2016].”

What the sources say

• Not checked yetcites Visconti and Grieco, 2009
• Not checked yetcites Reuter et al., 2010
• Not checked yetcites Perrone et al., 2016

In the paper

“In addition, the mismatch repair (MMR) pathway contributes to replication fidelity by more than 100-fold by correcting the rare errors that have escaped proofreading by replicative polymerases [Kunkel, 2004; Kunkel, 2009; Kunkel, 2011].”

What the sources say

• Not checked yetcites Kunkel, 2004
• Not checked yetcites Kunkel, 2009
• Not checked yetcites Kunkel, 2011

In the paper

“Another source of endogenous DNA damage results from the action of topoisomerase enzymes (for example: TOP I, TOP II, TOP III; 7 TOP genes are found in the human genome), which primarily remove superhelical tension on DNA during replication and transcription [Wang, 2002; Pommier et al., 2006].”

What the sources say

• Not checked yetcites Wang, 2002
• Not checked yetcites Pommier et al., 2006

In the paper

“Additional replication errors accumulate from strand slippage events at repetitive sequences causing insertions and deletions of nucleotides that can potentially change the reading frame [Viguera et al., 2001; Chatterjee N., 2013].”

What the sources say

• Not checked yetcites Viguera et al., 2001
• Not checked yetcites Chatterjee N., 2013

In the paper

“The majority of the endogenous DNA damage arises from the chemically active DNA engaging in hydrolytic and oxidative reactions with water and reactive oxygen species (ROS), respectively, that are naturally present within cells.”

In the paper

“Nevertheless, base substitutions and single base insertion and deletion errors still accumulate at a frequency of 10−6 to 10−8 per cell per generation [Kunkel, 2004; Kunkel, 2009].”

What the sources say

• Not checked yetcites Kunkel, 2004
• Not checked yetcites Kunkel, 2009

In the paper

“However, a battery of other DNA polymerases (α, β, σ, γ, λ, REV1, ζ, η, ι, κ, θ, ν, μ, Tdt and PrimPol) can carry out lower fidelity DNA synthesis during DNA replication or repair (Table 1) [Loeb and Monnat (2008)].”

What the sources say

• Not checked yetcites Loeb and Monnat (2008)

In the paper

“High fidelity DNA synthesis is a consequence of structural and biochemical attributes of replicative DNA polymerases, which ensure the insertion of a correct complementary deoxynucleotide opposite the template base.”

In the paper

“Abasic or AP (apurinic/apyrimidic) sites are continuously created in the DNA when the N-glycosyl bond, which links the nitrogenous base and the sugar phosphate backbone, either hydrolyzes spontaneously or gets cleaved by a DNA glycosylase to generate an intermediate in the BER pathway.”

In the paper

“Additionally, DNA adducts (from UV and benzene derivatives) and aberrant DNA structures (nicks, mismatches, abasic sites) can also irreversibly trap the TOP1-DNA cleavage complex into DNA lesions called suicidal complexes [Burgin et al., 1995; Pourquier and Pommier, 2001; Meng et al., 2003].”

What the sources say

• Not checked yetcites Burgin et al., 1995
• Not checked yetcites Pourquier and Pommier, 2001
• Not checked yetcites Meng et al., 2003

In the paper

“Misalignment of the 5′-OH DNA end stabilizes the cleavage complex to form a DNA lesion [Pommier and Cherfils, 2005; Pommier and Marchand, 2005].”

What the sources say

• Not checked yetcites Pommier and Cherfils, 2005
• Not checked yetcites Pommier and Marchand, 2005

In the paper

“From an evolutionary standpoint, cytosine deamination from endogenous and exogenous sources may serves as a source for genetic diversity [Fryxell and Zuckerkandl, 2000; Nabel et al., 2012].”

What the sources say

• Not checked yetcites Fryxell and Zuckerkandl, 2000
• Not checked yetcites Nabel et al., 2012

In the paper

“Abasic sites are inherently unstable and readily convert into single strand breaks (SSBs) from a β-elimination reaction that targets the 3′ phosphodiester bond of the leftover deoxyribose [Bailly and Verly, 1988; Waters and Walker, 2006; Tropp, 2011; Chan et al., 2013].”

What the sources say

• Not checked yetcites Bailly and Verly, 1988
• Not checked yetcites Waters and Walker, 2006
• Not checked yetcites Tropp, 2011

In the paper

“Consequently, the GC→AT transition at the CpG sequences accounts for one-third of the single site mutations responsible for hereditary diseases in humans [Cooper and Youssoufian, 1988; De Bont and van Larebeke, 2004].”

What the sources say

• Not checked yetcites Cooper and Youssoufian, 1988
• Not checked yetcites De Bont and van Larebeke, 2004

In the paper

“Similarly, the •OH radical produced as a byproduct of the Fenton reaction of H2O2 and Fe2+ induces an imidazole ring opening in guanine and adenine to form the fragmented purine structure formamidopyrimidine (Figure 1C) [Chetsanga et al., 1981; Errol C. Friedberg, 2005; C., 2006].”

What the sources say

• Not checked yetcites Chetsanga et al., 1981
• Not checked yetcites Errol C. Friedberg, 2005
• Not checked yetcites C., 2006

In the paper

“For example, AP sites are formed when uracil is removed from the DNA by uracil-DNA glycosylase [Lindahl and Barnes, 2000].”

What the sources say

• Not checked yetcites Lindahl and Barnes, 2000

In the paper

“TOP1-associated DNA damage is usually repaired by reversal of these complexes or is excised by TDP1 (tyrosyl DNA phosphodiesterase) and endonucleases [Pommier et al., 2006].”

What the sources say

• Not checked yetcites Pommier et al., 2006

In the paper

“For example, thymine glycol residues are generated from a •OH attack on the C5/C6 double bonds of thymine (Figure 1C).”

In the paper

“Interestingly, anticancer drugs such as camptothecin and many naturopathic compounds are known to stabilize the TOP1-DNA cleavage complexes [Staker et al., 2002; Han et al., 2008].”

What the sources say

• Not checked yetcites Staker et al., 2002
• Not checked yetcites Han et al., 2008

In the paper

“However, in excess, ROS species can cause a total of approximately 100 different oxidative base lesions and 2-deoxyribose modifications [Bjelland and Seeberg, 2003; Cadet et al., 2010; Cadet et al., 2011; Cadet et al., 2012; Ravanat et al., 2012; Cadet and Wagner, 2014].”

What the sources say

• Not checked yetcites Bjelland and Seeberg, 2003
• Not checked yetcites Cadet et al., 2010
• Not checked yetcites Cadet et al., 2011

In the paper

“In addition to the endogenous deamination sources, environmental exposure to UV radiation, intercalating agents, nitrous acid and sodium bisulfite can in general enhance base deamination rates in the DNA [Chen and Shaw, 1993; Moyer et al., 1993; Pfeifer et al., 2005; d’Ischia et al., 2011].”

What the sources say

• Not checked yetcites Chen and Shaw, 1993
• Not checked yetcites Moyer et al., 1993
• Not checked yetcites Pfeifer et al., 2005

In the paper

“In the case of deamination of cytosine, for instance, the native C:G base pairing alters to a U:A base pair in the first round of replication, which in the next round of replication results in a CG→TA mutation.”

In the paper

“The second class of direct reversal enzymes, the AlkB-related α-ketoglutarate-dependent dioxygenases (AlkB), reverse N-alkylated base adducts.”

In the paper

“In addition, chromatin remodeling is an important modulator of DDR response, whereby key post-translational modifications allow assembly of specific DDR and repair factors [Bekker-Jensen et al., 2006; Harper and Elledge, 2007; Misteli and Soutoglou, 2009; Polo and Jackson, 2011; Altmeyer and Lukas, 2013a; Altmeyer and Lukas, 2013b; House et al., 2014].”

What the sources say

• Not checked yetcites Bekker-Jensen et al., 2006
• Not checked yetcites Harper and Elledge, 2007
• Not checked yetcites Misteli and Soutoglou, 2009

In the paper

“For demethylation, the AlkB family proteins hydroxylate the alkyl group in a α-ketoglutarate and iron(II) dependent manner. The oxidized alkyl group is released as formaldehyde, leaving behind the original base [Drablos et al., 2004; Falnes et al., 2007].”

What the sources say

• Not checked yetcites Drablos et al., 2004
• Not checked yetcites Falnes et al., 2007

In the paper

“S-adenosylmethionine (SAM), which is used as a methyl donor by methyl transferases during normal methylation reactions, can also spontaneously generate up to 4000 N7-methylguanine, 600 N3-methyladenine and 10–30 O6-methylguanine residues per cell per day in mammals (Figure 1d) [Rydberg and Lindahl, 1982; Holliday and Ho, 1998; De Bont and van Larebeke, 2004].”

What the sources say

• Not checked yetcites Rydberg and Lindahl, 1982
• Not checked yetcites Holliday and Ho, 1998
• Not checked yetcites De Bont and van Larebeke, 2004

In the paper

“A single AGT molecule removes the alkylation adduct in a one step reaction by transferring the alkyl group from the oxygen of the DNA base to the cysteine residue in its catalytic pocket [Kaina et al., 2007].”

What the sources say

• Not checked yetcites Kaina et al., 2007

In the paper

“Finally, lipid peroxidation, the oxidation of lipid molecules by hydroxyl radicals, generates aldehyde products such as malondialdehyde and 4-hydroxynonenal, which can react with adenine, guanine and cytosine to form mutagenic adducts [Marnett, 2000; Plastaras et al., 2000; VanderVeen et al., 2001].”

What the sources say

• Not checked yetcites Marnett, 2000
• Not checked yetcites Plastaras et al., 2000
• Not checked yetcites VanderVeen et al., 2001

In the paper

“First, the O6- alkylguanine-DNA alkyltransferase (AGT/MGMT) enzyme reverses O-alkylated DNA lesions, such as the O6-methyl, ethyl, 2-chloroethyl, benzyl and aliphatic groups, the pyridyloxobutyl adducts of guanine, and even repair the O6–G-alkyl-O6- G interstrand cross-links [Tubbs et al., 2007; Fang et al., 2008; Pegg, 2011].”

What the sources say

• Not checked yetcites Tubbs et al., 2007
• Not checked yetcites Fang et al., 2008
• Not checked yetcites Pegg, 2011

In the paper

“Food preservatives [(sodium benzoate (SB), potassium benzoate (PB) and potassium sorbate (PS)] and food additives [(citric acid (CA), phosphoric acid (PA), brilliant blue (BB) and sunset yellow (SY)] are all known to cause DNA damage [Mamur et al., 2010; Zengin et al., 2011; Yilmaz et al., 2014; Pandir, 2016].”

What the sources say

• Not checked yetcites Mamur et al., 2010
• Not checked yetcites Zengin et al., 2011
• Not checked yetcites Yilmaz et al., 2014

In the paper

“Small subsets of DNA lesions—UV photolesions and alkylated bases—are simply reversed in an error-free manner.”

In the paper

“Other than attacking DNA bases, ROS radicals can also compromise the DNA backbone causing an estimated 2300 single strand breaks per cell per hour in mammalian cells [Giloni et al., 1981; R, 1981; Henner et al., 1983a; Henner et al., 1983b].”

What the sources say

• Not checked yetcites Giloni et al., 1981 source
• Not checked yetcites R, 1981
• Not checked yetcites Henner et al., 1983a

In the paper

“Additionally, plant protection products (PPPs) regularly used by orchard workers have also been associated with DNA damage [Kasiotis et al., 2012].”

What the sources say

• Not checked yetcites Kasiotis et al., 2012

In the paper

“For BER transactions, chromatin remodeling at the DNA damage site is followed by lesion recognition by a DNA glycosylase [Odell et al., 2013].”

What the sources say

• Not checked yetcites Odell et al., 2013

In the paper

“Recruitment of DDR factors is a spatiotemporally regulated process, in which the DDR factors are assembled at the site of damage in a sequential and coordinated manner, as verified by time-lapse microscopy of discrete foci [Harper and Elledge, 2007; Ciccia and Elledge, 2010; Polo and Jackson, 2011].”

What the sources say

• Not checked yetcites Harper and Elledge, 2007
• Not checked yetcites Ciccia and Elledge, 2010
• Not checked yetcites Polo and Jackson, 2011

In the paper

“Mutations affecting DDR network components are the cause of several cancer predisposition syndromes, reflecting their overall importance in avoiding DNA damage-induced human diseases [Ciccia and Elledge, 2010].”

What the sources say

• Not checked yetcites Ciccia and Elledge, 2010

In the paper

“On the other hand, lack of AGT expression is associated with certain group of cancers [Lee et al., 2011; Mokarram et al., 2013].”

What the sources say

• Not checked yetcites Lee et al., 2011
• Not checked yetcites Mokarram et al., 2013

In the paper

“In the nucleus, this repair process is mainly active in the G1 phase of the cell cycle [Dianov and Hubscher, 2013].”

What the sources say

• Not checked yetcites Dianov and Hubscher, 2013

In the paper

“In addition, alkyltransferase-like proteins (ATLs), a family of AGT homologs, inhibit the AGT enzyme by directing the repair of bulky alkyl damage to the NER pathway [Margison et al., 2007; Tubbs et al., 2009].”

What the sources say

• Not checked yetcites Margison et al., 2007
• Not checked yetcites Tubbs et al., 2009

In the paper

“BER corrects those forms of oxidative, deamination, alkylation and abasic single base damage that are not perceived as significant distortions to the DNA helix.”

In the paper

“butyl paraben (BP) and bisphenol A (BPA), found in cosmetics, pharmaceuticals, food-products and beverage processing, are linked to DNA damage in sperm cells [Oishi, 2002; Meeker et al., 2010a; Meeker et al., 2010b; Meeker et al., 2011].”

What the sources say

• Not checked yetcites Oishi, 2002
• Not checked yetcites Meeker et al., 2010a
• Not checked yetcites Meeker et al., 2010b

In the paper

“Next, the MutL complexes are recruited on to DNA and among the 4 known human MutL homologs; the MutLα heterodimer (MLH1/PMS2 heterodimer) plays a major role in MMR [Nicolaides et al., 1994; Papadopoulos et al., 1994; Li and Modrich, 1995; Lipkin et al., 2000].”

What the sources say

• Not checked yetcites Nicolaides et al., 1994
• Not checked yetcites Papadopoulos et al., 1994
• Not checked yetcites Li and Modrich, 1995

In the paper

“Recently, the Modrich lab has shown that MutL can trap MutS at the mismatch before it forms a sliding clamp [Qiu et al., 2015].”

What the sources say

• Not checked yetcites Qiu et al., 2015

In the paper

“downregulation of OGG1 is associated with aging, neurodegenerative disorders and cancer [Kovtun et al., 2007; Tian et al., 2009; Curtin, 2012; Mollersen et al., 2012; Chatterjee N., 2013; Krokan and Bjoras, 2013; Chatterjee et al., 2015].”

What the sources say

• Not checked yetcites Kovtun et al., 2007
• Not checked yetcites Tian et al., 2009
• Not checked yetcites Curtin, 2012

In the paper

“It involves the use of structure specific endonucleases XPF–ERCC1 and XPG (also known as ERCC5), which cuts the damaged strand short distances away from the 5′ and 3′ end of the lesion respectively [Fagbemi et al., 2011].”

What the sources say

• Not checked yetcites Fagbemi et al., 2011

In the paper

“In GG-NER, the main DNA damage sensor is the XPC (Xeroderma Pigmentosum, complementation group C) protein, complexed with RAD23B (UV excision repair protein Radiation sensitive 23B) protein and CETN2 (Centrin 2). This complex scans for the presence of transient single−stranded DNA (ssDNA) caused by disrupted base pairing due to the lesion [Masutani et al., 1994; Nishi et al., 2005].”

What the sources say

• Not checked yetcites Masutani et al., 1994
• Not checked yetcites Nishi et al., 2005

In the paper

“In terms of function, DNA glycosylases are either monofunctional, with only a glycosylase activity, such as the uracil glycosylases, N-methylpurine DNA Glycosylase (MPG), and MutY Homolog (MUTYH), or are bifunctional with a glycosylase and an additional β-lyase activity.”

In the paper

“To begin NER, chromatin remodeling mediated both by chromatin and NER components makes way for the NER machinery on the specified DNA lesions [Scharer, 2013].”

What the sources say

• Not checked yetcites Scharer, 2013

In the paper

“Nucleotide excision repair is the pathway of choice to remove bulky lesions such as CPDs and (6 – 4)PP from UV radiation, benzo[a]pyrene adducts, or damage from chemotherapeutic agents.”

In the paper

“Chromatin modifications have recently been shown to pave the way for the MMR proteins to gain access to the DNA lesion and initiate repair [Li et al., 2013; Li, 2014].”

What the sources say

• Not checked yetcites Li et al., 2013
• Not checked yetcites Li, 2014

In the paper

“However, like the BER pathway, NER contributes to the instability mechanisms in triplet repeat disorders [Lin et al., 2006; Hubert et al., 2011; Dion, 2014].”

What the sources say

• Not checked yetcites Lin et al., 2006
• Not checked yetcites Hubert et al., 2011
• Not checked yetcites Dion, 2014

In the paper

“NER deficiency results in a number of different human syndromes: Xeroderma Pigmentosum (XP), which is associated with a predisposition to skin cancers; Cockayne Syndrome (CS); rare UV-Sensitive Syndrome (UVSS); and Cerebro-Oculo-Facio-Skeletal syndrome (COFS) [Errol C. Friedberg, 2005; Vermeulen and Fousteri, 2013].”

What the sources say

• Not checked yetcites Errol C. Friedberg, 2005
• Not checked yetcites Vermeulen and Fousteri, 2013

In the paper

“It should be noted that 8-oxoguanine DNA glycosylase (OGG1) and NEIL3 function as both mono- and bifunctional glycosylases [Svilar et al., 2011].”

What the sources say

• Not checked yetcites Svilar et al., 2011

In the paper

“The replication proteins PCNA (proliferating cell nuclear antigen), RFC (replication factor C), POL δ, POL ε or POL κ, and LIG1 or XRCC1–LIG3 carry out the final step of gap−filling synthesis and ligation.”

In the paper

“These include the core NER factors (except for the GG−NER− specific UV–DDB and XPC complexes) and TC−NER−specific proteins, such as UVSSA (UV−stimulated scaffold protein A), USP7 (ubiquitin−specific−processing protease 7; also known as ubiquitin C−terminal hydrolase 7), XAB2 (XPA−binding protein 2; also known as pre−mRNA−splicing factor SYF1) and HMGN1 (high mobility group nucleosome−binding”

What the sources say

• Not checked yetcites Fousteri et al., 2006
• Not checked yetcites Schwertman et al., 2012

In the paper

“Mutations in the FA genes are the cause of the autosomal recessive FA disorder.”

In the paper

“The leading strand with the ICL becomes the template for new DNA synthesis—by TLS polymerases POL ι, POL κ, POL ν and REV1—that proceeds up to the lesion, bypasses it, and extends beyond the lesion until it reaches the first downstream Okazaki fragment [Minko et al., 2008; Raschle et al., 2008; Yamanaka et al., 2010; Ho et al., 2011; Klug et al., 2012].”

What the sources say

• Not checked yetcites Minko et al., 2008
• Not checked yetcites Raschle et al., 2008
• Not checked yetcites Yamanaka et al., 2010

In the paper

“In a yet unknown way, other FA core complex components (FANCA/B/C/E/F/G/L/T) assemble at the damaged site and activate the phosphorylated FANCI–FANCD2 heterodimer through FANCL-mediated monoubiquitination [Smogorzewska et al., 2007].”

What the sources say

• Not checked yetcites Smogorzewska et al., 2007

In the paper

“Replication fork remodeling stimulated by MFH and FANCM promotes Holliday junction migration and the creation of ssDNA gaps [Gari et al., 2008a; Gari et al., 2008b; Huang et al., 2010].”

What the sources say

• Not checked yetcites Gari et al., 2008a
• Not checked yetcites Gari et al., 2008b
• Not checked yetcites Huang et al., 2010

In the paper

“Interestingly, resolution of this HR intermediate depends on the FANCD2-FANCI complex.”

In the paper

“In replicating cells, the presence of ICL stalls the ongoing replication on the leading strand, as well as on the 5′ end of the lagging strand at some distance from the lesion [Raschle et al., 2008; Knipscheer et al., 2009].”

What the sources say

• Not checked yetcites Raschle et al., 2008
• Not checked yetcites Knipscheer et al., 2009

In the paper

“RPA bound ssDNA signals ATR activation [Zou and Elledge, 2003; Ben-Yehoyada et al., 2009].”

What the sources say

• Not checked yetcites Zou and Elledge, 2003
• Not checked yetcites Ben-Yehoyada et al., 2009

In the paper

“ATR phosphorylates downstream target CHK1, which in turn phosphorylates FANCE, FANCD2, FANCI and MRN [Andreassen et al., 2004; Smogorzewska et al., 2007; Wang et al., 2007a; Cui et al., 2009; Duquette et al., 2012].”

What the sources say

• Not checked yetcites Andreassen et al., 2004
• Not checked yetcites Smogorzewska et al., 2007
• Not checked yetcites Wang et al., 2007a

In the paper

“Next, XPF-ERCC1 and SNM1A induce incisions on either side of the lesion that unhook the ICL from the lagging strand, thereby producing a gap [Wang et al., 2011].”

What the sources say

• Not checked yetcites Wang et al., 2011

In the paper

“POL δ, RFC, HMGB1 (high mobility group box 1 protein) and LIG1 orchestrate the final steps of new DNA synthesis and ligation [Genschel and Modrich, 2003; Yuan et al., 2004; Guo et al., 2006].”

What the sources say

• Not checked yetcites Genschel and Modrich, 2003
• Not checked yetcites Yuan et al., 2004
• Not checked yetcites Guo et al., 2006

In the paper

“Subsequently, excision of the DNA strand (5′ and 3′) of the lesion is coordinated by structure specific endonucleases—XPF-ERCC1, MUS8-EME1, SLX4-SLX1, FAN1, SNM1A/SNM1B—in an as-yet unclear fashion [Clauson et al., 2013].”

What the sources say

• Not checked yetcites Clauson et al., 2013

In the paper

“EXO1 also carries out the 5′ directed mismatch excision creating a gap that is stabilized by RPA [Genschel and Modrich, 2003; Zhang et al., 2005].”

What the sources say

• Not checked yetcites Genschel and Modrich, 2003
• Not checked yetcites Zhang et al., 2005

In the paper

“These lesions are recognized and repaired by the Fanconi anemia (FA) proteins.”

In the paper

“Classically, FA is diagnosed by assessing cellular hypersensitivity—chromosomal breaks and chromosomal radial formations—to DNA ICL agents such as diepoxybutane (DEB) and MMC [D’Andrea, 2010].”

What the sources say

• Not checked yetcites D’Andrea, 2010

In the paper

“In non-replicating cells, ICL repair of psoralen, MMC, cisplatin, and alkyl ICLs depend on NER and TLS polymerases such as REV1 and POL ζ [Clauson et al., 2013].”

What the sources say

• Not checked yetcites Clauson et al., 2013

In the paper

“Upon ICL damage, FANCM is recruited to the damaged site along with FAAP24 (Fanconi Anemia associated protein of 24 kDa) and MFH (histone fold protein complex) [Ciccia et al., 2007; Niedernhofer, 2007; Yan et al., 2010].”

What the sources say

• Not checked yetcites Ciccia et al., 2007
• Not checked yetcites Niedernhofer, 2007
• Not checked yetcites Yan et al., 2010

In the paper

“Interstrand crosslink repair is initiated by chromatin loading of the FA proteins in a cell cycle-dependent manner [Mi and Kupfer, 2005; Kim et al., 2008].”

What the sources say

• Not checked yetcites Mi and Kupfer, 2005
• Not checked yetcites Kim et al., 2008

In the paper

“PCNA plays an important role in both the initiation step of MMR and in the subsequent DNA synthesis by interacting and localizing MutSα/β and MutLα complexes at the lesion site [Umar et al., 1996; Lau and Kolodner, 2003; Jiricny, 2006].”

What the sources say

• Not checked yetcites Umar et al., 1996
• Not checked yetcites Lau and Kolodner, 2003
• Not checked yetcites Jiricny, 2006

In the paper

“This activation of FANCI-D2 marks as the major activation switch for the FA pathway [Wang, 2008; Tomida et al., 2013].”

What the sources say

• Not checked yetcites Wang, 2008
• Not checked yetcites Tomida et al., 2013

In the paper

“After this step, the 3′ overhang of the leftover lagging strand invades the newly synthesized strand in a RAD51-dependent manner in a tightly coordinated manner [Long et al., 2011].”

What the sources say

• Not checked yetcites Long et al., 2011

In the paper

“In addition to mismatch repair and other cellular functions, the mismatch repair genes have recently been shown to be repressed in response to environmental stresses, such as hypoxia, benzo[a]pyrene, inflammation and even tumor microenvironment [Mihaylova et al., 2003; Bindra and Glazer, 2007; Nakamura et al., 2008; Edwards et al., 2009; Chen et al., 2013].”

What the sources say

• Not checked yetcites Mihaylova et al., 2003
• Not checked yetcites Bindra and Glazer, 2007
• Not checked yetcites Nakamura et al., 2008

In the paper

“These structural differences orient the thumb, fingers, palm, and little finger catalytic domains into a relatively larger open active site, while being aided by other physical features such as the polymerase-associated domain (PAD), wrist, and N-clasp region found in Y Family DNA polymerases that facilitate additional DNA binding.”

In the paper

“Interestingly, the TLS polymerases, REV1 and REV3, were also implicated in the development of chemoresistance in human cells and mice models, opening the possibility for a whole new class of promising chemotherapeutic drugs [Doles et al., 2010; Xie et al., 2010; Xu et al., 2013].”

What the sources say

• Not checked yetcites Doles et al., 2010
• Not checked yetcites Xie et al., 2010
• Not checked yetcites Xu et al., 2013

In the paper

“Single strand breaks (SSBs) are often generated from oxidative damage to the DNA, from abasic sites, or from erroneous activity of the DNA topoisomerase 1 (TOP1) enzyme [Wang, 2002; Hegde et al., 2008].”

What the sources say

• Not checked yetcites Wang, 2002
• Not checked yetcites Hegde et al., 2008

In the paper

“First, an ‘inserter’ TLS enzyme, usually a POL η, POL ι, or POL κ, and less often REV1 or POL ζ, incorporates a nucleotide opposite the DNA lesion [Korzhnev and Hadden, 2016].”

What the sources say

• Not checked yetcites Korzhnev and Hadden, 2016

In the paper

“The frequency of DNA synthesis errors during translesion synthesis depends on several factors, such as whether the lesion is a cognate for the particular TLS DNA polymerase, the biochemical characteristics of the particular TLS polymerase and the DNA sequence context [Pages and Fuchs, 2002; McCulloch et al., 2004; Waters and Walker, 2006].”

What the sources say

• Not checked yetcites Pages and Fuchs, 2002
• Not checked yetcites McCulloch et al., 2004
• Not checked yetcites Waters and Walker, 2006

In the paper

“Exogenous stressors—for example UV-C, MNNG, and BPDE—regulate the transcriptional expression of POL η, POL ι, POL κ and POL ζ [Zhu et al., 2003; Yu et al., 2004; Liu and Chen, 2006; Zhu et al., 2010; Zhu et al., 2012].”

What the sources say

• Not checked yetcites Zhu et al., 2003
• Not checked yetcites Yu et al., 2004
• Not checked yetcites Liu and Chen, 2006

In the paper

“This two-step model is proposed to direct both the error-free and error-prone translesion DNA synthesis across the damage [Shachar et al., 2009].”

What the sources say

• Not checked yetcites Shachar et al., 2009

In the paper

“For example, the FA pathway suppresses non-homologous end joining (NHEJ) by interacting with CtIP, and recruiting the NHEJ-inhibiting molecules—PARP1 and RAD18 to the DNA [Saberi et al., 2007; Ceccaldi et al., 2016a].”

What the sources say

• Not checked yetcites Saberi et al., 2007
• Not checked yetcites Ceccaldi et al., 2016a

In the paper

“Finally, the FA pathway has now been implicated in trinucleotide repeat instability [Chatterjee N., 2016].”

What the sources say

• Not checked yetcites Chatterjee N., 2016

In the paper

“In addition, loss of FANCD2 confers a synthetic lethal phenotype in POL θ null mice [Nguyen et al., 2014; Ceccaldi et al., 2015; Howard et al., 2015].”

What the sources say

• Not checked yetcites Nguyen et al., 2014
• Not checked yetcites Ceccaldi et al., 2015
• Not checked yetcites Howard et al., 2015

In the paper

“Notable features include the very limited sequence homology to replicative DNA polymerases, the absence of a 3′-5′ exonuclease domain to proofread incoming nucleotides, and their smaller thumb and finger domains, which make fewer contacts with the DNA than those found in replicative DNA polymerases [Rothwell and Waksman, 2005; Waters and Walker, 2006; Sale, 2013].”

What the sources say

• Not checked yetcites Rothwell and Waksman, 2005
• Not checked yetcites Waters and Walker, 2006
• Not checked yetcites Sale, 2013

In the paper

“TLS polymerases are specialized DNA polymerases that can replicate opposite and past aberrant DNA lesions in a relatively lower fidelity manner than replicative DNA polymerases [Sale, 2013].”

What the sources say

• Not checked yetcites Sale, 2013

In the paper

“Translesion synthesis is carried out by highly conserved TLS polymerases.”

In the paper

“In the second step, an extender TLS enzyme, a role usually fulfilled by POL ζ exclusively but in some cases by POL κ, replaces the inserter polymerase and extends the primer-template termini [Washington et al., 2002; Yuji Masuda, 2016].”

What the sources say

• Not checked yetcites Washington et al., 2002
• Not checked yetcites Yuji Masuda, 2016

In the paper

“Moreover, POLD3, which is part of the POL ζ4 complex, interacts with REV1 via its RIR, thereby assisting the switch from RIR directed insertion to POL ζ4-mediated extension during damage bypass [Pustovalova et al., 2016].”

What the sources say

• Not checked yetcites Pustovalova et al., 2016

In the paper

“In the polymerase switch model, TLS polymerases come together sequentially in a two-step process to replicate pass the DNA lesion at a stalled replication fork.”

In the paper

“In the gap-filling model, single strand gaps left behind by replicative polymerases during replication or via an incomplete DNA repair process, such as during immunoglobulin gene hypermutation, are the targets of TLS synthesis [Sale et al., 2009].”

What the sources say

• Not checked yetcites Sale et al., 2009

In the paper

“The TLS polymerases’ fascinating ability to help cells tolerate DNA damage arises from their structural and biochemical features [Rothwell and Waksman, 2005; Pavlov et al., 2006; Waters and Walker, 2006].”

What the sources say

• Not checked yetcites Rothwell and Waksman, 2005
• Not checked yetcites Pavlov et al., 2006
• Not checked yetcites Waters and Walker, 2006

In the paper

“Together, these structural features provide the TLS polymerases with a unique architecture that enable them to bypass DNA damage or fill ssDNA gaps [Trincao et al., 2001; Ling et al., 2003; Lone et al., 2007; Jansen et al., 2009a; Jansen et al., 2009b].”

What the sources say

• Not checked yetcites Trincao et al., 2001
• Not checked yetcites Ling et al., 2003
• Not checked yetcites Lone et al., 2007

In the paper

“The HR pathway consist of a set of related sub-pathways that utilize DNA strand invasion and template-directed DNA repair synthesis to effect a high-fidelity repair [Li and Heyer, 2008].”

What the sources say

• Not checked yetcites Li and Heyer, 2008

In the paper

“Finally, the TOP1-SSB pathway is a variant of the PARP1-dependent long patch repair in which the end-processing is carried out by the TDP1 (tyrosyl-DNA phosphodiesterase 1) enzyme that removes the TOP1 from the 3′-end [Caldecott, 2008].”

What the sources say

• Not checked yetcites Caldecott, 2008

In the paper

“Once the ends are bridged and stabilized, Artemis, PNKP, APLF, WRN, Aprataxin and Ku initiate DNA end processing, which involves removing groups that are blocking the ends and resecting the resultant naked strands [Ma et al., 2002; Bernstein et al., 2005; Ahel et al., 2006; Perry et al., 2006; Roberts et al., 2010; Li et al., 2011].”

What the sources say

• Not checked yetcites Ma et al., 2002
• Not checked yetcites Bernstein et al., 2005
• Not checked yetcites Ahel et al., 2006

In the paper

“We will briefly discuss the two major pathways—homologous recombination (HR) and non-homologous end joining (NHEJ)—that organisms have evolved to resolve the DSBs.”

In the paper

“At least two human genetic disorders, spinocerebellar ataxia with axonal neuropathy 1 (SCAN1) and ataxia-oculomotor apraxia 1 (AOA1), are associated with an abortive SSBR.”

In the paper

“Highly toxic DSBs are induced by various chemical and physical DNA damaging agents [Pfeiffer et al., 2000].”

What the sources say

• Not checked yetcites Pfeiffer et al., 2000

In the paper

“The gaps left behind after resection are filled by family X polymerases in a template-dependent (POL μ) or template-independent (POL λ) manner [Ramadan et al., 2004; Roberts et al., 2010].”

What the sources say

• Not checked yetcites Ramadan et al., 2004
• Not checked yetcites Roberts et al., 2010

In the paper

“Other recruited components include DNA-PKcs, XRCC4, LIG4 and XLF (XRCC4-like factor), APLF (Aprataxin-and-PNK-like factor) [and also TdT (terminal deoxynucleotidyl transferase) in lymphocytes] [Gottlieb and Jackson, 1993; Nick McElhinny et al., 2000; Costantini et al., 2007; Yano et al., 2008; Grundy et al., 2013].”

What the sources say

• Not checked yetcites Gottlieb and Jackson, 1993
• Not checked yetcites Nick McElhinny et al., 2000
• Not checked yetcites Costantini et al., 2007

In the paper

“Otherwise, the Holliday junction is collectively processed by the BLM-TOPOIII-RMI1-RMI2 complex, GEN1 endonuclease, the MUS81-EME1 complex and the SLX1-SLX4 complex [Chang et al., 2008; Ciccia et al., 2008; Xu et al., 2008; Fekairi et al., 2009; Rass et al., 2010].”

What the sources say

• Not checked yetcites Chang et al., 2008
• Not checked yetcites Ciccia et al., 2008
• Not checked yetcites Xu et al., 2008

In the paper

“For example, tobacco smoke causes telomere shortening via oxidative stress [Valdes et al., 2005; McGrath et al., 2007; Song et al., 2010; Babizhayev and Yegorov, 2011].”

What the sources say

• Not checked yetcites Valdes et al., 2005
• Not checked yetcites McGrath et al., 2007
• Not checked yetcites Song et al., 2010

In the paper

“Surprisingly, telomere maintenance requires the presence of some of the same components of DSBR/NHEJ components—for example, Ku and the MRN complex—complicating our understanding of the exact mechanism of telomere stability [Maser and DePinho, 2004; Marcand, 2014].”

What the sources say

• Not checked yetcites Maser and DePinho, 2004
• Not checked yetcites Marcand, 2014

In the paper

“For the strand to invade the template DNA, RAD54 and RAD54B remove RAD51 and allow the 3′-OH group to prime synthesis by Polymerases δ, κ and ν [Mazin et al., 2010; Sebesta et al., 2013].”

What the sources say

• Not checked yetcites Mazin et al., 2010
• Not checked yetcites Sebesta et al., 2013

In the paper

“Telomeres are well-conserved nucleoprotein structures found at the end of linear chromosomes that help differentiate normal chromosomal ends from DSBs [Longhese, 2008; Shammas, 2011].”

What the sources say

• Not checked yetcites Longhese, 2008
• Not checked yetcites Shammas, 2011

In the paper

“If the new DNA synthesis stops after a limited distance, as is the case in SDSA, the RTEL1 enzyme dissolves the D-loop [Barber et al., 2008].”

What the sources say

• Not checked yetcites Barber et al., 2008

In the paper

“Obesity has also been associated with accelerated shortening of telomeres in adipose tissue of mice, where levels of ROS were high [Song et al., 2010].”

What the sources say

• Not checked yetcites Song et al., 2010

In the paper

“Deprotected telomeres elicit a DNA damage response, recruiting DSBR components that attempt to repair the exposed ends, causing deleterious nucleolytic degradation, recombination, and chromosomal fusions [Longhese, 2008].”

What the sources say

• Not checked yetcites Longhese, 2008

In the paper

“Likewise, white blood cells of obese women harbor shorter telomeres than lean women [Valdes et al., 2005].”

What the sources say

• Not checked yetcites Valdes et al., 2005

In the paper

“However, robust DNA repair and damage tolerance pathways help remove or tolerate the lesions to allow survival (Figure 4).”

In the paper

“Finally, everyday stresses, including psychological stress, is known to shorten telomeres, whereas meditation and mindfulness may bring about an opposite effect [Epel et al., 2004; Cherkas et al., 2006; Simon et al., 2006; Epel et al., 2009; Mathur et al., 2016].”

What the sources say

• Not checked yetcites Epel et al., 2004
• Not checked yetcites Cherkas et al., 2006
• Not checked yetcites Simon et al., 2006

In the paper

“Critically shortened telomeres are associated with aging and cancer [Shammas, 2011].”

What the sources say

• Not checked yetcites Shammas, 2011

In the paper

“Genotoxic stressors such as certain pollutants (e.g. toluene and benzene, and PAHs) are also associated with telomere shortening [Hoxha et al., 2009; Pavanello et al., 2010; Trusina, 2014].”

What the sources say

• Not checked yetcites Hoxha et al., 2009
• Not checked yetcites Pavanello et al., 2010
• Not checked yetcites Trusina, 2014

In the paper

“Finally, everyday stresses, including psychological stress, is known to shorten telomeres, whereas meditation and mindfulness may bring about an opposite effect [Epel et al., 2004; Cherkas et al., 2006; Simon et al., 2006; Epel et al., 2009; Mathur et al., 2016].”

What the sources say

• Not checked yetcites Epel et al., 2009
• Not checked yetcites Mathur et al., 2016

In the paper

“Unresolved DNA damages are implicated in human diseases and cancers.”