CoChat
Sign Up
Cited by 44

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Tissue-specific knockouts of ACAT2 reveal that intestinal depletion is sufficient to prevent diet-induced cholesterol accumulation in the liver and blood

Zhang, Jun, Kelley, Kathryn L., Marshall, Stephanie M., Davis, Matthew A., Wilson, Martha D., Sawyer, Janet K., Farese, Robert V., Brown, J.Mark, Rudel, Lawrence L.·2012·Journal of Lipid Research
DOI 10.1194/jlr.m024356
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1194/jlr.m024356

Cites

1 of 1 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

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?

  • Free cholesterol deposited into the inner leaflet of the apical plasma membrane by NPC1L1 must subsequently move to the endoplasmic reticulum to be esterified by ACAT2.

    “Free cholesterol deposited into the inner leaflet of the apical PM by NPC1L1 must subsequently move to the ER to be esterified by ACAT2 (3–5).”

    From Aster-dependent nonvesicular transport facilitates dietary cholesterol uptake (2023) · cites this paper as [5]

    The Abstract identifies ACAT2 as an enzyme that uses free cholesterol to synthesize cholesteryl esters in intestinal cells. The Discussion describes NPC1L1-mediated uptake from the intestinal lumen, but neither passage establishes that NPC1L1 deposits cholesterol in the inner leaflet of the apical membrane or that it must then move to the ER. Page numbers are not available in our copy. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Both NPC1L1 and ACAT2 are key players in cholesterol absorption.

    “both proteins are recognized to be key players in the process of cholesterol absorption (5, 6).”

    From Aster-dependent nonvesicular transport facilitates dietary cholesterol uptake (2023) · cites this paper as [5]

  • ACAT2 is involved in cholesterol esterification.

    “the role of ACAT2 in cholesterol esterification are well documented”

    From Aster-dependent nonvesicular transport facilitates dietary cholesterol uptake (2023) · cites this paper as [5]

  • NPC1L1 facilitates entry of cholesterol into enterocytes.

    “The involvement of NPC1L1 in facilitating the entry of cholesterol into enterocytes”

    From Aster-dependent nonvesicular transport facilitates dietary cholesterol uptake (2023) · cites this paper as [5]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 28

  1. Joyce, 1999, Acyl-coenzyme A:cholesteryl acyltransferase 2, Curr. Opin. Lipidol., 10, 89, 10.1097/00041433-199904000-00002 · DOI
  2. Lee, 2004, Plasma cholesteryl esters provided by lecithin:cholesterol acyltransferase and acyl-coenzyme a:cholesterol acyltransferase 2 have opposite atherosclerotic potential, Circ. Res., 95, 998, 10.1161/01.RES.0000147558.15554.67 · DOI · Paper page
  3. Willner, 2003, Deficiency of acyl CoA:cholesterol acyltransferase 2 prevents atherosclerosis in apolipoprotein E-deficient mice, Proc. Natl. Acad. Sci. USA, 100, 1262, 10.1073/pnas.0336398100 · DOI
  4. Bell, 2006, Liver-specific inhibition of acyl-coenzyme a:cholesterol acyltransferase 2 with antisense oligonucleotides limits atherosclerosis development in apolipoprotein B100-only low-density lipoprotein receptor−/− mice, Arterioscler. Thromb. Vasc. Biol., 26, 1814, 10.1161/01.ATV.0000225289.30767.06 · DOI
  5. Brown, 2008, Targeted depletion of hepatic ACAT2-driven cholesterol esterification reveals a non-biliary route for fecal neutral sterol loss, J. Biol. Chem., 283, 10522, 10.1074/jbc.M707659200 · DOI
  6. Alger, 2010, Inhibition of acyl-coenzyme A:cholesterol acyltransferase 2 (ACAT2) prevents dietary cholesterol-associated steatosis by enhancing hepatic triglyceride mobilization, J. Biol. Chem., 285, 14267, 10.1074/jbc.M110.118422 · DOI
  7. Nguyen, 2012, Cholesterol esterification by ACAT2 is essential for efficient intestinal cholesterol absorption: evidence from thoracic lymph duct cannulation, J. Lipid Res., 53, 95, 10.1194/jlr.M018820 · DOI · Paper page
  8. Grundy, 1983, Absorption and metabolism of dietary cholesterol, Annu. Rev. Nutr., 3, 71, 10.1146/annurev.nu.03.070183.000443 · DOI
  9. Heider, 1983, Role of acyl CoA:cholesterol acyltransferase in cholesterol absorption and its inhibition by 57–118 in the rabbit, J. Lipid Res., 24, 1127, 10.1016/S0022-2275(20)37895-0 · DOI
  10. Krause, 1993, In vivo evidence that the lipid-regulating activity of the ACAT inhibitor CI-976 in rats is due to inhibition of both intestinal and liver ACAT, J. Lipid Res., 34, 279, 10.1016/S0022-2275(20)40755-2 · DOI
  11. Lee, 1996, Inhibitors of acyl-CoA: cholesterol O-acyl transferase (ACAT) as hypocholesterolemic agents. CI-1011: an acyl sulfamate with unique cholesterol-lowering activity in animals fed noncholesterol-supplemented diets, J. Med. Chem., 39, 5031, 10.1021/jm960674d · DOI
  12. Ramharack, 1998, CI-1011 lowers lipoprotein(a) and plasma cholesterol concentrations in chow-fed cynomolgus monkeys, Atherosclerosis, 136, 79, 10.1016/S0021-9150(97)00189-5 · DOI
  13. Suckling, 1985, Role of acyl-CoA: cholesterol acyltransferase in cellular cholesterol metabolism, J. Lipid Res., 26, 647, 10.1016/S0022-2275(20)34322-4 · DOI
  14. Buhman, 2000, Resistance to diet-induced hypercholesterolemia and gallstone formation in ACAT2-deficient mice, Nat. Med., 6, 1341, 10.1038/82153 · DOI · Paper page
  15. Repa, 2004, ACAT2 deficiency limits cholesterol absorption in the cholesterol-fed mouse: impact on hepatic cholesterol homeostasis, Hepatology, 40, 1088, 10.1002/hep.20439 · DOI
  16. Temel, 2005, Intestinal cholesterol absorption is substantially reduced in mice deficient in both ABCA1 and ACAT2, J. Lipid Res., 46, 2423, 10.1194/jlr.M500232-JLR200 · DOI
  17. Turley, 2010, Multiple mechanisms limit the accumulation of unesterified cholesterol in the small intestine of mice deficient in both ACAT2 and ABCA1, Am. J. Physiol. Gastrointest. Liver Physiol., 299, G1012, 10.1152/ajpgi.00190.2010 · DOI
  18. Lee, 2000, Differential expression of ACAT1 and ACAT2 among cells within liver, intestine, kidney, and adrenal of nonhuman primates, J. Lipid Res., 41, 1991, 10.1016/S0022-2275(20)32360-9 · DOI
  19. Parini, 2004, ACAT2 is localized to hepatocytes and is the major cholesterol-esterifying enzyme in human liver, Circulation, 110, 2017, 10.1161/01.CIR.0000143163.76212.0B · DOI
  20. Rudel, 1997, Hepatic origin of cholesteryl oleate in coronary artery atherosclerosis in African green monkeys. Enrichment by dietary monounsaturated fat, J. Clin. Invest., 100, 74, 10.1172/JCI119524 · DOI
  21. Goodman, 1962, The metabolism of chylomicron cholesterol ester in the rat, J. Clin. Invest., 41, 1886, 10.1172/JCI104645 · DOI
  22. Goodman, 1965, Cholesterol ester metabolism, Physiol. Rev., 45, 747, 10.1152/physrev.1965.45.4.747 · DOI
  23. Beltroy, 2007, Lysosomal unesterified cholesterol content correlates with liver cell death in murine Niemann-Pick type C disease, J. Lipid Res., 48, 869, 10.1194/jlr.M600488-JLR200 · DOI
  24. Beltroy, 2005, Cholesterol accumulation and liver cell death in mice with Niemann-Pick type C disease, Hepatology, 42, 886, 10.1002/hep.20868 · DOI
  25. Ramirez, 2011, Quantitative role of LAL, NPC2, and NPC1 in lysosomal cholesterol processing defined by genetic and pharmacological manipulations, J. Lipid Res., 52, 688, 10.1194/jlr.M013789 · DOI
  26. Ballantyne, 2005, Dose-comparison study of the combination of ezetimibe and simvastatin (Vytorin) versus atorvastatin in patients with hypercholesterolemia: the Vytorin Versus Atorvastatin (VYVA) study, Am. Heart J., 149, 464, 10.1016/j.ahj.2004.11.023 · DOI
  27. Bays, 2001, Effectiveness and tolerability of ezetimibe in patients with primary hypercholesterolemia: pooled analysis of two phase II studies, Clin. Ther., 23, 1209, 10.1016/S0149-2918(01)80102-8 · DOI
  28. van Heek, 2000, Comparison of the activity and disposition of the novel cholesterol absorption inhibitor, SCH58235, and its glucuronide, SCH60663, Br. J. Pharmacol., 129, 1748, 10.1038/sj.bjp.0703235 · DOI

Cited by

Sorted by citations

Metadata

Authors
Zhang, J., Kelley, K. L., Marshall, S. M., Davis, M. A., Wilson, M. D., Sawyer, J. K., Farese, R. V., Brown, J. M., & Rudel, L. L.
Venue
Journal of Lipid Research
Publisher
Elsevier BV
Published
2012-06
Volume
53
Issue
6
Pages
1144-1152
ISSN
0022-2275
DOI
10.1194/jlr.m024356
Cited by
44
References
1
Language
en
Licence

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.

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