Evidence map›Paper›PMID 25315780›Full record

ArticleThe Journal of biological chemistry2014

Comparative gene identification-58 (CGI-58) promotes autophagy as a putative lysophosphatidylglycerol acyltransferase.

Jun Zhang, Dan Xu, Jia Nie, Ruili Han, Yonggong Zhai, Yuguang Shi

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  4. Review
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  8. Article
  9. CGI-58: Versatile Regulator of Intracellular Lipid Droplet Homeostasis.Advances in experimental medicine and biology · 2020
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Regulation of autophagy by mitochondrial phospholipids in health and diseases.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017
    Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Jun Zhangthe Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033 From the Beijing Key Laboratory of Gene Resource and Molecular Development and College of Life Sciences, Beijing Normal University, Beijing 100875, China and.
Dan Xuthe Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033.
Jia Niethe Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033.
Ruili Hanthe Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033.
Yonggong ZhaiFrom the Beijing Key Laboratory of Gene Resource and Molecular Development and College of Life Sciences, Beijing Normal University, Beijing 100875, China and ygzhai@bnu.edu.cn.
Yuguang Shithe Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033 yus11@psu.edu.
Pennsylvania State University · USBeijing Normal University · CN

Funding

Regulation of Mitochondrial Dysfunction in Diet-Induced Obesity by ALCAT-1R01DK076685 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SHI, YUGUANG · 2008 to 2017
$2.8M
Regulation of Mitochondrial Dysfunction in Diet-Induced Obesity by ALCAT-1R56DK076685 · NIDDK · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI SHI, YUGUANG · 2007 to 2013
$228k
NIDDK NIH HHS DK076685NIDDK NIH HHS R01 DK076685NIDDK NIH HHS R56 DK076685
6 · The paper itself

Abstract

CGI-58 is a lipid droplet-associated protein that, when mutated, causes Chanarin-Dorfman syndrome in humans, which is characterized by excessive storage of triglyceride in various tissues. However, the molecular mechanisms underlying the defect remain elusive. CGI-58 was previously reported to catalyze the resynthesis of phosphatidic acid as a lysophosphatidic acid acyltransferase. In addition to triglyceride, phosphatidic acid is also used a substrate for the synthesis of various mitochondrial phospholipids. In this report, we investigated the propensity of CGI-58 in the remodeling of various phospholipids. We found that the recombinant CGI-58 overexpressed in mammalian cells or purified from Sf9 insect cells catalyzed efficiently the reacylation of lysophosphatidylglycerol to phosphatidylglycerol (PG), which requires acyl-CoA as the acyl donor. In contrast, the recombinant CGI-58 was devoid of acyltransferase activity toward other lysophospholipids. Accordingly, overexpression and knockdown of CGI-58 adversely affected the endogenous PG level in C2C12 cells. PG is a substrate for the synthesis of cardiolipin, which is required for mitochondrial oxidative phosphorylation and mitophagy. Consequently, overexpression and knockdown of CGI-58 adversely affected autophagy and mitophagy in C2C12 cells. In support for a key role of CGI-58 in mitophagy, overexpression of CGI-58 significantly stimulated mitochondrial fission and translocation of PINK1 to mitochondria, key steps involved in mitophagy. Furthermore, overexpression of CGI-58 promoted mitophagic initiation through activation of 5'-AMP-activated protein kinase and inhibition of mTORC1 mammalian target of rapamycin complex 1 signaling, the positive and negative regulators of autophagy, respectively. Together, these findings identified novel molecular mechanisms by which CGI-58 regulates lipid homeostasis, because defective autophagy is implicated in dyslipidemia and fatty liver diseases.

Indexed as

Autophagy1-Acylglycerol-3-Phosphate O-AcyltransferaseAcyltransferasesAMP-Activated Protein KinasesAnimalsBlotting, WesternCell LineChlorocebus aethiopsCOS CellsHEK293 CellsHomeostasisHumansKineticsLipid DropletsLipid MetabolismLysophospholipids1-Acylglycerol-3-Phosphate O-AcyltransferaseABHD5 protein, humanAcyltransferasesAMP-Activated Protein KinaseslysophosphatidylglycerolLysophospholipidsMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesPhosphatidylglycerolsTOR Serine-Threonine KinasesAutophagyLipid DropletLipid MetabolismMammalian Target of Rapamycin (mTOR)Mitochondria

Identifiers

PMID25315780
PMCPMC4239649
OpenAlexW1983064244

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.