Evidence map›Paper›PMID 27535804›Full record

ArticleScientific reports2016

The role of Rab6a and phosphorylation of non-muscle myosin IIA tailpiece in alcohol-induced Golgi disorganization.

Armen Petrosyan, Carol A Casey, Pi-Wan Cheng

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 28 citations in OpenAlex.

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  16. Unlocking Golgi: Why Does Morphology Matter?Biochemistry. Biokhimiia · 2019
    Review
  17. Pluronic block copolymers enhance the anti-myeloma activity of proteasome inhibitors.Journal of controlled release : official journal of the Controlled Release Society · 2019
    Article
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

Armen PetrosyanDepartment of Biochemistry and Molecular Biology, College of Medicine, the Fred and Pamela Buffett Cancer Center, 985870 Nebraska Medical Center, Omaha, NE 68198-5870, USA.
Carol A CaseyDepartment of Internal Medicine, University of Nebraska Medical Center, Omaha, NE, USA.
Pi-Wan ChengDepartment of Biochemistry and Molecular Biology, College of Medicine, the Fred and Pamela Buffett Cancer Center, 985870 Nebraska Medical Center, Omaha, NE 68198-5870, USA.
Nebraska Medical Center · USUniversity of Nebraska Medical Center · USVA Nebraska Western Iowa Health Care System · US

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI James Eudy · 1985 to 2026
$55.0M
Research Pilot Project ProgramP30GM106397 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI JOHNSON, KEITH R · 2013 to 2017
$4.9M
Alcohol effect on Golgi morphology and functionK01AA022979 · NIAAA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PETROSYAN, ARMEN · 2014 to 2018
$544k
ZEISS META 510 CONFOCAL IMAGING SYSTEM: PROSTATE, PANCREATIC CANCER, LYMPHOMAS10RR019278 · NCRR · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI CHRISTMAN, JUDITH K · 2006 to 2006
$379k
Glycosyltransferase Golgi Retention MechanismI01BX000985 · VA · OMAHA VA MEDICAL CENTER · PI CHENG, PI-WAN · 2011 to 2015
–
BLRD VA I01 BX000985NCI NIH HHS P30 CA036727NCRR NIH HHS S10 RR019278NIAAA NIH HHS K01 AA022979NIGMS NIH HHS P30 GM106397
6 · The paper itself

Abstract

Abnormalities in the Golgi apparatus function are important to the development of alcoholic liver injury. We recently reported that Golgi disorganization in ethanol (EtOH)-treated hepatocytes is caused by impaired dimerization of the largest Golgi matrix protein, giantin. However, little is known about the mechanism which forces fragmentation. Here, in both HepG2 cells overexpressing alcohol dehydrogenase and in rat hepatocytes, we found that EtOH administration reduces the complex between giantin and Rab6a GTPase and results in the S1943 phosphorylation of non-muscle Myosin IIA (NMIIA) heavy chain, thus facilitating NMIIA association with Golgi enzymes, as detected by biochemical approaches and 3D Structured Illumination Microscopy. We revealed that NMIIA-P-S1943 competes with giantin for the Rab6a dimer, which was converted to monomer after Golgi fragmentation. Therefore, Rab6a plays a dual role in the Golgi, serving as master regulator of Golgi organization and disorganization, and that NMIIA and giantin engage in a "tug-of-war". However, the inhibition of F-actin and downregulation of NMIIA or overexpression of NMHC-IIAΔtailpiece, as well the overexpression of dominant negative Rab6a(T27N), preserved a compact Golgi phenotype. Thus, the actomyosin complex forces EtOH-induced Golgi disorganization, and the targeting of NMIIA-P-S1943 may be important for preventing the damaging effects of alcohol metabolism on the cell.

Indexed as

Alcohol DehydrogenaseAnimalsCell Culture TechniquesEthanolGolgi ApparatusGolgi Matrix ProteinsHepatocytesHep G2 CellsHumansMaleNonmuscle Myosin Type IIAPhosphorylationrab GTP-Binding ProteinsRats, WistarAlcohol DehydrogenaseEthanolGolgi Matrix ProteinsmacrogolginNonmuscle Myosin Type IIARab6 proteinrab GTP-Binding Proteins

Identifiers

PMID27535804
PMCPMC4989220
OpenAlexW2508264592

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.