Evidence map›Paper›PMID 23396488›Full record

ArticleGlycobiology2013

A non-enzymatic function of Golgi glycosyltransferases: mediation of Golgi fragmentation by interaction with non-muscle myosin IIA.

Armen Petrosyan, Pi-Wan Cheng

Open access · greenAbstract read
In one paragraph

Article in Glycobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  4. Review
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  8. Article
  9. Unlocking Golgi: Why Does Morphology Matter?Biochemistry. Biokhimiia · 2019
    Review
  10. Article
  11. Article
  12. THE IMPACT OF ALCOHOL ON PRO-METASTATIC N-GLYCOSYLATION IN PROSTATE CANCER.Krimskii zhurnal eksperimental'noi i klinicheskoi meditsiny = Kryms'kyi zhurnal eksperymental'noi ta klinichnoi medytsyny = Crimean journal of experimental and clinical medicine · 2018
    Article
  13. Article
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  19. Onco-Golgi: Is Fragmentation a Gate to Cancer Progression?Biochemistry & molecular biology journal
    Article
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

2 authors at 1 institution in 1 country.

Armen PetrosyanDepartment of Research Service, VA Nebraska-Western Iowa Health Care System, Omaha, NE 68105 USA.
Pi-Wan Cheng
VA Nebraska Western Iowa Health Care System · US

Funding

BIOSYNTHESIS OF TRACHEAL MUCOUS GLYCOPROTEINSR01HL048282 · NHLBI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI CHENG, PI-WAN · 1995 to 2010
$2.2M
Control of Mucin Glycan Branching in Membrane-bound and Secreted MucinsR21HL097238 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI CHENG, PI-WAN · 2009 to 2010
$385k
NHLBI NIH HHS 1R21HL097238NHLBI NIH HHS 2R01HL48282
6 · The paper itself

Abstract

The Golgi apparatus undergoes morphological changes under stress or malignant transformation, but the precise mechanisms are not known. We recently showed that non-muscle myosin IIA (NMIIA) binds to the cytoplasmic tail of Core 2 N-acetylglucosaminyltransferase mucus-type (C2GnT-M) and transports it to the endoplasmic reticulum for recycling. Here, we report that Golgi fragmentation induced by brefeldin A (BFA) or coatomer protein (β-COP) knockdown (KD) in Panc1-bC2GnT-M (c-Myc) cells is accompanied by the increased association of NMIIA with C2GnT-M and its degradation by proteasomes. Golgi fragmentation is prevented by inhibition or KD of NMIIA. Using multiple approaches, we have shown that the speed of BFA-induced Golgi fragmentation is positively correlated with the levels of this enzyme in the Golgi. The observation is reproduced in LNCaP cells which express high levels of two endogenous glycosyltransferases--C2GnT-L and β-galactoside α2,3 sialyltransferase 1. NMIIA is found to form complexes with these two enzymes but not Golgi matrix proteins. The KD of both enzymes or the prevention of Golgi glycosyltransferases from exiting endoplasmic reticulum reduced Golgi-associated NMIIA and decreased the BFA-induced fragmentation. Interestingly, the fragmented Golgi detected in colon cancer HT-29 cells can be restored to a compact morphology after inhibition or KD of NMIIA. The Golgi disorganization induced by the microtubule or actin destructive agent is NMIIA-independent and does not affect the levels of glycosyltransferases. We conclude that NMIIA interacts with Golgi residential but not matrix proteins, and this interaction is responsible for Golgi fragmentation induced by β-COP KD or BFA treatment. This is a novel non-enzymatic function of Golgi glycosyltransferases.

Indexed as

Benzhydryl Compoundsbeta-Galactoside alpha-2,3-SialyltransferaseBrefeldin ACoatomer ProteinEndoplasmic ReticulumGolgi ApparatusHeat-Shock ProteinsHEK293 CellsHT29 CellsHumansMolecular Motor ProteinsMyosin Heavy ChainsN-AcetylglucosaminyltransferasesProteasome Endopeptidase ComplexProtein BindingProteolysisBenzhydryl Compoundsbeta-1,3-galactosyl-O-glycosyl-glycoprotein beta-1,6-N-acetylglucosaminyltransferase 3beta-Galactoside alpha-2,3-SialyltransferaseBrefeldin ACoatomer ProteinHeat-Shock ProteinsKNK 437Molecular Motor ProteinsMYH9 protein, humanMyosin Heavy ChainsN-AcetylglucosaminyltransferasesProteasome Endopeptidase ComplexPyrrolidinonesSialyltransferasesST3GAL1 protein, humanTunicamycinbrefeldin Aglycosyltransferasenon-muscle myosin IIArestoration of fragmented Golgi in cancer cells to a compact phenotypestress-induced Golgi fragmentation

Identifiers

PMID23396488
PMCPMC3641799
OpenAlexW2082573621

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.