Evidence map›Paper›PMID 27066481›Full record

ArticleFrontiers in cell and developmental biology2016

COG Complex Complexities: Detailed Characterization of a Complete Set of HEK293T Cells Lacking Individual COG Subunits.

Jessica Bailey Blackburn, Irina Pokrovskaya, Peter Fisher, Daniel Ungar, Vladimir V Lupashin

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 69 citations in OpenAlex.

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  12. Rapid COG Depletion in Mammalian Cell by Auxin-Inducible Degradation System.Methods in molecular biology (Clifton, N.J.) · 2023
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  19. Golgi-Dependent Copper Homeostasis Sustains Synaptic Development and Mitochondrial Content.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    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

5 authors at 2 institutions in 2 countries.

Jessica Bailey BlackburnDepartment of Physiology and Biophysics, University of Arkansas for Medical Sciences Little Rock, AR, USA.
Irina PokrovskayaDepartment of Physiology and Biophysics, University of Arkansas for Medical Sciences Little Rock, AR, USA.
Peter FisherDepartment of Biology, University of York York, UK.
Daniel UngarDepartment of Biology, University of York York, UK.
Vladimir V LupashinDepartment of Physiology and Biophysics, University of Arkansas for Medical Sciences Little Rock, AR, USA.
University of Arkansas for Medical Sciences · USUniversity of York · GB

Funding

Characterization of mammalian COG complex-interacting intra-Golgi trafficking macR01GM083144 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI VLADIMIR V LUPASHIN · 2008 to 2026
$6.5M
Super-Res Holographic Microscopy to Advance Research on Golgi Apparatus FunctionU54GM105814 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI BROOKER, GARY, LUPASHIN, VLADIMIR V · 2013 to 2017
$2.1M
Biotechnology and Biological Sciences Research Council BB/J014443/1NIGMS NIH HHS R01 GM083144NIGMS NIH HHS U54 GM105814
6 · The paper itself

Abstract

The Conserved Oligomeric Golgi complex is an evolutionarily conserved multisubunit tethering complex (MTC) that is crucial for intracellular membrane trafficking and Golgi homeostasis. The COG complex interacts with core vesicle docking and fusion machinery at the Golgi; however, its exact mechanism of action is still an enigma. Previous studies of COG complex were limited to the use of CDGII (Congenital disorders of glycosylation type II)-COG patient fibroblasts, siRNA mediated knockdowns, or protein relocalization approaches. In this study we have used the CRISPR approach to generate HEK293T knock-out (KO) cell lines missing individual COG subunits. These cell lines were characterized for glycosylation and trafficking defects, cell proliferation rates, stability of COG subunits, localization of Golgi markers, changes in Golgi structure, and N-glycan profiling. We found that all KO cell lines were uniformly deficient in cis/medial-Golgi glycosylation and each had nearly abolished binding of Cholera toxin. In addition, all cell lines showed defects in Golgi morphology, retrograde trafficking and sorting, sialylation and fucosylation, but severities varied according to the affected subunit. Lobe A and Cog6 subunit KOs displayed a more severely distorted Golgi structure, while Cog2, 3, 4, 5, and 7 knock outs had the most hypo glycosylated form of Lamp2. These results led us to conclude that every subunit is essential for COG complex function in Golgi trafficking, though to varying extents. We believe that this study and further analyses of these cells will help further elucidate the roles of individual COG subunits and bring a greater understanding to the class of MTCs as a whole.

Indexed as

COG complexCRISPRglycan processingglycosylationGolgi apparatustoxin traffickingvesicle tethering

Identifiers

PMID27066481
PMCPMC4813393
OpenAlexW2301892632

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.