Evidence map›Paper›PMID 26578865›Full record

ReviewFrontiers in neuroscience2015

Defects in the COG complex and COG-related trafficking regulators affect neuronal Golgi function.

Leslie K Climer, Maxim Dobretsov, Vladimir Lupashin

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

47 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Novel mutation ofMolecular genetics and metabolism reports · 2024
    Article
  7. Tumor TargetingMicroRNA (Shariqah, United Arab Emirates) · 2024
    Article
  8. Article
  9. Article
  10. Golgi-IP, a tool for multimodal analysis of Golgi molecular content.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Article
  12. Review
  13. GLIDER: function prediction from GLIDE-based neighborhoods.Bioinformatics (Oxford, England) · 2022
    Article
  14. Article
  15. Characterization of an Atypical eIF4E Ortholog inInternational journal of molecular sciences · 2021
    Article
  16. N-Glycomics of Human Erythrocytes.International journal of molecular sciences · 2021
    Article
  17. Article
  18. The role of the Golgi apparatus in disease (Review).International journal of molecular medicine · 2021
    Review
  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
  20. 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

3 authors at 1 institution in 1 country.

Leslie K ClimerDepartment of Physiology and Biophysics, College of Medicine, University of Arkansas for Medical Sciences Little Rock, AR, USA.
Maxim DobretsovDepartment of Anesthesiology, College of Medicine, University of Arkansas for Medical Sciences Little Rock, AR, USA.
Vladimir LupashinDepartment of Physiology and Biophysics, College of Medicine, University of Arkansas for Medical Sciences Little Rock, AR, USA.
University of Arkansas for Medical Sciences · US

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
NIGMS NIH HHS R01 GM083144NIGMS NIH HHS U54 GM105814
6 · The paper itself

Abstract

The Conserved Oligomeric Golgi (COG) complex is an evolutionarily conserved hetero-octameric protein complex that has been proposed to organize vesicle tethering at the Golgi apparatus. Defects in seven of the eight COG subunits are linked to Congenital Disorders of Glycosylation (CDG)-type II, a family of rare diseases involving misregulation of protein glycosylation, alterations in Golgi structure, variations in retrograde trafficking through the Golgi and system-wide clinical pathologies. A troublesome aspect of these diseases are the neurological pathologies such as low IQ, microcephaly, and cerebellar atrophy. The essential function of the COG complex is dependent upon interactions with other components of trafficking machinery, such as Rab-GTPases and SNAREs. COG-interacting Rabs and SNAREs have been implicated in neurodegenerative diseases like Alzheimer's disease and Parkinson's disease. Defects in Golgi maintenance disrupts trafficking and processing of essential proteins, frequently associated with and contributing to compromised neuron function and human disease. Despite the recent advances in molecular neuroscience, the subcellular bases for most neurodegenerative diseases are poorly understood. This article gives an overview of the potential contributions of the COG complex and its Rab and SNARE partners in the pathogenesis of different neurodegenerative disorders.

Indexed as

COGcongenital disorders of glycosylationconserved oligomeric Golgi complexglycosylationneurodegenerationRabSNAREvesicular trafficking

Identifiers

PMID26578865
PMCPMC4621299
OpenAlexW1857762931

What OpenQuestion holds

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LicenceCC BY
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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.