Evidence map›Paper›PMID 22772442›Full record

ReviewThe Journal of membrane biology2012

Degradation of connexins through the proteasomal, endolysosomal and phagolysosomal pathways.

Vivian Su, Kimberly Cochrane, Alan F Lau

Abstract readReview
PubMed Publisher
In one paragraph

Review in The Journal of membrane biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

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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 2 institutions in 1 country.

Vivian SuCancer Biology Program, University of Hawaii Cancer Center, University of Hawaii at Manoa, 651 Ilalo Street, BSB 222, Honolulu, HI 96813, USA. vsu@cc.hawaii.edu
Kimberly Cochrane
Alan F Lau
University of Hawaiʻi at Mānoa · USCancer Center of Hawaii · US

Funding

Regulation of Cx43 by Src and Novel Interacting ProteinsR01CA052098 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI LAU, ALAN F. F · 1991 to 2009
$2.6M
NCI NIH HHS CA052098-18
6 · The paper itself

Abstract

Connexins comprise gap junction channels, which create a direct conduit between the cytoplasms of adjacent cells and provide for intercellular communication. Therefore, the level of total cellular connexin protein can have a direct influence on the level of intercellular communication. Control of connexin protein levels can occur through different mechanisms during the connexin life cycle, such as by regulation of connexin gene expression and turnover of existing protein. The degradation of connexins has been extensively studied, revealing proteasomal, endolysosomal and more recently autophagosomal degradation mechanisms that modulate connexin turnover and, subsequently, affect intercellular communication. Here, we review the current knowledge of connexin degradation pathways.

Indexed as

AnimalsAutophagyConnexinsHumansLysosomesProteasome Endopeptidase ComplexConnexinsProteasome Endopeptidase Complex

Identifiers

PMID22772442
OpenAlexW2091457029

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.