Evidence map›Paper›PMID 22808311›Full record

ArticleCommunicative & integrative biology2012

The role of Connexin 46 promoter in lens and other hypoxic tissues.

Samuel A Molina, Dolores J Takemoto

Open access · goldAbstract read
In one paragraph

Article in Communicative & integrative biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Mutations of CX46/CX50 and Cataract Development.Frontiers in molecular biosciences · 2022
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Altered ubiquitin causes perturbed calcium homeostasis, hyperactivation of calpain, dysregulated differentiation, and cataract.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  9. 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.

Samuel A MolinaDepartment of Biochemistry; Kansas State University; Manhattan, KS USA.
Dolores J Takemoto
Kansas State University · US

Funding

PROTEIN KINASE C IN THE LENSR01EY013421 · NEI · KANSAS STATE UNIVERSITY · PI TAKEMOTO, DOLORES JEAN · 2001 to 2010
$3.0M
NEI NIH HHS R01 EY013421
6 · The paper itself

Abstract

Gap junctions are multimeric membrane protein channels that connect the cytoplasm of one cell to another. Much information about connexins regards electrophysiology and channel function but relatively little information is known about non-channel functions of connexins. Lens connexins, Cx43, Cx46 and Cx50, have been extensively studied for their role in lens homeostasis. Connexins allow the movement of small metabolically relevant molecules and ions between cells and this action in the lens prevents cataract formation. Interruption of Cx46 channel function leads to cataract formation due to dysregulation of lens homeostasis. The loss of Cx46 upregulates Cx43 in lens cell culture and suppresses tumor growth in breast and retinoblastoma tumor xenografts. Upregulation of Cx46 in hypoxic tissues has been noted and may be due in part to the effects of hypoxia and HIF activators. Here, we report that the Cx46 promoter is regulated by hypoxia and also offer speculation about the role of Cx46 in lens differentiation and solid tumor growth.

Indexed as

cellular differentiationConnexin 43Connexin 46connexin promoterhypoxialenstumorsxenografts

Identifiers

PMID22808311
PMCPMC3376042
OpenAlexW2066253577

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.