Evidence map›Paper›PMID 10085299›Full record

ArticleThe Journal of cell biology1999

Dissection of the molecular basis of pp60(v-src) induced gating of connexin 43 gap junction channels.

L Zhou, E M Kasperek, B J Nicholson

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 157 citations in OpenAlex.

  1. Cx45 regulation by kinases and impact of expression in heart failure.Journal of molecular and cellular cardiology · 2025
    Article
  2. Article
  3. Review
  4. Article
  5. The Role of Connexin 43 in Lung Disease.Life (Basel, Switzerland) · 2020
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Protein⁻Protein Interactions with Connexin 43: Regulation and Function.International journal of molecular sciences · 2018
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Role of connexins and pannexins in cardiovascular physiology.Cellular and molecular life sciences : CMLS · 2015
    Review
  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.

L ZhouDepartment of Biological Sciences, State University of New York at Buffalo, Buffalo, New York 14260, USA.
E M Kasperek
B J Nicholson
University at Buffalo, State University of New York · US

Funding

MECHANISMS OF CONTROL OF CELL GROWTH BY GAP JUNCTIONSR01CA048049 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI NICHOLSON, BRUCE J · 1989 to 2003
$1.1M
NCI NIH HHS CA 48049NCI NIH HHS R01 CA048049NIGMS NIH HHS GM 48773
6 · The paper itself

Abstract

Suppression of gap-junctional communication by various protein kinases, growth factors, and oncogenes frequently correlates with enhanced mitogenesis. The oncogene v-src appears to cause acute closure of gap junction channels. Tyr265 in the COOH-terminal tail of connexin 43 (Cx43) has been implicated as a potential target of v-src, although v-src action has also been associated with changes in serine phosphorylation. We have investigated the mechanism of this acute regulation through mutagenesis of Cx43 expressed in Xenopus laevis oocyte pairs. Truncations of the COOH-terminal domain led to an almost complete loss of response of Cx43 to v-src, but this was restored by coexpression of the independent COOH-terminal polypeptide. This suggests a ball and chain gating mechanism, similar to the mechanism proposed for pH gating of Cx43, and K+ channel inactivation. Surprisingly, we found that v-src mediated gating of Cx43 did not require the tyrosine site, but did seem to depend on the presence of two potential SH3 binding domains and the mitogen-activated protein (MAP) kinase phosphorylation sites within them. Further point mutagenesis and pharmacological studies in normal rat kidney (NRK) cells implicated MAP kinase in the gating response to v-src, while the stable binding of v-src to Cx43 (in part mediated by SH3 domains) did not correlate with its ability to mediate channel closure. This suggests a common link between closure of gap junctions by v-src and other mitogens, such as EGF and lysophosphatidic acid (LPA).

Indexed as

Gap JunctionsIon Channel GatingAnimalsBase SequenceCalcium-Calmodulin-Dependent Protein KinasesCell LineConnexin 43DNA PrimersEnzyme ActivationFemaleMutagenesis, Site-DirectedOncogene Protein pp60(v-src)PhosphorylationRatsTyrosineXenopusCalcium-Calmodulin-Dependent Protein KinasesConnexin 43DNA PrimersOncogene Protein pp60(v-src)Tyrosine

Identifiers

PMID10085299
PMCPMC2148195
OpenAlexW2030405538

What Socratic holds

Texttitle and abstract
LicenceCC BY-NC-SA
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 Socratic graph.