| PI3K/Akt signaling is involved in the disruption of gap junctional communication caused by v-Src and TNF-α. | |
| | |
MedLine Citation:
|
PMID: 20727856 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
Gap junctional communication, which is mediated by the connexin protein family, is essential for the maintenance of normal tissue function and homeostasis. Loss of intercellular communication results in a failure to coordinately regulate cellular functions, and it can facilitate tumorigenesis. Expression of oncogenes and stimulation with cytokines has been shown to suppress intercellular communication; however, the exact mechanism by which intercellular communication is disrupted by these factors remains uncertain. In this report, we show that Akt is essential for the disruption of gap junctional communication in v-Src-transformed cells. In addition, inhibition of Akt restores gap junctional communication after it is suppressed by TNF-α signaling. Furthermore, we demonstrate that the expression of a constitutively active form of Akt1, but not of Akt2 or Akt3, is sufficient to suppress gap junctional communication. Our results clearly define Akt1 as one of the critical regulators of gap junctional communication. |
| | |
Authors:
|
Satoko Ito; Toshinori Hyodo; Hitoki Hasegawa; Hong Yuan; Michinari Hamaguchi; Takeshi Senga |
Related Documents
:
|
717556 - Communality of surnames: a measures of biological interrelationships among thirty-one s... 6864636 - Language and communication problems in an asian community. 21790876 - Problems and consequences in the use of professional interpreters: qualitative analysis... 3990256 - Communication apprehension in esophageal and tracheoesophageal speakers. 15812926 - Bangkok 2004. sex workers and law reform in south africa. 2915866 - Brief sexual inquiry in gynecologic practice. |
Publication Detail:
|
Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-08-19 |
Journal Detail:
|
Title: Biochemical and biophysical research communications Volume: 400 ISSN: 1090-2104 ISO Abbreviation: Biochem. Biophys. Res. Commun. Publication Date: 2010 Sep |
Date Detail:
|
Created Date: 2010-09-20 Completed Date: 2010-10-13 Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 0372516 Medline TA: Biochem Biophys Res Commun Country: United States |
Other Details:
|
Languages: eng Pagination: 230-5 Citation Subset: IM |
Copyright Information:
|
Copyright © 2010 Elsevier Inc. All rights reserved. |
Affiliation:
|
Division of Cancer Biology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
1-Phosphatidylinositol 3-Kinase
/
genetics,
metabolism* Animals Cell Communication* Cell Line, Transformed Gap Junctions / enzymology, physiology* Mice Oncogene Protein pp60(v-src) / metabolism Proto-Oncogene Proteins c-akt / genetics, metabolism* Rats Signal Transduction Tumor Necrosis Factor-alpha / metabolism |
| Chemical | |
Reg. No./Substance:
|
0/Tumor Necrosis Factor-alpha; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 2.7.10.2/Oncogene Protein pp60(v-src); EC 2.7.11.1/Proto-Oncogene Proteins c-akt |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: The Dad1 subunit of the yeast kinetochore Dam1 complex is an intrinsically disordered protein.
Next Document: Ribosomal protein L2 associates with E. coli HtpG and activates its ATPase activity.