| RRC ID |
38307
|
| 著者 |
Ito S, Hyodo T, Hasegawa H, Yuan H, Hamaguchi M, Senga T.
|
| タイトル |
PI3K/Akt signaling is involved in the disruption of gap junctional communication caused by v-Src and TNF-α.
|
| ジャーナル |
Biochem Biophys Res Commun
|
| Abstract |
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.
|
| 巻・号 |
400(2)
|
| ページ |
230-5
|
| 公開日 |
2010-9-17
|
| DOI |
10.1016/j.bbrc.2010.08.045
|
| PII |
S0006-291X(10)01540-8
|
| PMID |
20727856
|
| MeSH |
Animals
Cell Communication*
Cell Line, Transformed
Gap Junctions / enzymology
Gap Junctions / physiology*
Mice
Oncogene Protein pp60(v-src) / metabolism
Phosphatidylinositol 3-Kinases / genetics
Phosphatidylinositol 3-Kinases / metabolism*
Proto-Oncogene Proteins c-akt / genetics
Proto-Oncogene Proteins c-akt / metabolism*
Rats
Signal Transduction
Tumor Necrosis Factor-alpha / metabolism
|
| IF |
2.985
|
| 引用数 |
13
|
|
WOS 分野
|
BIOPHYSICS
BIOCHEMISTRY & MOLECULAR BIOLOGY
|
| リソース情報 |
| ヒト・動物細胞 |
|
