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PKC phosphorylation disrupts gap junctional communication at G0/S phase in clone 9 cells.

Abstract：

:Gap junctional communication during the progression of cell cycle from quiescent G0 to S phase was examined in cultured clone 9 rat liver cells. The transfer of scrape-loaded fluorescent dye was suppressed immediately after the stimulation of cell cycle progression in a synchronized cell population. Northern blot analysis showed that the temporal disturbance of gap junctional communication in cells passing from G0 to S phase did not result from transcriptional down-regulation of connexin 43. It was also found that the PKC inhibitor, calphostin C, was able to restore intercellular communication in serum stimulated cells. Data suggest a control mechanism by PKC mediated phosphorylation in the regulation of gap junction function which is vulnerable to cell cycling. The loss of gap junctional communication correlated with the increased phosphorylation of connexin 43 on serine residues in clone 9 cells.

journal_name

Mol Cell Biochem

journal_title

Molecular and cellular biochemistry

authors

Koo SK,Kim DY,Park SD,Kang KW,Joe CO

doi

10.1023/a:1006831114120

subject

Has Abstract

pub_date

1997-02-01 00:00:00

pages

41-9

issue

1-2

eissn

0300-8177

issn

1573-4919

journal_volume

167

pub_type

杂志文章

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