THE CELLULAR SRC GENE-PRODUCT REGULATES JUNCTIONAL CELL-TO-CELL COMMUNICATION
THE CELLULAR SRC GENE-PRODUCT REGULATES JUNCTIONAL CELL-TO-CELL COMMUNICATION
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DOI：
10.1126/science.2447651
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发表时间：
1988-01-22
期刊：
影响因子：
56.9
通讯作者：
LOEWENSTEIN, WR
中科院分区：
文献类型：
--
作者：
AZARNIA, R;REDDY, S;LOEWENSTEIN, WR
NIH 3T3细胞中细胞src基因的过度表达导致400- 700道尔顿范围内分子在细胞间传递的减少。这种缝隙连接通讯的下调与基因产物蛋白酪氨酸激酶pp60c-src的活性相关。Tyr527点突变（pp60c-src中磷酸化并抑制激酶活性的位点）或将病毒-src替换为细胞-src的羧基端编码区，从而增强了下调。Tyr416 （Tyr527突变磷酸化位点）的突变抑制了Tyr527突变和基因过表达对通讯的下调。src对通讯的调控可能在胚胎发育和细胞生长的控制中起重要作用。
Overexpression of the cellular src gene in NIH 3T3 cells causes reduction of cell-to-cell transmission of molecules in the 400- to 700-dalton range. This down-regulation of gap junctional communication correlates with the activity of the gene product, the protein tyrosine kinase pp60c-src. The down-regulation was enhanced by point mutation of Tyr527 (a site that is phosphorylated in pp60c-src and that inhibits kinase activity) or by substitution of the viral-src for the cellular-src carboxyl-terminal coding region. Mutation of Tyr416 (a site phosphyrlated upon Tyr527 mutation) suppresses both the down-regulation of communication by Tyr527 mutation and that by gene overexpression. The regulation of communication by src may be important in the control of embryonic development and cellular growth.