v-ras and protein kinase C dedifferentiate thyroid cells by down-regulating nuclear cAMP-dependent protein kinase A.
v-ras and protein kinase C dedifferentiate thyroid cells by down-regulating nuclear cAMP-dependent protein kinase A.
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v-ras 和蛋白激酶 C 通过下调核 cAMP 依赖性蛋白激酶 A 使甲状腺细胞去分化。
DOI：
10.1101/gad.6.9.1621
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发表时间：
1992
影响因子：
10.5
通讯作者：
Avvedimento,EV
中科院分区：
文献类型：
--
作者：
Gallo,A;Benusiglio,E;Bonapace,IM;Feliciello,A;Cassano,S;Garbi,C;Musti,AM;Gottesman,ME;Avvedimento,EV
RAS蛋白是一种膜相关的信号转导系统，可将永恒的刺激信号传递给未知的细胞内靶点。结构性激活的v-ras癌基因可诱导甲状腺细胞去分化。V-RAS似乎通过刺激蛋白激酶C(PKC)发挥作用，PKC抑制cAMP依赖的蛋白激酶A(PKA)催化亚单位的核迁移。因此，依赖于PKA磷酸化的核组织特异性和管家反式作用因子被灭活。从细胞核中排除PKA亚基可能代表了RAS和PKC对细胞生长和分化的多效性作用的一般机制。
Ras proteins are membrane-associated transducers of eternal stimuli to unknown intracellular targets. The constitutively activated v-ras oncogene induces dedifferentiation in thyroid cells. v-Ras appears to act by stimulating protein kinase C (PKC), which inhibits the nuclear migration of the catalytic subunit of the cAMP-dependent protein kinase A (PKA). Nuclear tissue-specific and housekeeping trans-acting factors that are dependent on phosphorylation by PKA are thus inactivated. Exclusion of the PKA subunit from the nucleus could represent a general mechanism for the pleiotropic effects of Ras and PKC on cellular growth and differentiation.