Transformation by v-sis occurs by an internal autoactivation mechanism.

Transformation by v-sis occurs by an internal autoactivation mechanism.
复制标题

v-sis 的转化是通过内部自动激活机制发生的。

DOI:
10.1126/science.2551043
复制
发表时间:
1989
期刊:
Science (New York, N.Y.)
影响因子:
--
通讯作者:
Deuel,TF
Deuel,TF
中科院分区:
--
文献类型:
--
作者:
Bejcek,BE;Li,DY;Deuel,TF

文献摘要

参考文献

被引文献

相似文献

v-sis基因的转化似乎需要其蛋白产物p28 v-sis与血小板衍生生长因子(PDGF)受体的相互作用。然而,这种相互作用可能不会发生在细胞表面所预测的自分泌假说,因为表型转化不逆转孵育的SSV-NRK细胞与抗血清PDGF和因为形态学转化没有发生时,nontransformed NRK细胞连续培养p28 v-sis。构建了野生型v-sis基因的突变体,其编码针对内质网和高尔基体内保留的v-sis蛋白。NRK细胞表达的突变体v-sis基因没有分泌任何可检测的v-sis蛋白,但完全转化为野生型v-sis转染。结果支持了v-sisin转化的机制,即PDGF受体的内部激活发生在细胞表面p28 v-sisin或PDGF受体表达之前。
Transformation by the v-sisoncogene appears to require an interaction of its protein product, p28v-sis, with the receptor for the platelet-derived growth factor (PDGF). However, this interaction may not occur at the cell surface as predicted by the autocrine hypothesis because phenotypic transformation was not reversed by incubation of SSV-NRK cells with antisera to PDGF and because morphological transformation did not occur when nontransformed NRK cells were cultured continuously with p28v-sis. A mutant of the wild-type v-sisgene was constructed that encodes a v-sisprotein targeted for retention within the endoplasmic reticulum and Golgi. NRK cells expressing the mutant v-sisgene did not secrete any detectable v-sisprotein but were as fully transformed as wild-type v-sistransfectants. The results support a mechanism of transformation by v-sisin which internal activation of the PDGF receptor occurs before expression of either p28v-sisor the PDGF receptor at the cell surface.
DOI: --
发表时间: 1988
期刊: The Journal of biological chemistry
影响因子: --
作者:
Huang,SS;Huang,JS
通讯作者: Huang,JS
DOI: 10.1126/science.6304883
发表时间: 1983-01-01
期刊: SCIENCE
影响因子: 56.9
作者:
DOOLITTLE, RF;HUNKAPILLER, MW;ANTONIADES, HN
通讯作者: ANTONIADES, HN
患有纤维肉瘤的绒毛猴(Lagothrix spp.)肿瘤组织中的 C 型病毒。
DOI: 10.1093/jnci/47.4.881
发表时间: 1971
期刊: Journal of the National Cancer Institute
影响因子: --
作者:
G. Theilen;D. Gould;M. Fowler;D. Dungworth
通讯作者: D. Dungworth
DOI: 10.1126/science.6293053
发表时间: 1982-01-01
期刊: SCIENCE
影响因子: 56.9
作者:
ROBBINS, KC;DEVARE, SG;AARONSON, SA
通讯作者: AARONSON, SA
生长因子活性在肿瘤发生中的作用。
DOI: --
发表时间: 1984
期刊: Blood
影响因子: 20.3
作者:
Deuel,TF;Huang,JS
通讯作者: Huang,JS