Gillet G, Guerin M, Trembleau A, Brun G
Laboratoire de Biologie Moléculaire et Cellulaire, UMR 49 CNRS, LA-INRA, ENS Lyon, France.
EMBO J. 1995 Apr 3;14(7):1372-81. doi: 10.1002/j.1460-2075.1995.tb07123.x.
The oncoprotein p60v-src encoded by the Rous sarcoma virus (RSV) genome is the prototype of non-receptor tyrosine kinases. More than 50 targets of p60v-src have been described to date. However, the precise mechanisms of RSV transformation remain to be elucidated. Here, we present the study of a new v-src-activated gene, NR-13, which encodes a protein identified as a new member of the Bcl-2 family. This protein is localized in the membrane with a pattern already observed with Bcl-2. In quail embryos, this gene is mainly expressed in neural and muscular tissues. Its expression is dramatically down-regulated after embryonic day 7 (E7) in the optic tectum. To evaluate a possible role for NR-13 in the control of apoptotic processes in this particular brain area, in situ hybridization and DNA ladder fractionation studies were performed to correlate NR-13 expression with typical situations of apoptosis during brain development. Our results support the idea that RSV could activate anti-apoptotic functions of the host cell resulting in an increase of their lifespan, which could be particularly relevant to tumour formation.
劳氏肉瘤病毒(RSV)基因组编码的癌蛋白p60v-src是非受体酪氨酸激酶的原型。迄今为止,已描述了p60v-src的50多个靶点。然而,RSV转化的确切机制仍有待阐明。在此,我们展示了对一个新的v-src激活基因NR-13的研究,该基因编码一种被鉴定为Bcl-2家族新成员的蛋白质。这种蛋白质定位于细胞膜,其模式与Bcl-2已观察到的模式相同。在鹌鹑胚胎中,该基因主要在神经和肌肉组织中表达。在视顶盖中,其表达在胚胎第7天(E7)后显著下调。为了评估NR-13在该特定脑区凋亡过程控制中的可能作用,进行了原位杂交和DNA梯状条带分析研究,以将NR-13表达与脑发育过程中典型的凋亡情况相关联。我们的结果支持这样一种观点,即RSV可能激活宿主细胞的抗凋亡功能,从而延长其寿命,这可能与肿瘤形成特别相关。