A DNA damage and stress inducible G protein-coupled receptor blocks cells in G2/M.

A DNA damage and stress inducible G protein-coupled receptor blocks cells in G2/M.
复制标题

DOI:
10.1073/pnas.95.21.12334
复制
发表时间:
1998-10
影响因子:
11.1
通讯作者:
Zhigang Weng;Zhigang Weng;Anne Catherine Fluckiger;Anne Catherine Fluckiger;S. Nisitani;Matthew I. Wahl;Lu Q. Le;Charity A. Hunter;Anthony A. Fernal;M. L. Beau;Owen N. Witte
Zhigang Weng;Zhigang Weng;Anne Catherine Fluckiger;Anne Catherine Fluckiger;S. Nisitani;Matthew I. Wahl;Lu Q. Le;Charity A. Hunter;Anthony A. Fernal;M. L. Beau;Owen N. Witte
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Zhigang Weng;Zhigang Weng;Anne Catherine Fluckiger;Anne Catherine Fluckiger;S. Nisitani;Matthew I. Wahl;Lu Q. Le;Charity A. Hunter;Anthony A. Fernal;M. L. Beau;Owen N. Witte

文献摘要

被引文献

相似文献

Cell cycle progression is monitored by highly coordinated checkpoint machinery, which is activated to induce cell cycle arrest until defects like DNA damage are corrected. We have isolated an anti-proliferative cell cycle regulator named G2A (for G2 accumulation), which is predominantly expressed in immature T and B lymphocyte progenitors and is a member of the seven membrane-spanning G protein-coupled receptor family. G2A overexpression attenuates the transformation potential of BCR-ABL and other oncogenes, and leads to accumulation of cells at G2/M independently of p53 and c-Abl. G2A can be induced in lymphocytes and to a lesser extent in nonlymphocyte cell lines or tissues by multiple stimuli including different classes of DNA-damaging agents and serves as a response to damage and cellular stimulation which functions to slow cell cycle progression.