TY - JOUR
AU - 
AB - THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 273, No. 7, Issue of February 13, pp. 3799 –3802, 1998 Communication © 1998 by The American Society for Biochemistry and Molecular Biology, Inc. Printed in U.S.A. (12, 13), c-Abl-deficient cells are resistant to IR-induced apo- Regulation of Rad51 Function ptosis (14). Activation of c-Abl by genotoxic stress is associated by c-Abl in Response to DNA with interaction of c-Abl with the p53 tumor suppressor in the G arrest response (15, 16). Other signals dependent on c-Abl Damage* activation include induction of the stress-activated protein ki- nase and p38 mitogen-activated protein kinase by genotoxic (Received for publication, November 6, 1997, and revised form, agents (1, 2, 17). The findings that c-Abl contributes to the December 18, 1997) regulation of p53 and certain stress-induced kinases associated Zhi-Min Yuan, Yinyin Huang, Takatoshi Ishiko, with apoptosis have provided support for the activation of c-Abl Shuji Nakada, Taiju Utsugisawa, as a pro-apoptotic signal (14). In this context, expression of Surender Kharbanda, Rong Wang‡, c-Abl is associated with G phase growth arrest and induction Patrick Sung§, Akira Shinohara¶, Ralph Weichselbaumi, and Donald Kufe of apoptosis (14, 18, 19). Recombination plays a fundamental role in the repair of From 
TI - Regulation of Rad51 Function by c-Abl in Response to DNA Damage
JF - Journal of Biological Chemistry
DO - 10.1074/jbc.273.7.3799
DA - 1998-02-01
UR - https://www.deepdyve.com/lp/unpaywall/regulation-of-rad51-function-by-c-abl-in-response-to-dna-damage-Z8R3uKEFZL
DP - DeepDyve
ER -