TY - JOUR
AU - 
AB - THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 271, No. 34, Issue of August 23, pp. 20486–20493, 1996 © 1996 by The American Society for Biochemistry and Molecular Biology, Inc. Printed in U.S.A. Defect in Multiple Cell Cycle Checkpoints in Ataxia-Telangiectasia Postirradiation* (Received for publication, October 26, 1995, and in revised form, April 18, 1996) Heather Beamish‡, Richard Williams‡§, Philip Chen‡, and Martin F. Lavin‡§ From the ‡Queensland Cancer Fund Research Unit, Queensland Institute of Medical Research, Bancroft Centre, 300 Herston Road, Brisbane, Queensland 4029, Australia and the §Department of Surgery, University of Queensland, Royal Brisbane Hospital, Herston, Queensland 4029, Australia sis (15–16), and at longer times postirradiation they are irre- The recent description of a novel gene (ATM) mutated in ataxia-telangiectasia (A-T), with homologies to genes versibly delayed in G phase (9, 17, 18). Kastan et al. (8) encoding proteins involved in both G /S and G /M check- showed that A-T cells lacked the radiation induction of p53 1 2 point control, points to a common defect in cell cycle observed in normal cells. Khanna and Lavin (19) subsequently control in A-T operating through the cyclin-dependent revealed that the p53 response postirradiation is reduced kinases. In this report we 
TI - Defect in Multiple Cell Cycle Checkpoints in Ataxia-Telangiectasia Postirradiation
JF - Journal of Biological Chemistry
DO - 10.1074/jbc.271.34.20486
DA - 1996-08-01
UR - https://www.deepdyve.com/lp/unpaywall/defect-in-multiple-cell-cycle-checkpoints-in-ataxia-telangiectasia-BrlyxDOAeJ
DP - DeepDyve
ER -