K
Kevin M. Hopkins
Researcher at Columbia University
Publications - 33
Citations - 1564
Kevin M. Hopkins is an academic researcher from Columbia University. The author has contributed to research in topics: DNA repair & DNA damage. The author has an hindex of 21, co-authored 33 publications receiving 1494 citations. Previous affiliations of Kevin M. Hopkins include Science Applications International Corporation & Columbia University Medical Center.
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Journal ArticleDOI
Mammalian Rad9 Plays a Role in Telomere Stability, S- and G 2 -Phase-Specific Cell Survival, and Homologous Recombinational Repair
Raj K. Pandita,Girdhar G. Sharma,Andrei Laszlo,Kevin M. Hopkins,Scott Davey,Mikhail Chakhparonian,Arun Gupta,Raymund J. Wellinger,Junran Zhang,Simon N. Powell,Joseph L. Roti Roti,Howard B. Lieberman,Tej K. Pandita +12 more
TL;DR: Evidence of roles for mammalian Rad9 in telomere stability and HR repair as a mechanism for promoting cell survival after ionizing radiation (IR) exposure is provided.
Journal ArticleDOI
Human homologue of S. pombe Rad9 interacts with BCL-2/BCL-xL and promotes apoptosis
Kiyoshi Komatsu,Toshiyuki Miyashita,Haiying Hang,Kevin M. Hopkins,Wei Zheng,Sandy M. Cuddeback,Masao Yamada,Howard B. Lieberman,Hong Gang Wang +8 more
TL;DR: Using yeast two-hybrid and co-immunoprecipitation studies, it is shown that RAD9, a human protein involved in the control of a cell-cycle checkpoint, interacts with the anti-apoptotic Bcl-2-family proteins BCL-2 and BCL -xL, but not with the pro-APoptotic BAX and BAD.
Journal ArticleDOI
A human homolog of the Schizosaccharomyces pombe rad9+ checkpoint control gene
TL;DR: An underlying conservation of the molecular mechanisms of S and G2 checkpoint control pathways in most if not all eukaryotes is suggested.
Journal ArticleDOI
Phosphorylation of Human Rad9 Is Required for Genotoxin-activated Checkpoint Signaling *
Pia Roos-Mattjus,Kevin M. Hopkins,Andrea J. Oestreich,Benjamin T. Vroman,Kenneth L. Johnson,Stephen Naylor,Howard B. Lieberman,Larry M. Karnitz +7 more
TL;DR: It is demonstrated that the Rad9 phospho-tail is a key participant in the Chk1 activation pathway and point to additional roles for Rad9 in cellular responses to IR.
Journal ArticleDOI
Deletion of mouse rad9 causes abnormal cellular responses to DNA damage, genomic instability, and embryonic lethality.
Kevin M. Hopkins,Wojtek Auerbach,Xiang Yuan Wang,M. Prakash Hande,Haiying Hang,Debra J. Wolgemuth,Alexandra L. Joyner,Howard B. Lieberman +7 more
TL;DR: These investigations establish Mrad9 as a key mammalian genetic element of pathways that regulate the cellular response to DNA damage, maintenance of genomic integrity, and proper embryonic development.