S
Saurav De
Researcher at Memorial Sloan Kettering Cancer Center
Publications - 5
Citations - 765
Saurav De is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: DNA damage & Mutation. The author has an hindex of 5, co-authored 5 publications receiving 669 citations. Previous affiliations of Saurav De include Kettering University.
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Journal ArticleDOI
Loss of ATRX, genome instability, and an altered DNA damage response are hallmarks of the alternative lengthening of telomeres pathway.
Courtney A. Lovejoy,Wendi Li,Steven Reisenweber,Supawat Thongthip,Joanne Bruno,Titia de Lange,Saurav De,John H.J. Petrini,Patricia Sung,Maria Jasin,Joseph Rosenbluh,Yaara Zwang,Yaara Zwang,Barbara A. Weir,Charlie Hatton,Elena Ivanova,Laura E. MacConaill,Megan Hanna,William C. Hahn,William C. Hahn,Neal F. Lue,Roger R. Reddel,Roger R. Reddel,Yuchen Jiao,Kenneth W. Kinzler,Bert Vogelstein,Nickolas Papadopoulos,Alan K. Meeker +27 more
TL;DR: It is shown that loss of ATRX protein and mutations in the ATRRX gene are hallmarks of ALT–immortalized cell lines, and these attributes will facilitate the diagnosis and treatment ofALT positive human cancers.
Journal ArticleDOI
A recessive founder mutation in regulator of telomere elongation helicase 1, RTEL1, underlies severe immunodeficiency and features of Hoyeraal Hreidarsson syndrome.
Bari J. Ballew,Vijai Joseph,Saurav De,Grzegorz Sarek,Jean-Baptiste Vannier,Travis H. Stracker,Kasmintan A. Schrader,Trudy N. Small,Richard J. O'Reilly,Chris Manschreck,Megan Harlan Fleischut,Liying Zhang,John F. Sullivan,Kelly L. Stratton,Meredith Yeager,Kevin B. Jacobs,Neelam Giri,Blanche P. Alter,Joseph Boland,Laurie Burdett,Kenneth Offit,Simon J. Boulton,Sharon A. Savage,John H.J. Petrini +23 more
TL;DR: RTEL1 is implicates in the etiology of DC/HH and immunodeficiency and identifies the first known homozygous autosomal recessive disease-associated mutation in RTEL1, a helicase with critical telomeric functions in two unrelated families of Ashkenazi Jewish ancestry.
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Chemical Genetics Reveals a Specific Requirement for Cdk2 Activity in the DNA Damage Response and Identifies Nbs1 as a Cdk2 Substrate in Human Cells
Lara Wohlbold,Karl A. Merrick,Karl A. Merrick,Saurav De,Ramon Amat,Jun Hyun Kim,Stéphane Larochelle,Jasmina J. Allen,Chao Zhang,Kevan M. Shokat,John H.J. Petrini,Robert P. Fisher +11 more
TL;DR: It is shown that transient, selective inhibition of analog-sensitive (AS) Cdk2 after exposure to ionizing radiation (IR) enhances cell-killing and uncovers both a non-redundant requirement for Cdk 2 activity in response to DNA damage and a specific target of Cdk1 within the DNA repair machinery.
Journal ArticleDOI
Cell cycle- and DNA repair pathway-specific effects of apoptosis on tumor suppression
TL;DR: It is concluded that the oncogenic potential of double-strand breaks resulting from NHEJ deficiency is highly restricted by nonapoptotic functions of p53, suggesting that the particular facets of the DNA damage response required for tumor suppression are dictated by the proliferative status of the tumor-initiating cell.
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Rad50 Is Dispensable for the Maintenance and Viability of Postmitotic Tissues
TL;DR: The findings support the idea that the essential functions of the Mre11 complex are associated with DNA replication and further suggest that homologous recombination is not essential in nondividing cells.