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Yolanda Sanchez

Researcher at Dartmouth College

Publications -  46
Citations -  4370

Yolanda Sanchez is an academic researcher from Dartmouth College. The author has contributed to research in topics: G2-M DNA damage checkpoint & CHEK1. The author has an hindex of 21, co-authored 45 publications receiving 4129 citations. Previous affiliations of Yolanda Sanchez include Baylor College of Medicine & University of Cincinnati Academic Health Center.

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Conservation of the Chk1 checkpoint pathway in mammals: Linkage of DNA damage to Cdk regulation through Cdc25

TL;DR: Results suggest a model whereby in response to DNA damage, Chk1 phosphorylates and inhibits Cdc25C, thus preventing activation of the Cdc2-cyclin B complex and mitotic entry.
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Regulation of RAD53 by the ATM-Like Kinases MEC1 and TEL1 in Yeast Cell Cycle Checkpoint Pathways

TL;DR: Results indicate that RAD53 is a signal transducer in the DNA damage and replication checkpoint pathways and functions downstream of two members of the ATM lipid kinase family.
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Control of the DNA damage checkpoint by Chk1 and Rad53 protein kinases through distinct mechanisms

TL;DR: A model in which Chk1 and Rad53 function in parallel through Pds1 and Cdc5, respectively, to prevent anaphase entry and mitotic exit after DNA damage is supported, providing a possible explanation for the role of CDC5 in DNA damage checkpoint adaptation.
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von Hippel-Lindau protein binds hyperphosphorylated large subunit of RNA polymerase II through a proline hydroxylation motif and targets it for ubiquitination.

TL;DR: In this paper, the authors identified regions of Rpb1 and the adjacent subunit 6 of RNA polymerase II (Rpb6) that share sequence and structural similarity with the domain of hypoxia-inducible transcription factor 1α that binds von Hippel-Lindau tumor suppressor protein (pVHL).
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Chk1 in the DNA damage response: conserved roles from yeasts to mammals.

TL;DR: What is known about Chk1 activation and what downstream factors are regulated by Chk2 to counter replication blocks and DNA damage induced by UV, IR, and other genotoxic agents are discussed.