Zobrazeno 1 - 10
of 27
pro vyhledávání: '"Gloria G. Glick"'
Autor:
Kareem N Mohni, Petria S Thompson, Jessica W Luzwick, Gloria G Glick, Christopher S Pendleton, Brian D Lehmann, Jennifer A Pietenpol, David Cortez
Publikováno v:
PLoS ONE, Vol 10, Iss 5, p e0125482 (2015)
The DNA damage response kinase ATR may be a useful cancer therapeutic target. ATR inhibition synergizes with loss of ERCC1, ATM, XRCC1 and DNA damaging chemotherapy agents. Clinical trials have begun using ATR inhibitors in combination with cisplatin
Externí odkaz:
https://doaj.org/article/f9c69894fe6f41d8ba3ba6c828bd46d4
Publikováno v:
PLoS ONE, Vol 8, Iss 5, p e63149 (2013)
SMARCAL1 is an ATPase in the SNF2 family that functions at damaged replication forks to promote their stability and restart. It acts by translocating on DNA to catalyze DNA strand annealing, branch migration, and fork regression. Many SNF2 enzymes wo
Externí odkaz:
https://doaj.org/article/6a33b654f0d243c48227b01b10e41a31
Autor:
D. Reid Putney, Michael D. Feldkamp, Clinton Carroll, Gloria G. Glick, Thomas E. Bass, David Cortez, Walter J. Chazin, Gina Kavanaugh, Huzefa Dungrawala, Jessica W. Luzwick
Publikováno v:
Nature Cell Biology. 18:1185-1195
The ATR checkpoint kinase coordinates cellular responses to DNA replication stress. Budding yeast contain three activators of Mec1 (the ATR orthologue); however, only TOPBP1 is known to activate ATR in vertebrates. We identified ETAA1 as a replicatio
Autor:
David Cortez, Kareem N. Mohni, Kamakoti P. Bhat, Frank B. Couch, Kristie L. Rose, Huzefa Dungrawala, Gloria G. Glick
Publikováno v:
Molecular Cell. 59:998-1010
The ATR replication checkpoint ensures that stalled forks remain stable when replisome movement is impeded. Using an improved iPOND protocol combined with SILAC mass spectrometry, we characterized human replisome dynamics in response to fork stalling
Autor:
Manuel Ascano, M. Shane Hutson, Runxiang Zhao, Kareem N. Mohni, David Cortez, Monica E. Lacy, Gina Kavanaugh, Yan Guo, Gloria G. Glick
Publikováno v:
Molecular and Cellular Biology. 35:2979-2990
Accurate replication of DNA is imperative for the maintenance of genomic integrity. We identified Enhancer of Rudimentary Homolog (ERH) using a whole-genome RNA interference (RNAi) screen to discover novel proteins that function in the replication st
Autor:
Jun Qin, Sung Yun Jung, Clinton Carroll, Gloria G. Glick, David Cortez, Carol E. Bansbach, Frank B. Couch, Robert Driscoll, Karlene A. Cimprich, Rémy Bétous, Jessica W. Luzwick
Publikováno v:
Genes & Development. 27:1610-1623
The DNA damage response kinase ataxia telangiectasia and Rad3-related (ATR) coordinates much of the cellular response to replication stress. The exact mechanisms by which ATR regulates DNA synthesis in conditions of replication stress are largely unk
Autor:
David B. Friedman, Runxiang Zhao, David Cortez, Gloria G. Glick, Carol E. Bansbach, Edward A. Nam
Publikováno v:
Journal of Biological Chemistry. 286:28707-28714
The DNA damage response kinases ataxia telangiectasia-mutated (ATM), DNA-dependent protein kinase (DNA-PK), and ataxia telangiectasia-mutated and Rad3-related (ATR) signal through multiple pathways to promote genome maintenance. These related kinases
Publikováno v:
Genes & Development. 22:1478-1489
The ATR (ATM and Rad3-related) kinase and its regulatory partner ATRIP (ATR-interacting protein) coordinate checkpoint responses to DNA damage and replication stress. TopBP1 functions as a general activator of ATR. However, the mechanism by which Top
Autor:
Heather L. Ball, Mark Ehrhardt, David Cortez, Walter J. Chazin, Daniel A. Mordes, Gloria G. Glick
Publikováno v:
Molecular and Cellular Biology. 27:3367-3377
The ATR (ATM and Rad3-related) kinase is essential to maintain genomic integrity. ATR is recruited to DNA lesions in part through its association with ATR-interacting protein (ATRIP), which in turn interacts with the single-stranded DNA binding prote
Publikováno v:
Proceedings of the National Academy of Sciences. 101:10078-10083
The minichromosome maintenance (MCM) 2-7 helicase complex functions to initiate and elongate replication forks. Cell cycle checkpoint signaling pathways regulate DNA replication to maintain genomic stability. We describe four lines of evidence that A