A high-throughput, flow cytometry-based method to quantify DNA-end resection in mammalian cells.
about
DNA damage signaling assessed in individual cells in relation to the cell cycle phase and induction of apoptosisWRN regulates pathway choice between classical and alternative non-homologous end joiningRequirement for Parp-1 and DNA ligases 1 or 3 but not of Xrcc1 in chromosomal translocation formation by backup end joining.KAP-1 promotes resection of broken DNA ends not protected by γ-H2AX and 53BP1 in G₁-phase lymphocytes.Deregulated origin licensing leads to chromosomal breaks by rereplication of a gapped DNA template.Whole genome RNAi screens reveal a critical role of REV3 in coping with replication stress.DNA damage response factors from diverse pathways, including DNA crosslink repair, mediate alternative end joining.Sumoylation regulates EXO1 stability and processing of DNA damage.RNF4 regulates DNA double-strand break repair in a cell cycle-dependent mannerTetratricopeptide repeat factor XAB2 mediates the end resection step of homologous recombinationDual mode of cell death upon the photo-irradiation of a RuII polypyridyl complex in interphase or mitosis.RB localizes to DNA double-strand breaks and promotes DNA end resection and homologous recombination through the recruitment of BRG1.A flow cytometry-based method to simplify the analysis and quantification of protein association to chromatin in mammalian cells.Antibody Engineering for Pursuing a Healthier FutureSystematic characterization of deubiquitylating enzymes for roles in maintaining genome integritySustained E2F-Dependent Transcription Is a Key Mechanism to Prevent Replication-Stress-Induced DNA Damage.Coordinated nuclease activities counteract Ku at single-ended DNA double-strand breaks.CtIP tetramer assembly is required for DNA-end resection and repair.PRPF8 is important for BRCA1-mediated homologous recombination.PARP2 controls double-strand break repair pathway choice by limiting 53BP1 accumulation at DNA damage sites and promoting end-resection.BLM helicase regulates DNA repair by counteracting RAD51 loading at DNA double-strand break sites.DNA repair and cell cycle checkpoint defects in a mouse model of 'BRCAness' are partially rescued by 53BP1 deletion.Kinetics and Fidelity of the Repair of Cas9-Induced Double-Strand DNA Breaks.
P2860
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P2860
A high-throughput, flow cytometry-based method to quantify DNA-end resection in mammalian cells.
description
2012 nî lūn-bûn
@nan
2012 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2012 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
name
A high-throughput, flow cytome ...... resection in mammalian cells.
@ast
A high-throughput, flow cytome ...... resection in mammalian cells.
@en
A high-throughput, flow cytome ...... resection in mammalian cells.
@nl
type
label
A high-throughput, flow cytome ...... resection in mammalian cells.
@ast
A high-throughput, flow cytome ...... resection in mammalian cells.
@en
A high-throughput, flow cytome ...... resection in mammalian cells.
@nl
prefLabel
A high-throughput, flow cytome ...... resection in mammalian cells.
@ast
A high-throughput, flow cytome ...... resection in mammalian cells.
@en
A high-throughput, flow cytome ...... resection in mammalian cells.
@nl
P2860
P356
P1433
P1476
A high-throughput, flow cytome ...... resection in mammalian cells.
@en
P2093
Rachael V Walker
P2860
P304
P356
10.1002/CYTO.A.22155
P577
2012-08-14T00:00:00Z