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Junjie Chen

Researcher at University of Texas MD Anderson Cancer Center

Publications -  390
Citations -  36586

Junjie Chen is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: DNA damage & DNA repair. The author has an hindex of 92, co-authored 319 publications receiving 33469 citations. Previous affiliations of Junjie Chen include Carnegie Mellon University & University of Texas Health Science Center at Houston.

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Association of BRCA1 with Rad51 in Mitotic and Meiotic Cells

TL;DR: Findings suggest a functional interaction between BRCA1 and Rad51 in the meiotic and mitotic cell cycles, which, in turn, suggests a role for BRC a1 in the control of recombination and of genome integrity.
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Histone H2AX Is Phosphorylated in an ATR-dependent Manner in Response to Replicational Stress

TL;DR: It is reported that inhibition of DNA replication by hydroxyurea or ultraviolet irradiation also induces phosphorylation and foci formation of H2AX, and these phospho-H2AX foci colocalize with proliferating cell nuclear antigen, BRCA1, and 53BP1 at the arrested replication fork in S phase cells.
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RNF8 Transduces the DNA-Damage Signal via Histone Ubiquitylation and Checkpoint Protein Assembly.

TL;DR: This study implicates RNF8 as a novel DNA-damage-responsive protein that integrates protein phosphorylation and ubiquitylation signaling and plays a critical role in the cellular response to genotoxic stress.
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Structural Basis for the Methylation State-Specific Recognition of Histone H4-K20 by 53BP1 and Crb2 in DNA Repair

TL;DR: This study reveals an evolutionarily conserved molecular mechanism of targeting DNA repair proteins to DSBs by direct recognition of H4-K20me2 through direct binding of 53BP1 and Crb2 to histone H4.
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Dynamic Changes of BRCA1 Subnuclear Location and Phosphorylation State Are Initiated by DNA Damage

TL;DR: The data imply that the BRCA1 S phase foci are dynamic physiological elements, responsive to DNA damage, and that B RCA1-containing multiprotein complexes participate in a replication checkpoint response.