J
Junran Zhang
Researcher at Ohio State University
Publications - 70
Citations - 3707
Junran Zhang is an academic researcher from Ohio State University. The author has contributed to research in topics: DNA repair & Homologous recombination. The author has an hindex of 28, co-authored 56 publications receiving 2982 citations. Previous affiliations of Junran Zhang include Harvard University & University of Pittsburgh.
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Journal ArticleDOI
BACH1 is critical for homologous recombination and appears to be the Fanconi anemia gene product FANCJ
Rachel Litman,Min Peng,Zhe Jin,Fan Zhang,Junran Zhang,Simon N. Powell,Paul R. Andreassen,Sharon B. Cantor +7 more
TL;DR: In this article, the authors showed that cells deficient of the BRCA1-associated BACH1 helicase, also known as BRIP1, failed to elicit homologous recombination (HR) after DNA double-stranded breaks (DSBs).
Journal ArticleDOI
Chk2 Phosphorylation of BRCA1 Regulates DNA Double-Strand Break Repair
Junran Zhang,Henning Willers,Zhihui Feng,Jagadish C. Ghosh,Sang Kim,David T. Weaver,Jay H. Chung,Simon N. Powell,Fen Xia +8 more
TL;DR: A dual regulatory role for BRCA1 in maintaining genome integrity is proposed, whereby B RCA1 phosphorylation status controls the selectivity of repair events dictated by HR and error-prone NHR.
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ATF3 promotes erastin-induced ferroptosis by suppressing system Xc
Liyuan Wang,Liyuan Wang,Yichen Liu,Tingting Du,Tingting Du,Heng Yang,Lei Lei,Mengqi Guo,Han Fei Ding,Junran Zhang,Hongbo Wang,Xiaoguang Chen,Chunhong Yan +12 more
TL;DR: It is reported that activating transcription factor 3 (ATF3), a common stress sensor, can promote ferroptosis induced by erastin and add ATF3 to a short list of proteins that can regulate system Xc− and promote feroptosis repressed by this antiporter.
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The role of the BRCA1 tumor suppressor in DNA double-strand break repair.
Junran Zhang,Simon N. Powell +1 more
TL;DR: The idea that tumor suppression by BRCA1 depends on its control of DNA DSB repair, resulting in the promotion of error-free and the inhibition oferror-prone recombinational repair is explored.
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ATR/CHK1 inhibitors and cancer therapy.
TL;DR: The status of the development of ATR/CHK1 inhibitors is reviewed and the potential mechanisms by which ATR and CHK1 inhibition induces cell killing in the presence or absence of exogenous DNA damaging agents, such as RT and chemotherapeutic agents are discussed.