J
Jingmei Liu
Researcher at Rutgers University
Publications - 38
Citations - 776
Jingmei Liu is an academic researcher from Rutgers University. The author has contributed to research in topics: Medicine & DNA repair. The author has an hindex of 16, co-authored 28 publications receiving 688 citations. Previous affiliations of Jingmei Liu include University of Medicine and Dentistry of New Jersey & Colorado State University.
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Journal ArticleDOI
The BRCA2-interacting protein BCCIP functions in RAD51 and BRCA2 focus formation and homologous recombinational repair.
Huimei Lu,Xu Guo,Xiangbing Meng,Jingmei Liu,Chris Allen,Justin Wray,Jac A. Nickoloff,Zhiyuan Shen +7 more
TL;DR: It is shown that chromatin-bound BRCA2 colocalizes with BCCIP nuclear foci and that most radiation-induced RAD51 foci colocalize with BCC IP, indicating that BCCIP is critical for BRCa2- and RAD51-dependent responses to DNA damage and HRR.
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Regulation of double-strand break-induced mammalian homologous recombination by UBL1, a RAD51-interacting protein
Wenhui Li,Bahar Hesabi,Angela Babbo,Carol Pacione,Jingmei Liu,David J. Chen,Jac A. Nickoloff,Zhiyuan Shen +7 more
TL;DR: It is found that non-conjugated UBL1 forms a complex with RAD51 and RAD52 proteins in human cells and this results suggest a regulatory role for UBL 1 in homologous recombination.
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cDNA cloning, sequence analysis, and induction by aryl hydrocarbons of a murine cytochrome P450 gene, Cyp1b1.
TL;DR: The entire cDNA sequence of P450CMEF and the amino acid sequence deduced from it are reported and a comparison of the latter sequence with known cytochrome P450s indicates that P450 CMEF is in a new subfamily of family 1 of the P450 superfamily.
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Functional and mutational landscapes of BRCA1 for homology-directed repair and therapy resistance
Rachel W Anantha,Srilatha Simhadri,Tzeh Keong Foo,Susanna Miao,Jingmei Liu,Zhiyuan Shen,Shridar Ganesan,Bing Xia +7 more
TL;DR: The results define the functionality of the top 22 patient-derived BRCA1 missense variants and the contribution of different domains of BRC a1 and its E3 ubiquitin ligase activity to HDR and drug resistance, and demonstrate that the BRCa1-PALB2 interaction dictates the choice between HR and SSA.
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Distinct RAD51 associations with RAD52 and BCCIP in response to DNA damage and replication stress.
TL;DR: It is proposed that BCCIP-dependent repair of DSBs by HR is an early RAD51 response to ionizing radiation-induced DNA damage, and that RAD52-dependent HR occurs later to restart a subset of blocked or collapsed replication forks.