J
Jun Che
Researcher at University of Texas Health Science Center at San Antonio
Publications - 8
Citations - 205
Jun Che is an academic researcher from University of Texas Health Science Center at San Antonio. The author has contributed to research in topics: DNA repair & DNA replication. The author has an hindex of 6, co-authored 8 publications receiving 163 citations. Previous affiliations of Jun Che include Kunming Institute of Zoology.
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Journal ArticleDOI
Guidelines for DNA recombination and repair studies: Cellular assays of DNA repair pathways
Hannah L. Klein,Giedrė Bačinskaja,Jun Che,Anais Cheblal,Rajula Elango,Anastasiya Epshtein,Devon M. Fitzgerald,Belén Gómez-González,Sharik R. Khan,Sandeep Kumar,Bryan A Leland,Lea Marie,Qian Mei,Judith Miné-Hattab,Judith Miné-Hattab,Alicja Piotrowska,Erica J Polleys,Christopher D. Putnam,Christopher D. Putnam,Elina A. Radchenko,Anissia Ait Saada,Anissia Ait Saada,Cynthia J. Sakofsky,Eun Yong Shim,Mathew Stracy,Jun Xia,Zhenxin Yan,Yi Yin,Andrés Aguilera,Juan Lucas Argueso,Catherine H. Freudenreich,Susan M. Gasser,Dmitry A. Gordenin,James E. Haber,Grzegorz Ira,Sue Jinks-Robertson,Megan C. King,Richard D. Kolodner,Andrei Kuzminov,Sarah Lambert,Sarah Lambert,Sang Eun Lee,Kyle M. Miller,Kyle M. Miller,Sergei M. Mirkin,Thomas D. Petes,Susan M. Rosenberg,Rodney Rothstein,Lorraine S. Symington,Pawel Zawadzki,Nayun Kim,Michael Lisby,Anna Malkova +52 more
TL;DR: The most commonly used cellular assays, developed in microbial systems that provide the advantages of genetic and molecular reporters that can readily be manipulated are reviewed, discussed, and presented as the guidelines for future studies.
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DNA end recognition by the Mre11 nuclease dimer: insights into resection and repair of damaged DNA
Sihyun Sung,Fuyang Li,Young Bong Park,Jin Seok Kim,Ae Kyoung Kim,Ok kyu Song,Jiae Kim,Jun Che,Sang Eun Lee,Yunje Cho +9 more
TL;DR: The identified Mre11 interface binding DNA duplex ends is structurally conserved and shown to functionally contribute to efficient resection, non‐homologous end joining, and tolerance to DNA‐damaging agents when other resection enzymes are absent.
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Hyper-Acetylation of Histone H3K56 Limits Break-Induced Replication by Inhibiting Extensive Repair Synthesis
TL;DR: It is reported that deletion of HST3 and HST4, two redundant de-acetylases of histone H3 Lysine 56 (H3K56), inhibits BIR, sensitizes checkpoint deficient cells to deoxyribonucleotide triphosphate pool depletion, and elevates translocation-type gross chromosomal rearrangements (GCR).
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Rapid evolution and copy number variation of primate RHOXF2, an X-linked homeobox gene involved in male reproduction and possibly brain function
Ao-lei Niu,Ao-lei Niu,Yin-qiu Wang,Yin-qiu Wang,Hui Zhang,Cheng-hong Liao,Jinkai Wang,Rui Zhang,Jun Che,Bing Su +9 more
TL;DR: The rapid evolution and copy number changes of RHOXF2 had been driven by Darwinian positive selection acting on the male reproductive system and possibly also on the central nervous system, which sheds light on understanding the role of homeobox genes in adaptive evolution.
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Apn2 resolves blocked 3' ends and suppresses Top1-induced mutagenesis at genomic rNMP sites.
TL;DR: Genetic and biochemical analyses reveal that the nuclease Apn2 removes terminal cyclic phosphates that arise from ribonucleotide incorporation in the genome of budding yeast and identifies a role for Apn 2 in maintaining genome integrity during rNMP repair.