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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Liu Xiongxiong Li Qiang Institute of Modern Physics Chinese Academy of Sciences

Biochemistry and Molecular Biology DNA-dependent protein kinase catalytic subunit(DNA-PKcs) plays a critical role in non-homologous end joining(NHEJ) of DNA double-stand break(dsb) ***,we found genistein could sensitize cancer cells to low linear energy transfer(LET) X-rays via inhibiting DNA-PKcs ***,high-LET heavy ion produces more DNA dsbs than low-LET ***,it is more important to study the detailed molecular mechanisms of genistein on sensitizing cancer cells to heavy *** formation assays showed that genistein sensitized DNA-PKcs proficient but not deficient glioblastoma cells to high-LET carbon *** sensitizer enhancement ratio of genistein was similar to that of DNAPKcs specific inhibitor Nu7026 treatment or siRNA knockdown of *** and western blot experiments were performed to examine the DNA dsbs and their repair kinetics in two DNA-PKcs proficient glioblastoma cell *** current studies showed that genistein delayed the clearance of γ-H2 AX foci induced by carbon ions;moreover,it physically bound to DNA-PKcs and functionally inhibited the level of p-(T2609)-*** the kinase of DNAPK was not activated and the NHEJ repair pathway would be ***,although genistein did not decrease Ku70/80 induced by carbon ions,p-(T714)-Ku80 decreased *** Ku70/80 heterodimer preferentially bound to but not dissociated from the dsb site,which delayed the recruitment of Rad51 to the dsb ends,so that the homologous recombination(HR) repair was ***,our study demonstrated that genistein holds promise as a radiosensitizer for enhancing the efficacy of carbon ion radiotherapy via inhibiting NHEJ and delaying HR repair.

关键词： Genistein DNA-PKcs dsb repair

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Prevention of DNA re-replication in eukaryotic cells

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Journal of Molecular Cell Biology 2011年第1期3卷 13-22页

作者： Lan N.Truong Xiaohua Wu Department of Molecular and Experimental Medicine The Scripps Research InstituteLa JollaCA 92037USA

DNA replication is a highly regulated process involving a number of licensing and replication factors that function in a carefully orchestrated manner to faithfully replicate DNA during every cell *** of proper licensing control leads to deregulated DNA replication including DNA re-replication,which can cause genome instability and *** organisms have established several conserved mechanisms to prevent DNA re-replication and to counteract its potentially harmful *** mechanisms include tightly controlled regulation of licensing factors and activation of cell cycle and DNA damage *** licensing control and its associated compromised checkpoints have both been observed in tumor cells,indicating that proper functioning of these pathways is essential for maintaining genome *** this review,we discuss the regulatory mechanisms of licensing control,the deleterious consequences when both licensing and checkpoints are compromised,and present possible mechanisms to prevent re-replication in order to maintain genome stability.

关键词： DNA re-replication cell cycle checkpoints DNA damage response Cdt1 dsb repair genome stability tumorigenesis

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Cell polarity protein Par3 complexes with DNA-PK via Ku70 and regulates DNA double-strand break repair

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Cell Research 2007年第6期17卷 100-116页

作者： TimTakKwok SiuKaiKong BenjaminChen DavidJChen Graduate School of the Chinese Academy of Sciences Shanghai 200031China Department of Biochemistry The Chinese University of Hong KongHong Kong SARChina

The partitioning-defective 3 (Par3),a key component in the conserved Par3/Par6/aPKC complex,plays fundamentalroles in cell *** we report the identification of Ku70 and Ku80 as novel Par3-interacting proteins throughan in vitro binding assay followed by liquid chromatography-tandem mass ***70/Ku80 proteins are twokey regulatory subunits of the DNA-dependent protein kinase (DNA-PK),which plays an essential role in repairingdouble-strand DNA breaks (dsbs).We determined that the nuclear association of Par3 with Ku70/KuS0 was enhancedby y-irradiation (IR),a potent dsb ***,DNA-PKcs,the catalytic subunit of DNA-PK,interacted withthe Par3/Ku70/Ku80 complex in response to ***3 over-expression or knockdown was capable of up-or downregulat-ing DNA-PK activity,***,the Par3 knockdown cells were found to be defective in random plasmidintegration,defective in dsb repair following IR,and radiosensitive,phenotypes similar to that of Ku70 *** findings identify Par3 as a novel component of the DNA-PK complex and implicate an unexpected link ofcell polarity to dsb repair.

关键词： cell polarity dsb repair DNA-PK Ku70/Ku80/Par3

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Mechanisms of genome instability in Hutchinson-Gilford progeria

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Frontiers in Biology 2017年第1期12卷 49-62页

作者： Haoyue Zhang Kan Cao Department of Cell Biology and Molecular Genetics University of Maryland College Park MD 20742 USA

BACKGROUND： Hutchinson-Gilford progeria syndrome （HGPS） is a devastating premature aging disorder. It arises from a single point mutation in the LMNA gene. This mutation stimulates an aberrant splicing event and produces progerin, an isoform of the lamin A protein. Accumulation of progerin disrupts numerous physiological pathways and induces defects in nuclear architecture, gene expression, histone modification, cell cycle regulation, mitochondrial functionality, genome integrity and much more. OBJECTIVE： Among these phenotypes, genomic instability is tightly associated with physiological aging and considered a main contributor to the premature aging phenotypes. However, our understanding of the underlying molecular mechanisms of progerin-caused genome instability is far from clear. RESULTS AND CONCLUSION： In this review, we summarize some of the recent findings and discuss potential mechanisms through which, progerin affects DNA damage repair and leads to genome integrity.

关键词： HGPS DDR dsb repair

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53BP1 regulates heterochromatin through phase separation

53BP1 regulates heterochromatin through phase separation

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2021年全国生物相分离和相变学术研讨会

作者： Lei Zhang Xinran Geng Jinshan Tang Fangfang Wang Youwei Zhang National 111 Center for Cellular Regulation and Molecular Pharmaceutics Hubei University of Technology Department of Pharmacology Case Comprehensive Cancer CenterSchool of MedicineCase Western Reserve University

Human 53 BP1 is primarily known as a key player in regulating the DNA double strands break（dsb） repair choice;however,whether it is involved in other biological process is less well *** we report a previously uncharacterized function of 53 BP1 at heterochromatin,where it undergoes liquid-liquid phase separation（LLPS） with the heterochromatin protein HPla in a mutually dependent *** of 53 BP1 results in the loss of heterochromatin centers and the de-repression of heterochromatic tandem repetitive *** further identified domains and residues of 53 BP1 required for LLPS,which overlap with but are distinct from those involved in dsb ***,53 BP1 mutants that are defective in dsb repair but retain LLPS and heterochromatin maintenance function still protected cells from stress-induced DNA damage,growth inhibition and senescent *** study illustrates a critical role for 53 BP1 in maintaining the heterochromatin integrity and genome stability independent of dsb repair.

关键词： 53BP1 nuclear punctate heterochromatin liquid-liquid phase separation HP1α dsb repair DNA damage genome stability

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