浙江大学转化医学研究院及浙江大学医学院附属邵逸夫医院 谢安勇/冯依力博士实验室招收助理研究员2名

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因研究工作需要,浙江大学转化医学研究院及医学院附属邵逸夫医院谢安勇和冯依力博士实验室2021年公开招聘从事CRISPR基因编辑技术DNA双链断裂修复机制研究及技术改良的助理研究员两名。

研究内容

针对CRISPR基因编辑技术中DNA断裂产生及其构象的独特性,拟开展如下研究内容:1. 利用独特的DNA断裂(包括DNA双链断裂和单链断裂)修复分析系统,结合生物化学、分子生物学、细胞生物学、遗传学及生物信息学等手段,解析CRISPR基因编辑过程中DNA断裂修复机制与调节的独特性;2. 根据CRISPR基因编辑过程中独特的DNA断裂修复机制与调节,改进CRISPR基因编辑技术,提高基因编辑的效率和精准度,降低脱靶;3. 利用细胞模型和动物模型,测试改良的基因编辑技术在生物技术和临床医学应用中的转化潜力;4. 利用CRISPR工具研究DNA损伤修复异常与肿瘤基因组不稳定性之间的关系。

一、招聘要求

对申请人的要求:1.已获得或将在近期内获得生物学及医学相关领域的博士学位,具备较强的细胞生物学、分子生物学、生物化学或遗传学背景;2.具有强烈的科研兴趣、独立的实验设计能力和较强的动手能力,能够在PI的指导下开展富有创新性的科学研究;3.具有较强的语言表达能力,善于主动沟通,工作踏实勤奋,有责任心和团队精神;4.有高影响力论文的发表者优先。

二、待遇

浙江大学医学院附属邵逸夫医院正式编制,年薪25-30万,业绩优秀者或到岗后业绩突出,可申请特聘副研究员职位,年薪30-35万,配启动经费。获资助的国家级基金项目医院1:1 配套,发表论文及获资助基金按照医院规定给予业绩奖励。

三、应聘材料

1、个人简历(应包括个人学习和科研工作经历及感兴趣的研究方向的

简要介绍等,也应包括博士导师推荐信或联系信息);

2、博士学位证书和毕业证书复印件;

3、身份证复印件1份;

4、有工作经验者,请准备提供相关证明材料(如导师推荐信或导师联

系信息等)。

四、联系方式

有意向者请先将个人简历发至anyongxie@zju.edu.cn(谢安勇)或eric_feng@zju.edu.cn (冯依力)

五、谢安勇博士及其研究小组简介

谢安勇:浙江大学转化医学研究院及医学院附属邵逸夫医院教授、博导。先后获北京大学学士学位、中科院植物所硕士学位和美国University of Missouri-Columbia生物化学博士学位。2008年于Harvard Medical School和Beth Israel Deaconess Medical Center完成博士后训练,在加入浙江大学转化医学研究院和浙江大学医学院附属邵逸夫医院前任Harvard Medical School讲师。 

冯依力:浙江大学医学院附属邵逸夫医院特聘研究员、硕导,浙江大学医学院临床拔尖青年人才培育项目入选者。2008年宁波大学学士毕业,2013年获浙江大学生命科学研究院博士学位。

实验室组建于2014年,位于浙江大学华家池校区转化医学研究院内。转化医学研究院具有国际一流的跨学科研究平台和工作环境, 实验条件优良,科研氛围浓厚,并与浙江大学各附属医院相辅相成,开展转化医学的相关前沿科学研究。目前,实验室拥有1名教授,1名特聘研究员,1名助理研究员,1名技术员,1名博士后,8名硕博研究生,是一支年轻、富有活力与创造力的团队。实验室具备良好的的硬件条件、一流的科研平台和充足的科研经费。

课题组的三个主要研究方向:1.肿瘤基因组不稳定性及肿瘤靶向药物研发;2.CRISPR基因编辑机制研究、技术改良与应用;3.肝癌模型建立及肝癌发生机制研究与临床应用。


近期论文及代表作(#: 共同一作;*: 通讯作者):

1.Guo T#, Chen G-Q#, Li X-F#, Liu P-Y, Lin H, Xie A-Y*. Extrachromosomal tumor suppressor gene mutations drive evolution of intratumor heterogeneity in CRISPR-induced mouse liver cancer. In preparation.

2.Liu S-C#, Feng Y-L#, Sun X-N#, Chen R-D, Liu Q, Xiao J-J, Xiang J-F, Chen G-Q, Yang Y, Lou C, Li H-D, Xu S-M, Lin H, Xie A-Y*. Cas9-sgRNA target residence alters DNA double strand break repair pathway choices in CRISPR/Cas9 genome editing. Submitted.

3.Feng Y-L*, Liu S-C, Chen R-D, Xie A-Y*. Target binding and residence: a new determinant of DNA double strand break repair pathway choice in CRISPR/Cas9 genome editing. J Zhejiang Univ SCIENCE B 2021; 22(1): 73-86. (受邀综述)

4.Zhang F, Yan P, Yu H, Le H, Li Z, Chen J, Liang X, Wang S, Wei W, Liu L, Zhang Y, Ji X, Xie A, Chen W, Han Z, Pu WT, Chen S, Chen Y, Sun K, Ge B, Zhang B. LARP7 Is a BRCA1 ubiquitinase substrate and regulates genome stability and tumorigenesis. Cell Rep 2020; 32(4): 107974.

5.Kong N, Ji X, Wang J, Sun X, Chen G, Fan T, Liang W, Zhang H, Xie A*, Farokhzad OC, Tao W*. ROS-mediated selective killing effect of black phosphorus: mechanistic understanding and its guidance for safe biomedical applications. Nano Letters 2020; 20(5): 3943-3955. 

6.Guo T#, Feng Y-L#, Xiao J-J, Liu Q, Sun X-N, Xiang J-F, Kong N, Liu S-C, Chen G-Q, Wang Y, Dong M-M, Cai Z, Lin H, Cai X-J*, Xie A-Y*. Harnessing accurate non-homologous end joining for efficient precise deletion in CRISPR/Cas9-mediated genome editing. Genome Biol 2018; 19:170. 

7.Xie X, Hu H, Tong X, Li L, Liu X, Chen M, Yuan H, Xie X, Li Q, Zhang Y, Ouyang H, Wei M, Huang J, Liu P, Gan W, Liu Y, Xie A, Kuai X, Chirn GW, Zhou H, Zeng R, Hu R, Qin J, Meng FL, Wei W, Ji H, Gao D*. The mTOR–S6K pathway links growth signalling to DNA damage response by targeting RNF168. Nat Cell Biol 2018; 20: 320-331. 

8.Han J, Ruan C, Huen M, Wang J, Xie A, Fu C, Liu T, Huang J*. BRCA2 antagonizes 53BP1/RIF1/Artemis-dependent classical and alternative nonhomologous end-joining to prevent gross genomic instability. Nat Commun 2017; 8: 1470. 

9.Feng Y-L, Xiang J-F, Liu S-C, Guo T, Yan G-F, Feng Y, Kong N, Li H-D, Huang Y, Lin H, Cai X-J*, Xie A-Y*. H2AX facilitates classical non-homologous end joining at the expense of limited nucleotide loss at repair junctions. Nucleic Acids Res, 2017; 45: 10614-10633. 

10.Guirouilh-Barbat J, Gelot C, Xie A, Dardillac E, Scully R, Lopez BS*. 53BP1 protects against ctip-dependent capture of ectopic chromosomal sequences at the junction of distant double strand breaks. PLOS Genet, 2016; 12:e1006230. 

11.Tang J-C, Feng Y-L, Guo T, Xie A-Y*, Cai X-J*. Circulating tumor DNA in hepatocellular carcinoma: trends and challenges. Cell Biosci, 2016; 6:32. 

12.Feng Y-L,Xiang J-F,Kong N,Cai X-J*,Xie A-Y*. Buried territories: heterochromatic response to DNA double strand breaks. Acta Biochim Biophys Sin, 2016; 48:594-602 (受邀综述) 

13.Liu X-S, Chandramouly G, Rass E, Guan Y, Wang G, Hobbs RM, Rajendran A, Xie A, Shah JV, Davis AJ, Scully R*, Lunardi A*, Pandolfi PP*. LRF maintains genome integrity by regulating the non-homologous end joining pathway of DNA repair. Nat Commun, 2015; 6:8325. 

14.Liu P, Gan W, Guo C, Xie A, Gao D, Guo J, Zhang J, Willis N, Su A, Asara JM, Scully R, Wei W*. Akt-mediated phosphorylation of XLF impairs non-homologous end joining DNA repair. Mol Cell, 2015;57: 648–661. 

15.Hu Y, Petit SA, Ficarro SB, Toomire KJ, Xie A, Lim E, Cao SA, Park E, Eck MJ, Scully R, Brown M, Marto JA, Livingston DM*. PARP1-driven poly-ADP-ribosylation regulates BRCA1 function in homologous recombination-mediated DNA repair. Cancer Discov, 2014; 4:1430-1447. 

16.Rass E, Chandramouly G, Zha S, Alt FW, Xie A*. Ataxia telangiectasia mutated (ATM) is dispensable for endonuclease I-SceI-induced homologous recombination in mouse embryonic stem cells. J Biol Chem, 2013,288: 7086-7095. 

17.Xie A, Odate S, Chandramouly G, Scully R*. H2AX post-translational modifications in the ionizing radiation response and homologous recombination. Cell Cycle 2010; 9: 3602-3610. (Highlighted in News and Views in Cell Cycle, 2010; 9:3845). 

18.Xie A*, Kwok A, Scully R*. Role of mammalian Mre11 in classical and alternative nonhomologous end joining. Nat Struct Mol Biol 2009; 16:814-818 (*, Co-corresponding authorship). (Highlighted in News and Views in Nat Struct Mol Biol 2009; 16:798-800). 

19.Xie A, Hartlerode A, Stucki M, Odate S, Puget N, Kwok A, Nagaraju G, Yan C, Alt FW, Chen J, Jackson SP, Scully R*. Distinct roles of chromatin-associated factors MDC1 and 53BP1 in mammalian double strand break repair. Mol Cell 2007; 28:1045-1057. (Evaluated and recommended by Faculty of 1000). 

20.Xie A and Scully R*. Hijacking the DNA damage response to enhance viral replication: γ-Herpesvirus 68 orf36 phosphorylates histone H2AX. Mol Cell 2007; 27:178-179. 

21.Xie A, Puget N, Shim I, Odate S, Jarzyna I, Bassing CH, Alt FW, Scully R*. Control of sister chromatid recombination by histone H2AX. Mol Cell 2004; 16:1017-1025. 


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