标题：任瑞宝
个人履历
任瑞宝

主要教育背景及工作经历
学习经历1992 –1994 博士后，美国洛克菲勒大学David Baltimore 实验室。期间， 1994,7-1994,12 在美国麻省理工学 院。
1988 –1992 博士研究生, 美国纽约哥仑比亚大学医学院微生物系Vincent 
Racaniello实验室。
1983 –1986 中国北京医科大学（现北京大学医学部）微生物系 ，医学硕士研
究生
1978 –1983 中国北京医学院（现北京大学医学部），基础医学系本科生
工作经历1995-2000 美国布兰戴斯大学(BrandeisUniversity)生物系助理教授
2000-2008 美国布兰戴斯大学生物系副教授(tenured)
2008-2011 美国布兰戴斯大学生物系终生教授 
2010-2011 美国布兰戴斯大学生物系联席系主任
所获奖励1992 获美国哥仑比亚大学研究生院优秀研究生院长奖
1992 获Irvinton研究所博士后奖学金
1992-1995 获肿瘤研究所博士后奖学金
1996-1998 获美国癌症研究协会青年学者奖
1996-1998 获美国March of Dimes, Basil O’Connor 青年学者奖
1998-2003 获美国白血病及淋巴瘤协会学者奖
2003 获美国癌症研究协会研究学者称号
会员1998-至今 美国血液学协会会员
2002 美国血液学协会2002年年会慢性髓细胞白血病分会主席
2006-至今 美国癌症研究协会会员
委任职务2005-至今 美国国家卫生研究院血液学项目评审委员会委员
2006-至今 美国白血病及淋巴瘤协会评审委员会委员
2007-至今 美国国防部CML项目评审委员会主席
2006-至今 北京大学学报医学版特邀编委
2008-至今 美国Journal of Hematology and Oncology杂志常务副主编
2011-至今 美国Journal of Biological Chemistry杂志编委
2011-至今 医学前沿编委
科技创新成果任瑞宝教授长期从事分子生物学, 疾病学及治疗学研究。 在《Cell》, 《Nature》, 《Science》， 《Genes & Development》， 《PNAS》， 《Blood》， 《MCB》, 《Cancer Research》等重要学术期刊发表50多篇论文，引用率达6000次。 发表在《Science》杂志上的一篇论文在1993年全世界论文引用次数最多的十篇论文中排名第三。获美国国立卫生院, 美国国防部及美国肿瘤协会的多项研究基金。已培养了超过20名的博士研究生, 博士后和访问学者。先后获美国肿瘤协会, 美国March of Dimes, Basil O’Connor 和白血病及淋巴瘤协会学者奖。历任布兰戴斯大学终生教授，生物系联席系主任，布兰戴斯大学生物安全委员会主席， 美国国家卫生研究院血液学项目评审委员会委员， 白血病及淋巴瘤协会评审委员会委员， 美国国防部CML项目评审委员会主席。现任美国生物化学杂志（JBC）编委，美国血液与肿瘤学杂志（JHO）常务副主编，医学前沿编委及北京大学学报医学版特邀编委。2011年入选千人计划，全职回国任上海交通大学医学院附属瑞金医院上海血液学研究所常务副所长，研究员。
主要成就1. 将人小儿麻痹病毒受体转入小鼠而制成了小儿麻痹病毒受体的转基因小鼠模型，并用此模型做了大量深入的小儿麻痹病毒分子生物学研究。这个模型对研究小儿麻痹病毒的致病机理及小儿麻痹病毒疫苗的安全测试具有广泛的理论及应用价值。该动物模型获美国专利. 
2. 首次发现了存在于许多重要信号传导蛋白质中的SH3功能基团的功能及结合靶点。发表在《Science》杂志上的该论文在1993年全世界论文引用次数最多的十篇论文中排名第三。同时，在克隆3BP2基因后与Bruce Mayer 一道首次发现并命名了Pleckstrin homology功能基团（PHD）。
3. 研发了BCR/ABL诱导的人慢性髓细胞白血病（CML）及人急性淋巴细胞白血病（ALL），AML1/EVI1诱导的人急性髓细胞白血病（AML），及RAS诱导的人急性及慢性粒细胞及单核细胞白血病（AMML，CMML）的小鼠模型。 这些疾病模型对研究白血病致病机理，研发及测试白血病治疗具有重要的理论及应用价值。
4. 用CML小鼠模型系统的进行BCR/ABL功能与结构的研究。揭示了BCR/ABL蛋白质激酶活性对其诱导CML的必要性 – 为BCR/ABL蛋白质激酶抑制剂成功治疗CML 提供了理论基础。同时发现BCR/ABL蛋白质激酶外的功能集团对诱导CML 的重要作用 - 为研发抗BCR/ABL蛋白质激酶抑制剂耐药性治疗提供了理论基础。
5. RAS是人类最常见的癌基因（RAS基因突变见于30%人类肿瘤）。 任瑞宝教授的实验室首次建立了NRAS（白血病中最常见的RAS基因突变）诱导的AMML及CMML动物模型，并用此模型系统的进行NRAS功能与结构的研究。首次发现棕榈酰化（Palmitoylation）修饰对NRAS诱导白血病的必要性 – 为研发抗NRAS相关的白血病及其他癌的治疗奠定了理论基础。
NRAS肿瘤基因存在于25-30% 白血病， 肝癌及黑色素瘤中， 抑制NRAS棕榈酰化修饰对这些肿瘤应有有效的治疗作用。虽然很多肿瘤为KRAS4B肿瘤基因阳性， 而KRAS不需棕榈酰化修饰， 但进来发现KRAS4A （另一KRAS基因剪接产物）在KRAS阳性肿瘤， 如肺癌，发病过程中起重要作用，而KRAS4A需要棕榈酰化修饰。同时我们还发现抑制NRAS棕榈酰化修饰对RAS上游肿瘤蛋白有阻断作用, 因此抑制RAS棕榈酰化修饰对肿瘤应有广泛的治疗效果。该应用的专利申请正在审理中。
6. 三氧化二砷成功治疗急性早幼粒细胞白血病（APL）是中国的首创。三氧化二砷主要作用机理是诱导PML-RARα融合癌蛋白降解。任瑞宝教授的实验室发现三氧化二砷也诱导EVI1癌蛋白降解。EVI1的异常表达见于10%AML病人及90%以上宫颈癌病人。 上述发现为扩大三氧化二砷治疗这些疾病提供了理论基础。
7. 干扰素调节因子4（IRF4）最初被发现为癌蛋白， 对多发性骨髓癌癌细胞生存的维系起重要作用。近来，任瑞宝教授的实验室首次发现IRF4 在早期B-淋巴细胞及髓细胞中的功能为癌抑制蛋白。 这一发现对发展多发性骨髓癌及白血病的治疗具有重要指导作用。IRF4癌抑制功能及应用的专利申请正在审理中。
发表论著1. Racaniello,V.R., C.L. Mendelsohn, M. Morrison, M. Freistadt, G. Kaplan, E. Moss, and R.Ren. 1990. Molecular genetics of cellular receptors forpoliovirus. In: "Positive StrandRNA Viruses" (M.A. Brinton and F.X. Heinz, eds). American Society for Microbiology,Washington, DC. pp. 278-286.
2. Ren,R., E. G. Moss, V. R. Racaniello. 1991. Identification of twodeterminants that attenuate vaccine-related type 2 poliovirus. J. Virol. 65:1377-1382.
3. Newlon,C. S., L. R. Lipchitz, I. Collins, A. Deshpande, R. J. Devenish, R. P. Green,H. L. Klein, T. G Palzkill, R. Ren, S. Synn, and S. T. Woody. 1991. Analysis of a circular derivative ofSaccharomyces cerevisiae chromosome III: A physical map and identification andlocation of ARS elements. Genetics. 129: 343-357.
4. Racaniello,V.R., E. Moss, G. Kaplan, R. Ren. 1991. Interaction of polioviruswith its immunoglobulin-like cell receptor. In: "Microbial Adhesion" (M. Hook and L. Switalski, eds)Springer Verlag, Berlin.
5. Ren,R., V. R. Racaniello. 1992. Humanpoliovirus receptor gene expression and poliovirus tissue tropism in transgenicmice. J. Virol. 66: 296-304.
6. Ren,R., V. R. Racaniello. 1992. Poliovirusspreads from muscle to the central nervous system by neural pathways. J.Infect. Dis. 166: 747-752
7. Racaniello,V.R., R. Ren, M. Bouchard. 1992. Poliovirus attenuation and pathogenesis in atransgenic mouse model for poliomyelitis. Develop. Biol. Standard. 78:105-112.
8. Ren,R., B. J. Mayer, P. Ciccheti, and D. Baltimore. 1993. Identification of a ten-amino acid proline-rich SH3 binding site.Science. 259: 1157-1161. (the third-most-frequently cited paper in 1993,Science Watch. 5[1]:1).
9. Mayer,B. J., R. Ren, K. L. Clark, D. Baltimore. 1993. A putative modular domainpresent in diverse signaling proteins. Cell. 73: 629-630.
10. Ren,R., Z. Ye, D. Baltimore. 1994. Ablprotein-tyrosine kinase selects Crk adapter as a substrate using SH3 bindingsites. Genes Dev. 8: 783-795
11. Songyang,Z., S. E. Shoelson, J. McGlade, P. Olivier, T. Pawson, R. X. Bustelo, H.Hanafusa, T. Yi, R. Ren, D. Baltimore, S. Ratnofsky, R. A. Feldman, L. C.Cantley. 1994. Specific motifs recognized by the SH2 domains of csk, 3BP2,fes/fpd, Grb2, SHPTP1, SHC, Syk and vav. Mol. Cell. Biol. 14: 2777-2785 
12. Feller,S. M., R. Ren, H. Hanafusa, and D. Baltimore. 1994. SH2 and SH3 domains insignal transduction - the interactions of Crk and Abl. TIBS. 19:453-458.
13. Racaniello,V.R., R. Ren. 1994. Transgenic mice and the pathogenesis of poliomyelitis. ArchVirol Suppl. 9:79-86.
14. Cohen,G., R. Ren, D. Baltimore. 1995. Modular binding domains in signal transduction.Cell: 80:237-48.
15. BaltimoreD; Ren R; Cheng G; Alexandropoulos K; Cicchetti P. 1995. A nuclear tyrosine kinase becomes acytoplasmic oncogene. Ann N Y Acad Sci 758:339-344.
16. Kharbanda,S., R. Ren (co-first-author), P. Pandey, T. D. Shafman, J. Kyriakis, R. R.Weichselbaum, D. Kufe. 1995. Activation of the c-Abl tyrosine kinase in the stress response toDNA-damage agents. Nature. 376: 785-788
17. Racaniello,V. R., R. Ren. 1996. Poliovirus biology and pathogenesis. In: “Transgenic Model of Human Viral and ImmunologicalDisease” (F. V. Chisari and M. B. A. Oldstane, eds). Springer-Verlag, Berlin Heidelberg New York.pp. 305-326.
18. Freeman,N. L., K. A. Mintzer, T. Lila, Z. Chen, A. J. Pahk, R. Ren, and J. Field. 1996. A domain containing a conserved SH3 binding site on the Saccharomycescerevisiae cyclase associated proteinmodulates cytoskeletal interactions and RAS signaling. Mol. Cell. Biol. 16:548-556
19. KharbandaS; P. Pandey; R. Ren; B. Mayer; L. Zon; D. Kufe. 1996. c-Abl activation regulates induction of theSEK1/stress-activated protein kinase pathway in the cellular response to1-beta-D-arabinofuranosylcytosine. J Biol. Chem. 270: 30278-81
20. Kharbanda,S., A. Bharti, D. Pei, J. Wang, P. Pandey, R. Ren, R. Weichselbaum, C. Walsh,and D. Kufe. 1996. The stress responseto ionizing radiation involves c-Abl-Dependent phosphorylation of SHPTP1. Proc. Natl. Acad. Sci. USA. 93: 6898-901
21. Holmes,T. C., D. A. Fadool, R. Ren, and I. B. Levitan. 1996. Association of Src tyrosine kinase with a human potassium channelmediated by SH3 domain. Science. 274: 2089-91
22. Chen,M., H., She, E. M., Davis, C. M., Spicer, L., Kim, R., Ren, M. M., Le Beau, W.,Li. 1998. Identification of Nck family genes, chromosomal localization,expression, and signaling specificity. J. Biol. Chem. 273: 25171
23. Zhang,X. and R. Ren. 1998. Bcr-Abl efficiently induces a myeloproliferative diseaseand production of excess IL-3 and GM-CSF in mice: a novel model for chronicmyelogenous leukemia. Blood. 92: 3829-3840
24. Skourides,P. A., Perera, S. A., and R. Ren. 1999. Polarized distribution of Bcr-Abl inmigrating myeloid cells and co-localization of Bcr-Abl and its target proteins.Oncogene. 18: 1165-1176
25. Gross,A., X. Zhang, and R. Ren. 1999. Bcr-Ablwith an SH3 deletion retains the ability to induce a myeloproliferative diseasein mice, yet c-Abl activated by SH3 deletion induces only lymphoid malignancy.Mol. Cell. Biol. 19: 6918-6928
26. Hao,S. X., and R. Ren. 2000. Expression of ICSBP is downregulated in Bcr-Abl-inducedmurine CML-like disease, and forced coexpression of ICSBP inhibits theBcr-Abl-induced myeloproliferative disorder. Mol. Cell. Biol. 20: 1149-1161.
27. Cuenco,G. M., G. Nucifora, and R. Ren. 2000.Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML)in mice: a novel model for human AML. Proc. Natl. Acad. Sci. USA. 97:1760-1765.
28. GrossA. W. and R. Ren. 2000. Bcr-Abl has a greater intrinsic capacity than v-Abl toinduce the neoplastic expansion of myeloid cells in vivo. Oncogene. 19:6286-6296
29. ZhangX, R. Wong, S. X. Hao, W. S. Pear, and R. Ren. 2001. The SH2 domain of Bcr-Abl is not required to induce a murinemyeloproliferative disease; however, SH2 signaling influences disease latencyand phenotype. Blood. 97: 277-287. 
30. ZhangX, R. Subrahmanyam, R. Wong, A. W. Gross and R. Ren. 2001. The NH2-terminalcoiled-coil domain and tyrosine 177 play important roles in induction of amyeloproliferative disease in mice by Bcr-Abl. Mol. Cell. Biol. 21: 840-853
31. Cuenco,M. G. and R. Ren. 2001. Cooperation of BCR-ABL and AML1/MDS1/EVI1 in blockingmyeloid differentiation and rapid induction of an Acute Myelogenous Leukemia.Oncogene. 20:8236-8248
32. He,Y., J. A. Wertheim, L. Xu, J. P. Miller, F. G. Karnell, J. K. Choi, R. Ren, andW. S. Pear. 2002. The coiled-coildomain and Tyr177 of bcr are required to induce a murine chronic myelogenousleukemia-like disease by bcr/abl. Blood.99: 2957-2968.
33. Ren,R. 2002. Dissecting the molecular mechanism of chronic myelogenous leukemiausing murine models. Leukemia and Lymphoma. 8: 1549-1561
34. Ren,R. 2002. The molecular mechanism of chronic myelogenous leukemia and itstherapeutic implications: studies in a murine model. Oncogene. 21: 8629-8642.
35. Wertheim,J. A., S. A. Perera, D. Hammer, R. Ren, D. Boettiger and W. S. Pear. 2003. Localization of BCR-ABL to F-actinregulates cell adhesion but does not attenuate CML development. Blood.102:2220-8
36. Dinulescu,D. M., L. J. Wood, L. Shen, M. Loriaux, C. L. Corless, A. W. Gross, R. Ren, M.W..N. Deininger & B. J. Druker. 2003. c-CBL is not required for leukemiainduction by Bcr-Abl in mice. Oncogene. 22:8852-60
37. Ren,R. 2003. Overriding BCR/ABL mitotic signal by ICSBP-induced differentiation.Inside blood, Blood. 102:4251-52
38. Cuenco,G. M. and R. Ren. 2004. Both AML1 andEVI1 oncogenic components are required to the cooperation of AML1/MDS1/EVI1with BCR/ABL in induction of acute myelogenous leukemia in mice. Oncogene.23:569-79
39. Ren,R. 2004. Modeling the dosage effect of oncogenes in leukemogenesis. CurrentOpinion in Hematology. 11:25-34
40. Ren,R. 2004. Restraing CML by adhesives. Blood. 104:1917-18
41. Ren,R. 2005. Mechanisms of BCR-ABL in the pathogenesis of chronic myelogenousleukaemia. Nature Reviews Cancer. 5(3):172-83.
42. Ren,R. 2005. Oncogenic forms of Abl family kinases. in "Abl family kinases indevelopment and disease" (A. Koleske, ed). Landes Publishing.
43. Parikh,C. R. Subrahmanyam and R. Ren. 2006. Oncogenic NRAS rapidly and efficientlyinduces CMML- and AML-like diseases in mice. Blood. 108:2349-57.
44. Cuiffo,B. and R. Ren. 2006. Models of hematopoietic malignancies: chronic myeloidleukemia. Drug Discovery Today: Disease Models. 3:183-189
45. Shackelford,D., C. Kenific, A. Blusztajn, S. Waxman and R. Ren. 2006. Targeted Degradationof the AML1/MDS1/EVI1 oncoprotein by Arsenic Trioxide. Cancer Research.66:11360-11369
46. YanM, JK Luo, KJ Ritchie, I Sakai, K Takeuchi, R Ren, DE Zhang. 2007. Ubp43regulates BCR-ABL leukemogenesis via the Type I interferon receptor signaling.Blood. 110:305-12.
47. Parikh,C., R. Subrahmanyam and R. Ren. 2007. Oncogenic NRAS, KRAS and HRAS exhibitdifferent leukemogenic potentials in mice. Cancer Research. 67:7139-46
48. Zhang,S. J., L. Y. Ma, Q. H. Huang, G. Li, B. W. Gu, X. D. Gao, J. Y. Shi, Y. Y.Wang, L. Gao, X. Cai, R. Ren, J. Zhu, Z. Chen, S. J. Chen. 2008.Gain-of-function mutation of GATA-2 in acute myeloid transformation of chronicmyeloid leukemia. Proc. Natl. Acad. Sci. USA. 105: 2076-81.
49. Parikh,C. and R. Ren. 2008. Mouse model for NRAS-induced leukemogenesis. MethodsEnzymol. 439:15-24.
50. BaumKJ, R. Ren. 2008. Effect of Ras Inhibition in Hematopoiesis and BCR/ABLLeukemogenesis. J Hematol Oncol. 1:5.
51. Acquaviva,J. X. Chen and R. Ren. 2008. IRF-4 functions as a tumor suppressor in earlyB-cell development. Blood. 110:3798-806.
52. JaganiZ, K. Song, J. L. Kutok, M. R. Dewar, A. Melet, T. Santos, A. Grassian, S.Ghaffari, C. Wu, H. Yeckes-Rodin, R. Ren, K. Miller, R. Khosravi-Far. 2009.Proteasome inhibition causes regression of leukemia and abrogatesBCR-ABL-induced evasion of apoptosis in part through regulation of forkheadtumor suppressors. Cancer Research. 69:6546-55.
53. Cuiffo,B., and R. Ren. 2010. Palmitoylation of oncogenic NRAS is essential forleukemogenesis. Blood. 115:3598-605. PMID: 20200357
54. Jo,S., J. Schatz, J. Acquaviva, H. Singh and R. Ren. 2010. Cooperation betweendeficiencies of IRF-4 and IRF-8 promotes both myeloid and lymphoidtumorigenesis. Blood. 116:2759-67. PMID: 20585039 
55. Wang,Y.Y., L.J. Zhao, C.F. Wu, P. Liu, L. Shi, Y. Liang, S.M. Xiong, J.Q. Mi, Z.Chen, R. Ren (co-corresponding author), S.J. Chen. 2011. C-KIT mutation cooperates withfull-length AML1-ETO to induce acute myeloid leukemia in mice. Proc. Natl.Acad. Sci. USA. 108: 2450-5. PMID: 21262832 
56. Jo,S. and R. Ren. 2012. IRF-4 suppresses BCR/ABL transformation of myeloid cellsin a DNA binding-independent manner. J Biol Chem. 287:1770-8. PMID:22110133