個人履歷
任瑞寶
中文名：任瑞寶
英文名：Ruibao Ren
性別：男
學位：博士（M.D./Ph.D.）
主要教育背景及工作經(jīng)歷
學習經(jīng)歷
1992 u20131994 博士后，美國洛克菲勒大學David Baltimore 實驗室。期間， 1994,7-1994,12 在美國麻省理工學 院。
1988 u20131992 博士研究生, 美國紐約哥侖比亞大學醫(yī)學院微生物系Vincent
Racaniello實驗室。
1983 u20131986 中國北京醫(yī)科大學（現(xiàn)北京大學醫(yī)學部）微生物系 ，醫(yī)學碩士研
究生
1978 u20131983 中國北京醫(yī)學院（現(xiàn)北京大學醫(yī)學部），基礎醫(yī)學系本科生
工作經(jīng)歷
1995-2000 美國布蘭戴斯大學(BrandeisUniversity)生物系助理教授
2000-2008 美國布蘭戴斯大學生物系副教授(tenured)
2008-2011 美國布蘭戴斯大學生物系終生教授
2010-2011 美國布蘭戴斯大學生物系聯(lián)席系主任
所獲獎勵
1992 獲美國哥侖比亞大學研究生院優(yōu)秀研究生院長獎
1992 獲Irvinton研究所博士后獎學金
1992-1995 獲腫瘤研究所博士后獎學金
1996-1998 獲美國癌癥研究協(xié)會青年學者獎
1996-1998 獲美國March of Dimes, Basil Ou2019Connor 青年學者獎
1998-2003 獲美國白血病及淋巴瘤協(xié)會學者獎
2003 獲美國癌癥研究協(xié)會研究學者稱號
會員
1998-至今 美國血液學協(xié)會會員
2002 美國血液學協(xié)會2002年年會慢性髓細胞白血病分會主席
2006-至今 美國癌癥研究協(xié)會會員
委任職務
2005-至今 美國國家衛(wèi)生研究院血液學項目評審委員會委員
2006-至今 美國白血病及淋巴瘤協(xié)會評審委員會委員
2007-至今 美國國防部CML項目評審委員會主席
2006-至今 北京大學學報醫(yī)學版特邀編委
2008-至今 美國Journal of Hematology and Oncology雜志常務副主編
2011-至今 美國Journal of Biological Chemistry雜志編委
2011-至今 醫(yī)學前沿編委
2017-至今 上海血液研究所所長
科技創(chuàng)新成果
任瑞寶教授長期從事分子生物學, 疾病學及治療學研究。 在《Cell》, 《Nature》, 《Science》， 《Genes & Development》， 《PNAS》， 《Blood》， 《MCB》, 《Cancer Research》等重要學術期刊發(fā)表50多篇論文，引用率達6000次。 發(fā)表在《Science》雜志上的一篇論文在1993年全世界論文引用次數(shù)最多的十篇論文中排名第三。獲美國國立衛(wèi)生院, 美國國防部及美國腫瘤協(xié)會的多項研究基金。已培養(yǎng)了超過20名的博士研究生, 博士后和訪問學者。先后獲美國腫瘤協(xié)會, 美國March of Dimes, Basil Ou2019Connor 和白血病及淋巴瘤協(xié)會學者獎。歷任布蘭戴斯大學終生教授，生物系聯(lián)席系主任，布蘭戴斯大學生物安全委員會主席， 美國國家衛(wèi)生研究院血液學項目評審委員會委員， 白血病及淋巴瘤協(xié)會評審委員會委員， 美國國防部CML項目評審委員會主席�，F(xiàn)任美國生物化學雜志（JBC）編委，美國血液與腫瘤學雜志（JHO）常務副主編，醫(yī)學前沿編委及北京大學學報醫(yī)學版特邀編委。2011年全職回國任上海交通大學醫(yī)學院附屬瑞金醫(yī)院上海血液學研究所常務副所長、所長，研究員。
主要成就
1. 將人小兒麻痹病毒受體轉(zhuǎn)入小鼠而制成了小兒麻痹病毒受體的轉(zhuǎn)基因小鼠模型，并用此模型做了大量深入的小兒麻痹病毒分子生物學研究。這個模型對研究小兒麻痹病毒的致病機理及小兒麻痹病毒疫苗的安全測試具有廣泛的理論及應用價值。該動物模型獲美國專利.
2. 首次發(fā)現(xiàn)了存在于許多重要信號傳導蛋白質(zhì)中的SH3功能基團的功能及結合靶點。發(fā)表在《Science》雜志上的該論文在1993年全世界論文引用次數(shù)最多的十篇論文中排名第三。同時，在克隆3BP2基因后與Bruce Mayer 一道首次發(fā)現(xiàn)并命名了Pleckstrin homology功能基團（PHD）。
3. 研發(fā)了BCR/ABL誘導的人慢性髓細胞白血�。–ML）及人急性淋巴細胞白血�。ˋLL），AML1/EVI1誘導的人急性髓細胞白血�。ˋML），及RAS誘導的人急性及慢性粒細胞及單核細胞白血�。ˋMML，CMML）的小鼠模型。 這些疾病模型對研究白血病致病機理，研發(fā)及測試白血病治療具有重要的理論及應用價值。
4. 用CML小鼠模型系統(tǒng)的進行BCR/ABL功能與結構的研究。揭示了BCR/ABL蛋白質(zhì)激酶活性對其誘導CML的必要性 u2013 為BCR/ABL蛋白質(zhì)激酶抑制劑成功治療CML 提供了理論基礎。同時發(fā)現(xiàn)BCR/ABL蛋白質(zhì)激酶外的功能集團對誘導CML 的重要作用 - 為研發(fā)抗BCR/ABL蛋白質(zhì)激酶抑制劑耐藥性治療提供了理論基礎。
5. RAS是人類最常見的癌基因（RAS基因突變見于30%人類腫瘤）。 任瑞寶教授的實驗室首次建立了NRAS（白血病中最常見的RAS基因突變）誘導的AMML及CMML動物模型，并用此模型系統(tǒng)的進行NRAS功能與結構的研究。首次發(fā)現(xiàn)棕櫚�；≒almitoylation）修飾對NRAS誘導白血病的必要性 u2013 為研發(fā)抗NRAS相關的白血病及其他癌的治療奠定了理論基礎。
NRAS腫瘤基因存在于25-30% 白血病， 肝癌及黑色素瘤中， 抑制NRAS棕櫚酰化修飾對這些腫瘤應有有效的治療作用。雖然很多腫瘤為KRAS4B腫瘤基因陽性， 而KRAS不需棕櫚酰化修飾， 但進來發(fā)現(xiàn)KRAS4A （另一KRAS基因剪接產(chǎn)物）在KRAS陽性腫瘤， 如肺癌，發(fā)病過程中起重要作用，而KRAS4A需要棕櫚酰化修飾。同時我們還發(fā)現(xiàn)抑制NRAS棕櫚�；揎棇AS上游腫瘤蛋白有阻斷作用, 因此抑制RAS棕櫚�；揎棇δ[瘤應有廣泛的治療效果。該應用的專利申請正在審理中。
6. 三氧化二砷成功治療急性早幼粒細胞白血病（APL）是中國的首創(chuàng)。三氧化二砷主要作用機理是誘導PML-RARα融合癌蛋白降解。任瑞寶教授的實驗室發(fā)現(xiàn)三氧化二砷也誘導EVI1癌蛋白降解。EVI1的異常表達見于10%AML病人及90%以上宮頸癌病人。 上述發(fā)現(xiàn)為擴大三氧化二砷治療這些疾病提供了理論基礎。
7. 干擾素調(diào)節(jié)因子4（IRF4）最初被發(fā)現(xiàn)為癌蛋白， 對多發(fā)性骨髓癌癌細胞生存的維系起重要作用。近來，任瑞寶教授的實驗室首次發(fā)現(xiàn)IRF4 在早期B-淋巴細胞及髓細胞中的功能為癌抑制蛋白。 這一發(fā)現(xiàn)對發(fā)展多發(fā)性骨髓癌及白血病的治療具有重要指導作用。IRF4癌抑制功能及應用的專利申請正在審理中。
發(fā)表論著
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
57. Jiao, B., Z.H. Ren, P. Liu, L.J Chen, J.Y. Shi, Y. Dong, J. Ablain, L. Shi, L. Gao, J.P. Hu, R. Ren, H. de Thé, Z. Chen, and S.J. Chen. 2013. 8-CPT-cAMP/all-trans retinoic acid targets t(11;17) acute promyelocytic leukemia through enhanced cell differentiation and PLZF/RARα degradation.Proc. Natl. Acad. Sci. USA.110:3495-500
58. Liu, Y.J., H.B. Fan, Y. Jin, C.G. Ren, X.E. Jia, L. Wang, Y. Chen, M. Dong, K.Y. Zhu, Z.W. Dong, B.X. Ye, Z. Zhong, M. Deng, T.X. Liu and R. Ren. 2013.Cannabinoid receptor 2suppresses leukocyte inflammatory migration by modulating the JNK/c-Jun/Alox5pathway.J Biol Chem.288:13551-62.
59. Ren C.G., L. Wang, X.E. Jia, Y.J. Liu, Z.W. Dong, Y. Jin, Y. Chen, M. Deng, Y. Zhou, Y. Zhou, R. Ren(co-corresponding author), W.J. Pan and T.X. Liu. 2013. Activated N-Ras signaling regulates arterial-venous specification in zebrafish.J Hematol Oncol.6:34 doi: 10.1186/1756-8722-6-34.
60. Fredericks J. and R. Ren. 2013. The role of RAS effectors in BCR/ABL induced chronic myelogenous leukemia.Front Med.7:452-61.
61.Du T.T., P.F. Xu, Z.W. Dong, H.B. Fan, Y. Jin, M. Dong, Y. Chen, W.J. Pan, R. Ren, T.X. Liu, M. Deng, and Q.H. Huang. 2014. Setdb2 controls convergence and extension movements during zebrafish gastrulation by transcriptional regulation of dvr1.Dev Biol.392:233-44
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