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肠道疾病课题组

2019年02月25日 来源:

  简介:

  韩晓男,2000年毕业于中国医学科学院和中国协和医科大学病理系,获博士学位。随后于2000-2003年在美国匹茨堡医学院重症分子医学中心,病理和分子细胞生物学系做博士后研究。于2003年至2006年在辛辛那提儿童医学中心从事消化道疾病研究。从2006年至2016年分别任辛辛那提儿童医院胃肠,肝和营养系讲师,儿科助理教授和消化病中心副研究员。现为中国医学科学院,中国协和医科大学医学动物研究所研究员。他的课题组发表包括最后联系作者 SCI论文70余篇包括Gastroenterology, Gut, PNAS, EMBO Molecular Medicine, Stem Cell Reports等。韩教授目前为美国胃肠学会(AGA),生理学会(APS), 细胞生学(ASCB)和药物和实验治疗学会(APET)会员。曾获美国国防部科研探索奖 (Discover Award 2013),美国胃肠学会(AGA)-爱唯(Elsevier 2012)奖,美国克隆氏病和结肠病学会年轻科学家奖(Young Investigator Award 2006), 科研发展奖(Career Development Award 2005)和资深科研奖(Senior Research Award 2016)等。

  研究方向:
  肠道感染和炎症病理学、肠道干细胞生物学。

  人员组成:

 
 
李海凤
助理研究员
刘瑞雪
技师

  联系方式:010-63132343
  科研成果:

  1)Liu R, Moriggl R, Zhang D, Li H, Ruan H, Karns1 R, Mayhew C, Watson C, Bangar H, Cha S, Haslam D, Zhang T, Helmrath M, Wells J, Denson L, Han X*. Constitutive STAT5 Activation Regulates Paneth and Paneth-like Cells to Control C. difficile Ileocolitis. Life Science Alliance. 2019 Apr 4;2(2). PMID: 30948494

  2) Li H, Liu R, Zhang D, Li N, Cai J, Moriggl R, Wells, J, Denson L, Han X*. Regulation of Paneth Cell Lineages for Reginal Immune Specification to Control Comorbidity of C. Difficile Infection with IBD. Gastroenterology, Volume 154, Issue 1, Supplement, January 2018, Page S50

  3)Liu R, Li H, Cai J, Wei Q, Han X*,Lgr5+ intestinal stem cell sorting and organoid culture. Animal Model Exp Med,2019,00:1-4.

  4)Zhao M, Xiong X, Ren K, Xu B, Cheng M, Sahu C, Wu K, Nie Y, Huang Z, Blumberg RS, Han X, Ruan HB. Deficiency in intestinal epithelial O-GlcNAcylation predisposes to gut inflammation. EMBO Mol Med. 2018 Aug;10(8). pii: e8736. PMID: 29941542.

  5)Rauth M, Freund P, Orlova A, Grünert S, Tasic N, Han X, Ruan HB, Neubauer HA, Moriggl R. Cell Metabolism Control Through O-GlcNAcylation of STAT5: A Full or Empty Fuel Tank Makes a Big Difference for Cancer Cell Growth and Survival. Int J Mol Sci. 2019 Feb 27;20(5). pii: E1028. doi: 10.3390/ijms20051028. Review. PMID: 30818760

  6)Ballweg R, Lee S, Han X, Maini P, Byme H, Hong C, Zhang T. Unraveling the control of cell cycle period during intestinal stem cell differentiation. Biophysical Journal, 2018, 115, 1-9. PMID: 30467024.

  7)Kaltenecker D, Themanns M, Mueller KM, Spirk K, Suske T, Merkel O, Kenner L, Luís A, Kozlov A, Haybaeck J, Müller M, Han X, Moriggl R. Hepatic growth hormone - JAK2 - STAT5 signalling: Metabolic function, non-alcoholic fatty liver disease and hepatocellular carcinoma progression. Cytokine. 2018 Oct 30. 2018.10.010. PMID: 30389231.

  8)Wingelhofer B, Neubauer H, Valent P, Han X, Constantinescu S, Gunning P, Müller M, Moriggl R. Implications of STAT3 and STAT5 signaling on gene regulation and 1 chromatin remodeling in hematopoietic cancer. 2018 Mar 27. doi: 10.1038/s41375-018-0117-x. PMID: 29728695

  9)Kramer N, Schmöllerl J, Unger C, Nivarthi H, Rudisch A, Unterleuthner D, Scherzer M, Riedl A, Artaker M, Crncec I, Lenhardt D, Schwarz T, Prieler B, Han X, Hengstschläger M, Schüler J, Eferl R, Moriggl R, Sommergruber W, Dolznig H. Autocrine WNT2 signaling in fibroblasts promotes colorectal cancer progression. Oncogene. 2017 Sep 28;36(39):5460-5472. PMID: 28553956

  10)Friedrich K, Dolznig H, Han X, Moriggl R. Steering of carcinoma progression by the YIN/YANG interaction of STAT1/STAT3. Biosci Trends. 2017 Feb 2. doi: 10.5582/bst.2016.01250. PMID: 28154246

  11)Freund P, Kerenyi MA, Hager M, Wagner T, Wingelhofer B, Pham HTT, Elabd M, Han X, Valent P, Gouilleux F, Sexl V, Krämer OH, Groner B, Moriggl R. O-GlcNAcylation of STAT5 controls tyrosine phosphorylation and oncogenic transcription in STAT5-dependent malignancies. Leukemia. 2017 Oct;31(10):2132-2142. PMID: 28074064

  12) Zhang R1, Gilbert S1, Yao X, Vallance J, Steinbrecher K, Moriggl R, Eluri M, Shroyer N, Cao H, Denson L, Han X*. Methyl Protodiosin Protests against Mucosal Injury by Promoting Commensal-induced Epithelial Innate Immunity. Pharmacology Research & Perspectives, 2015 2015 Mar;3(2):e00118.

  13)Gilbert S, Zhang R, Denson L, Moriggl R, Steinbrecher K, Shroyer N, Lin J, Han X*. Enterocyte STAT5 promotes mucosal wound healing via suppression of myosin light chain kinase-mediated loss of barrier function and inflammation. EMBO Mol Med. 2012 Feb;4(2):109-24.