题目：Endogenous MAP4K4 is activated by diverse cardiac stress signals and plays an essential role in the ceramide death pathway
主讲人：美国Baylor大学医学院谢敏博士
时间：2007年5月22日4PM
地点：综合楼三层东头学术报告厅
主办：医学院
来自下面这个组的。
http://www.bcm.edu/db/db_fac-schneider.htmlMichael D. Schneider
E-mail:
michaels@bcm.tmc.eduProfessor, Baylor College of Medicine
Co-Director, Center for Cardiovascular Development
M.D. Anderson Foundation Professor
A.B., Harvard College, Cambridge, MA, 1972
M.D., University of Pennsylvania School of Medicine, 1976
Clinical Associate, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, 1978-84
Cardiac growth and differentiation
Current research in Dr. Schneider's laboratory is aimed at the molecular genetics of cardiac muscle, with heavy reliance on mouse genetic models. Morphogenesis: a heart-specific knockout of the type IA receptor for bone morphogenetic proteins results in death at mid-gestation, with cardiac septal defects. Hypertrophy: a gain-of-function mutation that mimics the activation of the mitogen-activated protein kinase TAK1 (as seen after a mechanical load) suffices to precipitate heart failure in mice. Survival: cardiac-specific expression of Bcl-2 can reduce the extent of cardiac death by 50% and preserves cardiac mechanical performance, after ischemia-reperfusion injury. In addition to mouse models, extensive use is made of adenoviral gene transfer, to dissect cardiac life and death cascades.
Selected Publications
Zhang D, Gaussin V, Taffet GE, Belaguli NS, Yamada M, Schwartz RJ, Michael LH, Overbeek PA, Schneider MD (2000) TAK1 is activated in the myocardium after pressure overload and is sufficient to provoke heart failure in transgenic mice. Nature Medicine 6:556-563.
Oh H, Taffet GE, Youker KA, Entman ML, Overbeek PA, Michael LH, Schneider MD (2001) Telomerase reverse transcriptase promotes cardiac muscle cell proliferation, hypertrophy, and survival. Proceedings of the National Academy of Sciences U.S.A. 98:10308-10313.
Gaussin V, Van de Putte T, Mishina Y, Hanks MC, Zwijsen A, Huylebroeck D, Behringer RR, Schneider MD (2002) Endocardial cushion and myocardial defects after cardiac myocyte-specific conditional deletion of the bone morphogenetic protein receptor ALK3. Proceedings of the National Academy of Sciences U.S.A. 99:2878-2883.
Minamino T, Yujiri T, Terada N, Taffet GE, Michael LH, Johnson GL, Schneider MD (2002) MEKK1 is essential for cardiac hypertrophy and dysfunction induced by Gq. Proceedings of the National Academy of Sciences U.S.A. 99:3866-3871.
Wei L, Imanaka-Yoshida K, Wang L, Zhan S, Schneider MD, DeMayo FJ, Schwartz RJ (2002) Inhibition of Rho family GTPases by Rho GDP dissociation inhibitor disrupts cardiac morphogenesis and inhibits cardiomyocyte proliferation. Development 129:1705-1714.
Sano M, Abdellatif M, Oh H, Xie M, Bagella L, Giordano A, Michael LH, DeMayo FJ, Schneider MD (2002) Activation and function of cyclin T-Cdk9 (positive transcription elongation factor-b) in cardiac muscle-cell hypertrophy. Nature Medicine 8:1310-1317.
Nakamura T, Sano M, Songyang Z, Schneider MD (2003) A Wnt- and β-catenin-dependent pathway for mammalian cardiac myogenesis. Proceedings of the National Academy of Sciences U.S.A. 100:5834-5839.
Oh H, Bradfute SB, Gallardo TD, Nakamura T, Gaussin V, Mishina Y, Pocius J, Michael LH, Behringer RR, Garry DJ, Entman ML, Schneider MD (2003) Cardiac progenitor cells from adult myocardium: homing, differentiation, and fusion after infarction. Proceedings of the National Academy of Sciences U.S.A. 100:12313-12318.
Contact Information
Michael D. Schneider, M.D.
Department of Medicine
Baylor College of Medicine
One Baylor Plaza 506C
Houston, Texas 77030, U.S.A.
Tel: (713) 798-6683
Fax: (713) 798-7437
E-mail:
michaels@bcm.tmc.edu
