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水生所11月21日创新系列讲座预告(2016-11)
作者: | 2016-11-18 | 浏览量:

  时间:2016年11月21日 星期一 上午10:00

  地点:标本馆506报告厅

  报告专家: Dr. Wenbiao Chen Vanderbilt University

  报告题目:Molecular Mechanisms of Islet Cell Compensation and Decompensation During Metabolic Stress in Zebrafish

  专家简介:

  陈文标博士于1997年在Oregon Health Sciences University获得博士学位,1997-2001年在Massachusetts Institute of Technology做博士后工作。2013年至今,受聘于Vanderbilt University,任副教授一职。陈文标博士2015年曾经获得VICB文章引用率最高殊荣,并于2016年入选Chancellor Faculty Fellow,陈博士曾经在NATURE, CELL, PNAS等国际顶级知名期刊发表学术论文若干,同时也是该学科领域多家期刊的审稿人。

  研究方向:

  Pancreatic alpha and beta cells secrete glucagon and insulin respectively to maintain glucose homeostasis. In conditions that impair the signaling of these hormones, alpha and beta cells compensate by increasing their number and augmenting their secretion. Defects in the compensatory responses lead to defects in glucose homeostasis. The molecular mechanisms underlying the compensatory responses remain incompletely understood. The Chen laboratory found that compensatory responses of pancreatic alpha cells and beta cells is conserved in zebrafish, a vertebrate model amenable for live imaging as well as large-scale genetic and chemical screens. We combine genetic, pharmacological, and imaging techniques to identify genes essential for the compensatory responses and to define their roles in diabetes.

  报告摘要:

  The pancreatic islet employs several mechanisms to maintain glucose homeostasis. In addition to the acute change of glucagon and insulin secretion from alpha and beta cells in response to low and high blood glucose, respectively, insufficient action of glucagon and insulin also triggers compensatory hyperplasia of the cognate cells. Defects in beta -cell compensation and beta-cell maintenance result in diabetes, and compensatory alpha-cell hyperplasia can lead to endocrine tumors. I will present our recent work on using zebrafish as a model to understand the molecular mechanisms of overnutrition-induced beta-cell genesis, glucagon deficiency-induced alpha-cell hyperplasia, and chronic overnutrition-induced beta-cell death.

  代表性发表文章:

  1. Lu D, Willard D, Patel IR, Kadwell S, Overton L, Kost T, Luther M, Chen W, Woychik RP, Wilkison WO, and Cone RD (1994). Agouti protein is an antagonist of the melanocyte-stimulating-hormone receptor. Nature 371, 799-802.

  2. Chen W, Kelly MA, Opitz-Araya X, Thomas RE, Low MJ, and Cone RD. (1997). Exocrine glands dysfunction in MC5-R-deficient mice: Evidence for coordinated regulation of exocrine gland function by melanocortin peptides. Cell 91,789-798.

  3. Zhang C, Song Y, Thompson DA, Madonna MA, Milhauser GL, Toro S, Varga Z, Westerfield M, Gamse J, Chen W, and Cone RD. (2010) A Pineal-specific Agouti Protein Regulates Teleost Background Color Adaptation. PNAS 107(47):20164-71.

  4. Ni TT, Lu J, Zhu M, Maddison LA, Huskey LC, Boyd K, Ju B, Hesselson D, Zhong TP, Page-McCaw PS, Stainier DY, Chen W. (2012) Conditional control of gene function by an invertible gene trap in zebrafish. PNAS, 109:15389-94. (Featured with commentary)

  5. Jao LE, Wente S, Chen W. (2013) Efficient multiplex biallelic zebrafish genome editing using the CRISPR nuclease. PNAS 110(34):13904-9.

  6. Lin CY, ErkekS, Tong, Y, Yin L, Federation AJ, Zapatka M, Haldipur P, Kawauchi D, Risch T, Warnatz HJ, Worst BC, Ju B, Orr BA, Zeid R, Polaski DR, Segura-Wang M, Waszak SM, Jones DTW, Kool M, Hovestadt V, Buchhalter I, Sieber L, Johann P, Chavez L, Gröschel S, Ryzhova M, Korshunov A, Chen W, Chizhikov VV, Millen KJ, Amstislavskiy V, Lehrach H, Yaspo M, Eils R, Lichter P, Korbel JO, Pfister SM, Bradner, JE and Northcott PA. (2016) Active medulloblastoma enhancers reveal subgroup-specific cellular origins. Nature 530(7588):57-62.

  7. Michel M, Page-McCaw, PS, Chen W, Cone RD. (2016) Leptin Signaling Regulates Glucose Homeostasis, but not Adipostasis, in the Zebrafish. PNAS 113(11):3084-9 (Epub Feb 22, 2016).

  8. Li M, Zhao L, Page-McCaw PS, Chen W (2016) Zebrafish genome engineering using the CRISPR-Cas9 system. Trends in Genetics (accepted).

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