INCREASED A7/B1 INTEGRIN SIGNALING SECONDARY TO DAPC DISSOCIATION

DAPC 解离后 A7/B1 整合素信号传导增强

• 批准号: 7959742
• 负责人: STEPHEN C ARMSTRONG
• 金额: $ 21.83万
• 依托单位: SANFORD RESEARCH/USD
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-07-01 至 2010-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7959742
• 关键词: Area; Breeding; Cardiovascular system; Centers of Research Excellence; Chicago; Communication; Complement; Complex; Computer Retrieval of Information on Scientific Projects Database; Dilated Cardiomyopathy; Dissociation; Doctor of Medicine; Doctor of Philosophy; Dystrophin; Funding; Glycogen Synthase Kinase 3; Grant; Institution; Integrins; Knock-out; Knockout Mice; Life; Limb-Girdle Muscular Dystrophies; Mediating; Mus; Muscle Development; Muscular Dystrophies; Nevada; Patients; Protein Kinase; Regenerative Medicine; Regulation; Research; Research Personnel; Resources; Sarcoglycans; Secondary to; Signal Transduction; Skeletal Muscle; Source; Transgenic Organisms; United States National Institutes of Health; Universities; Weaning; human ITGA7 protein; mouse model; muscle regeneration; muscular dystrophy mouse model; novel; programs; pup; response; skeletal muscle differentiation; therapeutic development; transcription factor

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. COBRE Project 2 examines the hypothesis that communication of the dystrophin and integrin complexes regulates dilated cardiomyopathy in a ¿-sarcoglycan knock out mouse model of Limb Girdle Muscular Dystrophy 2F. Our mouse colony has developed rapidly since it inception, 8-20-08, with the establishment of two ¿sarcoglycan knock out breeding pairs from Elizabeth McNally, M.D., Ph.D; University of Chicago. We established three breeding pairs of alpha 7 integrin knock-out mice from Dean Burkin, Ph.D (Nevada Transgenic Facility) on 11-20-08. We initiated two ¿7 KO (B) X ¿SG KO (@) crosses on 3-13-09. These crosses were successful with both pairings producing live pups. These pups will be weaned on 4-26-09 and 4-28-09 and matured for assessment of dilated cardiomyopathy. We predict that the characterization of this novel cross will yield unique information that will guide the development of therapeutic approaches to dilated cardiomyopathy in patients with muscular dystrophy. We developed a program that examines skeletal muscle development in these mouse models of muscular dystrophy. This complements our studies on dilated cardiomyopathy in that we will examine pharmacologic approaches to the differentiation of skeletal muscle. Specifically, we will examine the hypothesis that inactivation of the protein kinase, GSK-3, reverses the negative regulation of transcription factors that is mediated by GSK-3. This hypothesis is the focus of an NIH Challenge Grant, entitled "GSK-3 Inactivation and Skeletal Muscle Regeneration in Muscular Dystrophy", that was submitted in response to the broad challenge area, Regenerative Medicine.

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