INCREASED A7/B1 INTEGRIN SIGNALING SECONDARY TO DAPC DISSOCIATION

DAPC 解离后 A7/B1 整合素信号传导增强

基本信息

批准号：
8168343
负责人：
STEPHEN C ARMSTRONG
金额：
$ 4.97万
依托单位：
SANFORD RESEARCH/USD
依托单位国家：
美国
项目类别：
财政年份：
2010
资助国家：
美国
起止时间：
2010-07-01 至 2011-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8168343
关键词：
Area Breeding 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 Secondary to Signal Transduction Skeletal Muscle Source Transgenic Organisms United States National Institutes of Health Universities Weaning delta Sarcoglycan human ITGA7 protein mouse model muscle regeneration muscular dystrophy mouse model novel programs pup response skeletal muscle differentiation therapeutic development transcription factor

项目摘要

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 delta-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 deltasarcoglycan 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.

该副本是利用众多研究子项目之一由NIH/NCRR资助的中央赠款提供的资源调查员（PI）可能已经从其他NIH来源获得了主要资金，因此，在列出的机构中可能会被压制对于中心，这不一定是调查员的工厂。 Cobre Project 2研究了肌营养不良蛋白和整合素的通讯在Oglycan敲除肢体肌肉肌营养不良2F的Oglycan敲除模型中，我们的小鼠菌落群体迅速发展了ITCEPTION，8-20-08，并建立了8-20-0-08，并建立伊丽莎白·麦克纳利（Elizabeth McNally），芝加哥大学（University of Chicago）的伊丽莎白·麦克纳利（Elizabeth McNally）敲打了两名sarcoglycan » 7 ko（b）x¿ SG KO（@）在3-13-09上交叉。肌营养不良症患者的囊性心肌病的疗法发展。我们在这些肌肉营养不良的小鼠模型中开发了一个骨骼肌肉的发展，这将检查骨骼肌肉的分化药物。蚂蚁，标题为“ GSK-3失活和骨骼肌再生肌营养不良症”，该蚂蚁是在重生挑战区，再生医学的Rewsoney中。