GONADOTROPIN-RELEASING HORMONE ACTION

促性腺激素释放激素作用

• 批准号: 8173169
• 负责人: P. MICHAEL CONN
• 金额: $ 4.76万
• 依托单位: OREGON HEALTH & SCIENCE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2011-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8173169
• 关键词: Cell physiology; Computer Retrieval of Information on Scientific Projects Database; Disease; Enzymes; Frequencies; Funding; Gonadotropin Hormone Releasing Hormone; Grant; Institution; Ion Channel; Molecular Chaperones; Post-Translational Regulation; Proteins; Publishing; Regulation; Research; Research Personnel; Resources; Route; Signal Transduction; Source; Therapeutic; Therapeutic Agents; United States National Institutes of Health; analog; base; mutant; receptor; translational study

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. These are highly translational studies in which we have observed that the underlying basis of mutational disease is frequently the mis-routing of otherwise functional proteins, in this case a receptorbut other labs have now confirmed this for other receptors, ion channels and enzymes. We have shown that these mutant receptors can be rescued and restored to function by pharmacological chaperones. We have determined that the regulation of routing is also a normal type of post-translational regulation that occurs in routine cell function and can be controlled. During the prior period we have shown that misfolded hGnRHR can be refolded so that therapeutic agents need not be continuously present. We have also shown that control of hGnRHR helps explain the basics of the ability of this receptor to respond to both amplitude and frequency modulated signals. GnRHR analogs were screened for potential therapeutic action and a review was published.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 这些是高度转化的研究，我们观察到，突变疾病的基本基础通常是对其他功能蛋白的误用，在这种情况下为受体，但其他实验室现在已经证实了其他受体，离子通道和酶。我们已经表明，这些突变受体可以被药理学伴侣救援并恢复以功能。我们已经确定路由的调节也是常规的翻译后调节类型，它发生在常规细胞功能中，并且可以控制。在上一时期，我们表明可以重折叠错误的HGNRHR，以便不必连续存在治疗剂。我们还表明，HGNRHR的控制有助于解释该受体对振幅和频率调制信号响应能力的基础。筛选了GNRHR类似物的潜在治疗作用，并发表了审查。