PRMT1 MEDIATED ARG METHYLATION OF INHIBITORY SMADS IN TGF-BETA SIGNALLING

PRMT1 介导 TGF-β 信号传导中抑制性 SMAD 的 ARG 甲基化

• 批准号: 8363822
• 负责人: RIK M DERYNCK
• 金额: $ 1.03万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-06-01 至 2012-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8363822
• 关键词: Arginine; Development; Funding; Goals; Grant; Mass Spectrum Analysis; Mediating; Methylation; Molecular; National Center for Research Resources; Principal Investigator; Regulation; Research; Research Infrastructure; Resources; Role; Signal Transduction; Source; Transforming Growth Factor beta; United States National Institutes of Health; base; cost; response

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. This project aims to define the role of PRMT1 mediated arginine methylation of inhibitory Smads in the regulation of TGF-beta/BMP signaling. We aim to elucidate the molecular mechanism underlying PRMT1 mediated arginine methylation through identifying specific arginine resudes that are methylated, and examine the alteration of signaling response when this methylation is ablated. Assistance from UCSF Mass Spectrometry Facility is critical for achieving our research goals in that mass spectrometric analysis will help us identify target arginine resudes and confirm their methylation status. This will serve as the basis for our project development.

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 本项目旨在明确PRMT1介导的抑制性Smads精氨酸甲基化在调节转化生长因子-β/骨形态发生蛋白信号转导中的作用。我们的目的是通过鉴定特定的甲基化精氨酸结果来阐明PRMT1介导的精氨酸甲基化的分子机制，并检测当这种甲基化被去除时信号反应的变化。来自加州大学旧金山分校质谱学设施的帮助对于实现我们的研究目标至关重要，因为质谱学分析将帮助我们识别目标精氨酸结果并确认其甲基化状态。这将作为我们项目开发的基础。