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

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 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。

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. 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.