MAPPING SITES OF PHOSPHORYLATION ON SUPPRESSOR OF CYTOKINE SIGNALING 1 (SOCS-1)

绘制细胞因子信号传导抑制剂 1 (SOCS-1) 磷酸化位点

• 批准号: 7359138
• 负责人: Paul B Rothman
• 金额: $ 2.71万
• 依托单位: UNIVERSITY OF MICHIGAN AT ANN ARBOR
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-08-01 至 2007-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7359138
• 关键词: MAPPING; SITES; PHOSPHORYLATION; SUPPRESSOR; CYTOKINE

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. Bypassing SOCS-1 activity may be an essential step during cellular transformation by Jak-dependent oncogenes. SOCS-1 over expression is unable to inhibit transformation by v-Abl oncogenes that suggests the activity of SOCS-1 is decreased. The Rothman laboratory has evidence that the phosphorylation of SOCS-1 on non-tyrosine residues has a role in modulating the activity of SOCS-1. The determination of the sites of phosphorylation would be very useful in understanding this important regulatory event.

这个子项目是利用由NIH/NCRR资助的中心拨款提供的资源的许多研究子项目之一。子项目和调查员(PI)可能从另一个NIH来源获得了主要资金，因此可能会出现在其他CRISE条目中。列出的机构是针对中心的，而不一定是针对调查员的机构。在JAK依赖癌基因的细胞转化过程中，绕过SOCS-1活性可能是必不可少的一步。SOCS-1过表达不能抑制v-Abl癌基因的转化，提示SOCS-1活性降低。罗斯曼实验室有证据表明，SOCS-1在非酪氨酸残基上的磷酸化在调节SOCS-1的活性方面具有作用。磷酸化位点的确定将非常有助于理解这一重要的调控事件。