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: 7602898
• 负责人: Paul B Rothman
• 金额: $ 2.33万
• 依托单位: UNIVERSITY OF MICHIGAN AT ANN ARBOR
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-08-01 至 2008-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7602898
• 关键词: Bypass; Computer Retrieval of Information on Scientific Projects Database; Cytokine Inducible SH2-Containing Protein; Event; Funding; Grant; Institution; Laboratories; Maps; Oncogenes; Phosphorylation; Phosphorylation Site; Research; Research Personnel; Resources; Role; Source; Tyrosine; United States National Institutes of Health; abl Oncogene; metaplastic cell transformation

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.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 激活SOCS-1活性可能是Jak依赖性癌基因转化细胞过程中的一个重要步骤。SOCS-1过表达不能抑制v-Abl癌基因的转化，这表明SOCS-1的活性降低。Rothman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的活性中起作用。磷酸化位点的确定对于理解这一重要的调控事件是非常有用的。