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ISGF3 Transcription Factor Family in Cytokine Signaling

细胞因子信号转导中的 ISGF3 转录因子家族

基本信息

批准号：
7758248
负责人：
David E Levy
金额：
$ 61.52万
依托单位：
NEW YORK UNIVERSITY SCHOOL OF MEDICINE
依托单位国家：
美国
项目类别：
财政年份：
1990
资助国家：
美国
起止时间：
1990-01-01 至 2012-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7758248
关键词：
Achievement Animal Cancer Model Animals Antibodies Binding Biochemical Biological Biological Process Biology C-terminal Cancer Biology Cell Cycle Cells Cellular biology Characteristics Collection Competence Complex Cytokine Signaling Cytoplasm Data Development Diagnosis Dimerization Disease Drug Delivery Systems Embryonic Development Family Family member Future Gene Expression Genetic Genetic Transcription Goals Immune Inflammatory Response Maintenance Malignant - descriptor Malignant Neoplasms Mediating Modeling Molecular Motivation Normal Cell Nuclear Translocation Oncogene Proteins Pathway interactions Play Process Proteins Regulation Research Resources Role STAT protein STAT1 gene STAT3 gene Signal Transduction Stem cells Stimulus Therapeutic Transactivation Transducers Tumor Suppressor Proteins Tyrosine Tyrosine Phosphorylation activating transcription factor animal tissue base extracellular genetic regulatory protein human disease interferon-stimulated gene factor 3 mutant novel novel strategies src Homology Region 2 Domain tool trophoblast tumor tumor progression

项目摘要

Signal Transducers and Activators of Transcription (STAT) proteins were originally characterized as latent transcription factors activated by signal-dependent tyrosine phosphorylation. Two founding members of this family, STAT1 and STATS, interact genetically and biochemically and have been shown to function in innate immune and inflammatory responses. Recent evidence also shows that STAT1 has characteristics of a tumor suppressor and STAT3 has characteristics of an oncogene, and these proteins play important but as yet poorly understood roles in cancer progression. A large body of research has fleshed out details of the JAK-STAT pathway, demonstrating the importance of tyrosine phosphorylation, dimerization, nuclear translocation, DMA binding, and transcription induction, features that fit the originally postulated role of STAT proteins as direct transducers of extracellular signals. While this paradigm has served to explain many aspects of STAT function, emerging data suggest that some biological functions of STAT1 and 3 are independent of one or more of the cornerstones of the canonical pathway.We proopse to explore the molecular mechanisms and biological consequences of STAT-dependent processes that are not fully explained by current models of JAK-STAT signaling. We propose to pursue the following specific aims: 1. Characterize the essential role of STATS in trophectoderm function and embryonic development. 2. Characterize the role of STATS in Ras-induced cancer. 3. Characterize the regulation, interaction, and function of STAT1 and STATS during the cell cycle. This research will be facilitated by our extensive collection of genetic and biochemical resources, including single and double mutant cells and animals, tissue-specific mutant animals, animal models of cancer, and antibody and molecular tools specific for STAT proteins. Achievement of the goals of this proposal will increase our understanding of the complex roles of these proteins in normal biology and cancer, will bridge a major gap in our current understanding of the mechanisms of STAT function, will further our efforts towards optimization of therapeutic strategies targeting STATS,and will facilitate development of novel strategies for better diagnosis and treatment of human disease.

信号转导和转录激活因子（STAT）蛋白最初被描述为