PROLACTIN REGULATES THE UTERINE RESPONSE TO PROGESTERONE

催乳素调节子宫对黄体酮的反应

• 批准号: 2201882
• 负责人: Beverly S. Chilton
• 金额: $ 16万
• 依托单位: TEXAS TECH UNIVERSITY HEALTH SCIS CENTER
• 依托单位国家: 美国
• 财政年份: 1993
• 资助国家: 美国
• 起止时间: 1993-12-01 至 1996-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2201882
• 关键词: DNA binding protein; DNA footprinting; cell type; complementary DNA; gel mobility shift assay; genetic library; genetic promoter element; genetic regulation; genetic transcription; glycoproteins; hormone receptor; hormone regulation /control mechanism; immunocytochemistry; in situ hybridization; laboratory rabbit; messenger RNA; molecular cloning; northern blottings; progesterone; prolactin; protein sequence; recombinant proteins; tissue /cell culture; uterus; western blottings

DESCRIPTION (Adapted from the applicant's abstract): The ultimate objective of this work is to understand how receptors and other DNA-binding proteins interact to regulate the transcription of tissue- and hormone-specific genes. The aim of this proposal is to understand how PRL augments the progesterone-dependent transcription of the UG gene by regulating as many as four proteins that bind to the UG promoter. This goal will be achieved by 1) cloning and characterizing the cDNAs for PRL/progesterone-dependent proteins that bind to the UG promoter; 2) determining whether PRL, in combination with progesterone, regulates the sequence-specific binding activity of the UG promoter binding (UGPB) proteins; 3) quantifying hormone-dependent changes in the expression of mRNA for UGPB proteins by specific uterine cell types; 4) characterizing the interactions of PRL and progesterone in the regulation of the UG promoter in an in vitro cell transfection system.

描述（改编自申请人的摘要）：最终的 这项工作的目的是了解受体和其他 DNA 结合的方式 蛋白质相互作用来调节组织和 激素特异性基因。 本提案的目的是了解 PRL 如何 通过以下方式增强 UG 基因的黄体酮依赖性转录 调节多达四种与 UG 启动子结合的蛋白质。 这 通过以下方式实现目标： 1) 克隆和表征 cDNA 与 UG 启动子结合的 PRL/孕酮依赖性蛋白； 2） 确定 PRL 与黄体酮结合是否可以调节 UG 启动子结合 (UGPB) 的序列特异性结合活性 蛋白质； 3）量化激素依赖性表达变化 特定子宫细胞类型的 UGPB 蛋白 mRNA； 4）表征 PRL 和孕酮在 UG 调节中的相互作用 体外细胞转染系统中的启动子。