Mitogen activated protein kinases regulation-PTH/PTHrP

丝裂原激活蛋白激酶调节-PTH/PTHrP

• 批准号: 7046686
• 负责人: HESHAM A TAWFEEK
• 金额: $ 13.23万
• 依托单位: MASSACHUSETTS GENERAL HOSPITAL
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-04-01 至 2008-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7046686
• 关键词: 3T3 cells; apoptosis; cell differentiation; cell growth regulation; cell proliferation; cell surface receptors; enzyme induction /repression; focal adhesion kinase; genetically modified animals; hormone regulation /control mechanism; immunoprecipitation; laboratory mouse; mitogen activated protein kinase; osteoblasts; parathyroid hormone related protein; parathyroid hormones; phosphorylation; protein tyrosine kinase; receptor binding; receptor expression; tissue /cell culture; western blottings

DESCRIPTION (provided by applicant): The ultimate goal of this K01 proposal is to provide the applicant with additional training in basic science and molecular biology to establish himself as an independent scientist. The project elucidates the molecular mechanisms and the function of PTH/PTHrP receptor regulation of Extracellular signal regulated (ERK) mitogen-activated protein (MAP) kinases. The role of non-receptor tyrosine kinases as well as the role of receptor phosphorylation in PTH activation of ERK1/2 MAP kinases in osteoblastic cell lines will be explored. Furthermore, the role of ERK1/2 MAP kinases in osteoblastic cell proliferation, differentiation and apoptosis will be investigated. Primary osteoblastic cell culture from wild type and genetically engineered mice as well as several other biochemical and pharmacological tools will be employed to achieve the goals of the study.

描述（由申请人提供）： 本K 01提案的最终目标是为申请人提供基础科学和分子生物学方面的额外培训，以使其成为独立的科学家。本项目旨在阐明PTH/PTHrP受体对细胞外信号调节（ERK）丝裂原活化蛋白（MAP）激酶的调节作用及其分子机制。将探讨成骨细胞系中非受体酪氨酸激酶的作用以及受体磷酸化在PTH激活ERK 1/2 MAP激酶中的作用。此外，ERK 1/2 MAP激酶在成骨细胞增殖、分化和凋亡中的作用也将被研究。将采用野生型和基因工程小鼠的原代成骨细胞培养物以及其他几种生化和药理学工具来实现研究目标。