ADAPTIVE REGULATION IN 3T3 L1 ADIPOCYTES

3T3 L1 脂肪细胞的自适应调节

• 批准号: 6176604
• 负责人: SUSAN Cooke FROST
• 金额: $ 17.45万
• 依托单位: UNIVERSITY OF FLORIDA
• 依托单位国家: 美国
• 财政年份: 1992
• 资助国家: 美国
• 起止时间: 1992-05-01 至 2003-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6176604
• 关键词: 3T3 cells; adipocytes; animal genetic material tag; antisense nucleic acid; gene induction /repression; glucose; glucose metabolism; glucose transport; glucose transporter; intermolecular interaction; laboratory mouse; nutrition related tag; protein structure function; site directed mutagenesis; transfection /expression vector

DESCRIPTION: Carbohydrate regulated genes provide a mechanism for integrating cellular responses with resource utilization in the entire body. This coordinated effort provides exquisite regulation in maintaining the circulating levels of glucose in humans within a fairly narrow range. Glucose deprivation increases the rate of glucose transport by the GLUT-1 receptor in a number cel types by a protein synthesis dependent mechanism. However, the expression of the GLUT1 glucose transporter does not change. This proposal focuses on the discovery of a unique 50 kDa protein whose synthesis is regulated by glucose availability. The studies proposed test the hypothesis that this 50 Kda protein modulates the activity of GLUT 1 to affect changes in glucose uptake. The research plan involves a series of specific aims which define the expression of the p50 protein at the transcriptional and translational level in 3T3-L1 adipocytes and the mouse. Experiments are designed to examine the interaction of p50 with GLUT! and the effect of that interaction on transport activity. Finally, studies are proposed to examine the role of p50 in transport function, in vivo, using antisense technology to inhibit it expression and adenovirus transduction system to stimulate overexpression.

描述：碳水化合物调节基因提供了一种机制， 将蜂窝响应与整个系统中的资源利用相结合 身体这种协调的努力提供了精致的调节， 人体内葡萄糖的循环水平在一个相当窄的范围内。 葡萄糖剥夺增加了GLUT-1的葡萄糖转运速率 受体通过蛋白质合成依赖性机制在多种细胞类型中表达。 然而，GLUT 1葡萄糖转运蛋白的表达没有改变。 该提案的重点是发现一种独特的50 kDa蛋白质， 合成受葡萄糖可用性调节。 该研究提出的测试 这一50 Kda蛋白调节GLUT 1活性的假设 影响葡萄糖摄取的变化。 该研究计划涉及一系列 的特定目标，其定义了p50蛋白的表达， 在3 T3-L1脂肪细胞中的转录和翻译水平， 老鼠.实验旨在研究p50与 GLUT！ 以及这种相互作用对运输活动的影响。 最后， 建议研究p50在转运功能中的作用， 在体内，利用反义技术抑制其表达， 转导系统以刺激过表达。