UVR 诱导黑色素生成中的染色质重塑-猫眼课题宝

UVR 诱导黑色素生成中的染色质重塑

批准号：

7263913

负责人：

IVANA L DE LA SERNA

金额：

$10.55万

依托单位：

UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS

依托单位国家：

美国

项目类别：

财政年份：

2005

资助国家：

美国

项目状态：

已结题

起止时间：

2005-09-01 至 2009-07-31

来源：

https://reporter.nih.gov/project-details/7263913

关键词：

ATP Hydrolysis Address Apoptosis Apoptotic Binding CDKN1A gene Cell Cycle Cell Cycle Arrest Cell Cycle Regulation Cell Death Cell Survival Cells Chromatin Remodeling Factor Chromatin Structure Complex Condition Cutaneous DNA Damage DNA Repair Data Development Dominant-Negative Mutation Dopachrome isomerase Drosophila snf protein Enzymes Epidermis Event Exposure to G1 Phase Gene Activation Gene Expression Gene Expression Regulation Genes Genetic Transcription Malignant - descriptor Malignant Neoplasms Mammals Mediating Melanins Melanogenesis Molecular Monitor Monophenol Monooxygenase Mutate Oncogenic Pathway interactions Physiological Pigmentation physiologic function Pigments Play Process Reporting Research Personnel Resistance Role Role playing therapy Skin Skin Cancer Stimulus Tumor Suppressor Proteins Tyrosinase related protein-1 UV Radiation Exposure Ultraviolet Rays Yeasts cell growth chromatin remodeling environmental agent human TYRP1 protein melanocyte melanoma microphthalmia-associated transcription factor oncoprotein p21 programs promoter research study response transcription factor ultraviolet

项目摘要

项目成果

IVANA L DE LA SERNA的其他基金

相似基金

相关文献

中文摘要

翻译

点击翻译按钮获取中文摘要

英文摘要

DESCRIPTION (provided by applicant) Cutaneous melanocytes provide the major physiologic defense against the DNA damaging effects of ultraviolet (UV) radiation by synthesizing and distributing melanin to surrounding cells. Exposure to UV radiation is highly correlated with the transformation of normal melanocytes into melanoma. The mechanisms regulating the response to UV radiation and the steps leading to the oncogenic state have not been elucidated. A hallmark of exposure to UV radiation is an increase in pigmentation by enhanced transcription of genes required for melanin synthesis. Cells also respond to UV radiation by activation of pathways leading to cell cycle arrest, DNA repair, and apoptosis. To understand how a melanocyte responds to UV radiation, it is necessary to characterize the molecular mechanism involved. Activation of gene expression often involves alterations in chromatin structure to make it more accessible to the transcriptional machinery. SWI/SNF enzymes are multisubunit complexes that utilize the hydrolysis of ATP to remodel chromatin structure and facilitate transcription factor binding. They act as tumor suppressors, and are involved in gene regulation and cell cycle control. Preliminary evidence suggests that SWI/SNF enzymes are required for the activation of melanocyte specific genes (tyrosinase, trp1, and trp2) and for genes regulating cell cycle arrest (p21) and apoptosis (Bcl2). This proposal seeks to investigate the role that SWI/SNF enzymes play in the response to UV radiation. Specific Aim 1 will determine whether SWI/SNF enzymes are required for the enhanced expression of tyrosinase, trp1, and trp2 and for the modulation of other genes upon exposure to UV radiation. Specific Aim 2 will identify the mechanisms by which UV radiation results in activation of a melanocyte specific gene tyrosinase, by looking at changes in chromatin structure and transcription factor binding. Specific Aim 3 will determine a role for SWI/SNF enzymes in cell cycle control.

期刊论文(5)

专著(0)

科研奖励(0)

会议论文