Mechanisms of post-transcriptional regulation of MeCP2

MeCP2转录后调控机制

• 批准号: 6506556
• 负责人: CAROL S LUTZ
• 金额: $ 7.78万
• 依托单位: UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-07-01 至 2004-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6506556
• 关键词: CpG islands; RNase protection assay; Rett syndrome; biological signal transduction; cell line; gene expression; genetic regulation; genetic regulatory element; messenger RNA; molecular cloning; northern blottings; nucleic acid sequence; polyadenylate; posttranscriptional RNA processing; site directed mutagenesis; tissue /cell culture; transcription factor

DESCRIPTION (provided by applicant): The goal of this application is to uncover the sequences and factors involved in the regulation of the formation and function of the unusually large 3' untranslated region of the MeCP2 gene. This approximately 8.5 kb 3' UTR likely contains elements that regulate gene expression at the post-transcriptional level. First, the investigators will identify auxiliary regulatory elements and factors that play a role in alternative polyadenylation of the MeCP2 gene, the process that determines the size of the 3' UTR in a tissue- and developmental-specific fashion. Second, they will test the hypothesis that the long 3' UTR plays a role in determining differential stability or translation of the MeCP2 mRNA. These studies represent under-explored areas of MeCP2 expression that may have a critical influence in the tissue-specific effects observed in Rett syndrome.

描述（由申请人提供）：本申请的目的是发现调节MECP2基因异常大的3'未翻译区域的形成和功能所涉及的序列和因素。 大约8.5 kb 3'UTR可能包含在转录后水平调节基因表达的元素。 首先，研究人员将确定在MECP2基因的替代聚腺苷酸化中起作用的辅助调节元素和因素，该过程决定了在组织和发育特异性的方式中确定3'UTR的大小。 其次，他们将检验以下假设：长3'UTR在确定MECP2 mRNA的差异稳定性或翻译中起作用。 这些研究代表了MECP2表达的爆发较低的区域，这些区域可能对RETT综合征观察到的组织特异性作用产生关键影响。