IKAROS 调节血管活性肠肽受体-猫眼课题宝

IKAROS 调节血管活性肠肽受体

批准号：

6500293

负责人：

GLENN Paul DORSAM

金额：

$4.2万

依托单位：

UNIVERSITY OF CALIFORNIA, SAN FRANCISCO

依托单位国家：

美国

项目类别：

财政年份：

2001

资助国家：

美国

项目状态：

未结题

起止时间：

2001-09-01 至

来源：

https://reporter.nih.gov/project-details/6500293

关键词：

DNA footprinting T lymphocyte antileukemic agent binding sites biological signal transduction cell growth regulation cell line gel mobility shift assay gene induction /repression genetic promoter element hemolymph neoplasm /cancer genetics neuropeptide receptor protein isoforms protein structure function receptor expression transcription factor vasoactive intestinal peptide

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中文摘要

翻译

锌指造血限制性转录因子Ikaros在某些人类白血病中发生突变。此外，Ikaros DNA结合域的遗传缺失与小鼠中的侵袭性T淋巴细胞白血病相关。因此，Ikaros对生长调节基因的转录调节可能是某些白血病发展的重要潜在原因。最近，我们收集了新的数据表明，Ikaros转录调节VIP-PACAP受体1（VPAC-1）的表达，这已被证明是传递抗增殖信号。因此，我们建议研究VPAC-1的转录调控Ikaros在T淋巴细胞。

英文摘要

The zinc-finger hemolymphopoietic-restricted transcription factor, Ikaros, is mutated in some human leukemias. Moreover, genetic deletions of the Ikaros DNA-binding domain were associated with an aggressive T lymphocyte leukemia in mice. Thus, the transcriptional regulation of growth-modulating genes by Ikaros may be an important underlying cause for the development of certain leukemias. Recently, we have collected novel data suggesting that Ikaros transcriptionally regulates the expression of VIP-PACAP receptor 1 (VPAC-1), which has been demonstrated to transmit anti-proliferative signals. Therefore, we propose to investigate the transcriptional regulation of VPAC-1 by Ikaros in T lymphocytes.

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