HSB-2 cells stably expressing LDB1 or mutant LDB1 proteins
收藏干细胞与再生医学数据中心2022-02-20 更新2024-03-06 收录
下载链接：
http://data.iscr.ac.cn/Article?id=3f12df325a935d8d4eb4e8836cfd179e
下载链接
链接失效反馈官方服务：
资源简介：
LMO2 is a component of multisubunit DNA-binding transcription factor complexes that regulate gene expression in hematopoietic stem and progenitor cell development. Enforced expression of LMO2 causes leukemia by inducing hematopoietic stem cell-like features in T-cell progenitor cells, but the biochemical mechanisms of LMO2 function have not been fully elucidated. In this study we systematically dissected the LMO2/LDB1 binding interface to investigate the role of this interaction in T-cell leukemia. Alanine scanning mutagenesis of the LIM interaction domain of LDB1 revealed a discrete motif R320LITR required for LMO2 binding. Most strikingly, co-expression of full length, wild type LDB1 increased LMO2 steady state abundance, whereas co-expression of mutant proteins deficient in LMO2 binding compromised LMO2 stability. These mutant LDB1 proteins also exerted dominant negative effects on growth and transcription in diverse leukemic cell lines. Raw gene expression data on HSB-2 cells is presented here.
提供机构：
Vanderbilt Cancer Center
创建时间：
2022-02-20
