Genetically engineered mouse models of FK506‐binding protein 5

FKBP5型 生物 糖皮质激素受体 FKBP公司 计算生物学 基因剔除小鼠 表型 神经科学 表观遗传学 条件基因敲除 共同伴侣 核受体 基因 细胞生物学 遗传学 生物信息学 转录因子 热休克蛋白90 热休克蛋白
作者
Niat T. Gebru,Shannon E. Hill,Laura J. Blair
出处
期刊:Journal of Cellular Biochemistry [Wiley]
被引量:4
标识
DOI:10.1002/jcb.30374
摘要

Abstract FK506 binding protein 51 (FKBP51) is a molecular chaperone that influences stress response. In addition to having an integral role in the regulation of steroid hormone receptors, including glucocorticoid receptor, FKBP51 has been linked with several biological processes including metabolism and neuronal health. Genetic and epigenetic alterations in the gene that encodes FKBP51, FKBP5 , are associated with increased susceptibility to multiple neuropsychiatric disorders, which has fueled much of the research on this protein. Because of the complexity of these processes, animal models have been important in understanding the role of FKBP51. This review examines each of the current mouse models of FKBP5 , which include whole animal knockout, conditional knockout, overexpression, and humanized mouse models. The generation of each model and observational details are discussed, including behavioral phenotypes, molecular changes, and electrophysiological alterations basally and following various challenges. While much has been learned through these models, there are still many aspects of FKBP51 biology that remain opaque and future studies are needed to help illuminate these current gaps in knowledge. Overall, FKBP5 continues to be an exciting potential target for stress‐related disorders.
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