School of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore.
Curr Opin Pharmacol. 2011 Aug;11(4):354-9. doi: 10.1016/j.coph.2011.04.013. Epub 2011 May 14.
FKBP38, a noncanonical member of the immunosuppressive drug FK506 binding protein (FKBP) family members, possesses an inducible rotamase. FKBP38 interacts with several proteins and regulates multiple signaling pathways such as cell survival, apoptosis, proliferation, and metastasis. Deregulation of apoptosis is associated with chemoresistance and tumor relapse. The antiapoptotic protein Bcl-2 is a key player for increasing the apoptotic threshold in response to various cytotoxic drugs. The molecular interaction of Bcl-2 with FKBP38 potentiates the biological function of Bcl-2 and contributes to tumorigenesis and chemoresistance. Here, we discuss recent advances in the role of FKBP38 in connection with Bcl-2 and its possible link to chemotherapeutic resistance.
FKBP38 是免疫抑制药物 FK506 结合蛋白 (FKBP) 家族成员中的一个非典型成员,具有可诱导的旋转酶。FKBP38 与几种蛋白质相互作用,调节多种信号通路,如细胞存活、细胞凋亡、增殖和转移。细胞凋亡的失调与化疗耐药和肿瘤复发有关。抗凋亡蛋白 Bcl-2 是增加对各种细胞毒性药物的细胞凋亡阈值的关键因素。Bcl-2 与 FKBP38 的分子相互作用增强了 Bcl-2 的生物学功能,并有助于肿瘤发生和化疗耐药。在这里,我们讨论了 FKBP38 与 Bcl-2 相关的作用的最新进展及其与化疗耐药的可能联系。