Structural highlights
Disease
GIMA5_HUMAN The disease may be caused by variants affecting the gene represented in this entry.
Function
GIMA5_HUMAN Plays a role in T lymphocyte development and the optimal generation of CD4/CD8 double-positive thymocytes (By similarity). Inhibitor of GSK3A, possibly by sequestering GSK3A in cytoplasmic vesicles and impairing its translocation to the nucleus. Consequently, impairs GSK3A-dependent transcriptional program and regulation of the DNA damage response occurring during T cells proliferation (PubMed:29382851). Required for the survival of peripheral T cells, natural killer (NK) and NK T-cell development and the maintenance of normal liver function (By similarity). May promote the survival of mature T lymphocytes upon cytokine withdrawal (By similarity). May regulate Ca(2+) homeostasis by modulating lysosomal Ca(2+) stores, preventing its accumulation in the absence of T cell activation (By similarity). May play a role in mitochondrial DNA segregation in hematopoietic tissues (By similarity). Is a regulator of liver endothelial cell homeostasis (By similarity).[UniProtKB:Q8BWF2][UniProtKB:Q8K3L6][1]
References
- ↑ Patterson AR, Endale M, Lampe K, Aksoylar HI, Flagg A, Woodgett JR, Hildeman D, Jordan MB, Singh H, Kucuk Z, Bleesing J, Hoebe K. Gimap5-dependent inactivation of GSK3β is required for CD4(+) T cell homeostasis and prevention of immune pathology. Nat Commun. 2018 Jan 30;9(1):430. PMID:29382851 doi:10.1038/s41467-018-02897-7
