myelin-oligodendrocyte-glycoprotein-(35-55) and Hyperplasia

myelin-oligodendrocyte-glycoprotein-(35-55) has been researched along with Hyperplasia* in 1 studies

Other Studies

1 other study(ies) available for myelin-oligodendrocyte-glycoprotein-(35-55) and Hyperplasia

ArticleYear
Armc5 deletion causes developmental defects and compromises T-cell immune responses.
    Nature communications, 2017, 02-07, Volume: 8

    Armadillo repeat containing 5 (ARMC5) is a cytosolic protein with no enzymatic activities. Little is known about its function and mechanisms of action, except that gene mutations are associated with risks of primary macronodular adrenal gland hyperplasia. Here we map Armc5 expression by in situ hybridization, and generate Armc5 knockout mice, which are small in body size. Armc5 knockout mice have compromised T-cell proliferation and differentiation into Th1 and Th17 cells, increased T-cell apoptosis, reduced severity of experimental autoimmune encephalitis, and defective immune responses to lymphocytic choriomeningitis virus infection. These mice also develop adrenal gland hyperplasia in old age. Yeast 2-hybrid assays identify 16 ARMC5-binding partners. Together these data indicate that ARMC5 is crucial in fetal development, T-cell function and adrenal gland growth homeostasis, and that the functions of ARMC5 probably depend on interaction with multiple signalling pathways.

    Topics: Adrenal Glands; Animals; Armadillo Domain Proteins; Cell Differentiation; Cell Line; Cell Proliferation; Encephalomyelitis, Autoimmune, Experimental; Female; Fetal Development; Germ-Line Mutation; Humans; Hyperplasia; Immunity, Cellular; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Mutation; Myelin-Oligodendrocyte Glycoprotein; Peptide Fragments; Sequence Deletion; Severity of Illness Index; T-Lymphocytes; Transplantation Chimera

2017