Skip to Main content Skip to Navigation
New interface
Journal articles

Armc5 deletion causes developmental defects and compromises T-cell immune responses.

Abstract : 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.
Document type :
Journal articles
Complete list of metadata

Cited literature [47 references]  Display  Hide  Download
Contributor : Michel Courcelles Connect in order to contact the contributor
Submitted on : Wednesday, June 7, 2017 - 9:07:39 PM
Last modification on : Monday, July 20, 2020 - 12:33:14 PM
Long-term archiving on: : Wednesday, December 13, 2017 - 9:54:28 AM


Publication funded by an institution


Distributed under a Creative Commons Attribution 4.0 International License




Yan Hu, Linjiang Lao, Jianning Mao, Wei Jin, Hongyu Luo, et al.. Armc5 deletion causes developmental defects and compromises T-cell immune responses.. Nature Communications, 2017, 8, pp.13834. ⟨10.1038/ncomms13834⟩. ⟨pasteur-01534656⟩



Record views


Files downloads