Calcium modulating ligand (CAMLG or CAML), also known as calcium-modulating cyclophilin ligand, is a signalling protein recognized by the TNF receptorTACI.[5][6]
Function
The immunosuppressant drug cyclosporin A blocks a calcium-dependent signal from the T-cell receptor (TCR) that normally leads to T-cell activation. When bound to cyclophilin B, cyclosporin A binds and inactivates the key signaling intermediate calcineurin. The protein encoded by this gene functions similarly to cyclosporin A, binding to cyclophilin B and acting downstream of the TCR and upstream of calcineurin by causing an influx of calcium. This integral membrane protein appears to be a new participant in the calcium signal transduction pathway, implicating cyclophilin B in calcium signaling, even in the absence of cyclosporin.[6]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Bram RJ, Valentine V, Shapiro DN, Jenkins NA, Gilbert DJ, Copeland NG (March 1997). "The gene for calcium-modulating cyclophilin ligand (CAMLG) is located on human chromosome 5q23 and a syntenic region of mouse chromosome 13". Genomics. 31 (2): 257–60. doi:10.1006/geno.1996.0044. PMID8824814.
von Bülow GU, Bram RJ (1997). "NF-AT activation induced by a CAML-interacting member of the tumor necrosis factor receptor superfamily". Science. 278 (5335): 138–41. doi:10.1126/science.278.5335.138. PMID9311921.
Larramendy ML, Niini T, Elonen E, Nagy B, Ollila J, Vihinen M, Knuutila S (2003). "Overexpression of translocation-associated fusion genes of FGFRI, MYC, NPMI, and DEK, but absence of the translocations in acute myeloid leukemia. A microarray analysis". Haematologica. 87 (6): 569–77. PMID12031912.
