Biology:TMEM38B
Trimeric intracellular cation-selective channel B (TRIC-B) is a monovalent cation channel in the ER membrane encoded by the transmembrane protein 38B (TMEM38B) gene.[1][2] It is one of two known TRIC proteins, the other being TRIC-A.
Function
TRIC-B is permeable to both Na+ and K+ but not divalent cations like Ca2+.[1] The channel exhibits marked voltage-dependence, becoming more open when the cytosol is more positively charged than the ER lumen. There at least four major sub-conductance states (with 80%, 60%, 46% and 30% of the conductance of the fully-opened channel).[1] TMEM38B-knockout mice exhibit reduced IP3-receptor-mediated Ca2+ release.[1] As such, K+ flux into the ER through TRIC-B is thought to support IP3-induced efflux of Ca2+ ions through IP3-gated Ca2+ channels in the ER membrane.
Clinical significance
Null mutations in TMEM38B reduce the levels of functional TRIC-B in heterozygotes and abolish expression of functional TRIC-B in homozygotes. Such mutations are an uncommon but relatively severe cause of autosomal recessive osteogenesis imperfecta or "brittle bone disease".[2]
See also
References
- ↑ 1.0 1.1 1.2 1.3 Venturi, Elisa; Sitsapesan, Rebecca; Yamazaki, Daiju; Takeshima, Hiroshi (15 December 2012). "TRIC channels supporting efficient Ca2+ release from intracellular stores". European Journal of Physiology 465 (2): 187–195. doi:10.1007/s00424-012-1197-5. PMID 23242030. https://link.springer.com/article/10.1007/s00424-012-1197-5.
- ↑ 2.0 2.1 Cabral, Wayne A.; Ishikawa, Masaki; Garten, Matthias; Makareeva, Elena N.; Sargent, Brandi M.; Weis, MaryAnn; Barnes, Aileen M.; Webb, Emma A. et al. (21 July 2016). "Absence of the ER Cation Channel TMEM38B/TRIC-B Disrupts Intracellular Calcium Homeostasis and Dysregulates Collagen Synthesis in Recessive Osteogenesis Imperfecta". PLOS Genetics 12 (7): e1006156. doi:10.1371/journal.pgen.1006156. PMID 27441836.
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