J Physiol
Department of Pharmacology, Southern Illinois University School of Medicine, Springfield, IL, USA.
Published: May 2019
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http://dx.doi.org/10.1113/JP278089 | DOI Listing |
Cell Death Dis
December 2023
Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, 606-8501, Japan.
TRIC-A and TRIC-B proteins form homotrimeric cation-permeable channels in the endoplasmic reticulum (ER) and nuclear membranes and are thought to contribute to counterionic flux coupled with store Ca release in various cell types. Serious mutations in the TRIC-B (also referred to as TMEM38B) locus cause autosomal recessive osteogenesis imperfecta (OI), which is characterized by insufficient bone mineralization. We have reported that Tric-b-knockout mice can be used as an OI model; Tric-b deficiency deranges ER Ca handling and thus reduces extracellular matrix (ECM) synthesis in osteoblasts, leading to poor mineralization.
View Article and Find Full Text PDFJ Gen Physiol
November 2023
Department of Pharmacology, University of Oxford, Oxford, UK.
Trimeric intracellular cation channels (TRIC-A and TRIC-B) are thought to provide counter-ion currents to enable charge equilibration across the sarco/endoplasmic reticulum (SR) and nuclear membranes. However, there is also evidence that TRIC-A may interact directly with ryanodine receptor type 1 (RyR1) and 2 (RyR2) to alter RyR channel gating. It is therefore possible that the reverse is also true, where the presence of RyR channels is necessary for fully functional TRIC channels.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
February 2023
Department of Molecular Medicine, Biochemistry Unit, University of Pavia, Pavia, Italy.
Introduction: Trimeric intracellular potassium channels TRIC-A and -B are endoplasmic reticulum (ER) integral membrane proteins, involved in the regulation of calcium release mediated by ryanodine (RyRs) and inositol 1,4,5-trisphosphate (IPRs) receptors, respectively. While TRIC-A is mainly expressed in excitable cells, TRIC-B is ubiquitously distributed at moderate level. TRIC-B deficiency causes a dysregulation of calcium flux from the ER, which impacts on multiple collagen specific chaperones and modifying enzymatic activity, leading to a rare form of osteogenesis imperfecta (OI Type XIV).
View Article and Find Full Text PDFPflugers Arch
March 2021
Department of Surgery, The Ohio State University Columbus, Columbus, OH, 43210, USA.
Trimeric intracellular cation (TRIC) channels have been identified as monovalent cation channels that are located in the ER/SR membrane. Two isoforms discovered in mammals are TRIC-A (TMEM38a) and TRIC-B (TMEM38b). TRIC-B ubiquitously expresses in all tissues, and TRIC-B mice is lethal at the neonatal stage.
View Article and Find Full Text PDFNeuroscience
March 2021
Department of Pediatrics, USA. Electronic address:
Pain is a major health problem, affecting over fifty million adults in the US alone, with significant economic cost in medical care and lost productivity. Despite evidence implicating nicotinic acetylcholine receptors (nAChRs) in pathological pain, their specific contribution to pain processing in the spinal cord remains unclear given their presence in both neuronal and non-neuronal cell types. Here we investigated if loss of neuronal-specific TMEM35a (NACHO), a novel chaperone for functional expression of the homomeric α7 and assembly of the heteromeric α3, α4, and α6-containing nAChRs, modulates pain in mice.
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