Last update 19 Sep 2024

TRPM6

Last update 19 Sep 2024

Basic Info

Synonyms

CHAK2, Channel kinase 2, FLJ22628

+ [7]

Introduction

Essential ion channel and serine/threonine-protein kinase. Crucial for magnesium homeostasis. Has an important role in epithelial magnesium transport and in the active magnesium absorption in the gut and kidney. Isoforms of the type M6-kinase lack the ion channel region.

Drugs associated with TRPM6

L-687

Target

TRPC3 x TRPM6

Mechanism

TRPC3 antagonists [+1]

Active Org.

Kyoto University [+2]

Originator Org.

Kyoto University

Active Indication

Fibrosis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with TRPM6

100 Translational Medicine associated with TRPM6

0 Patents (Medical) associated with TRPM6

396

Literatures (Medical) associated with TRPM6

01 Sep 2024·Physiological Genomics

Genetic drivers of age-related changes in urinary magnesium excretion

Article

Author: van Megen, Wouter H. ; van Megen, Wouter H ; Hoenderop, Joost G J ; de Baaij, Jeroen H. F. ; Churchill, Gary A ; Hoenderop, Joost G. J. ; Korstanje, Ron ; Devuyst, Olivier ; de Baaij, Jeroen H F ; Churchill, Gary A.

Aging increased urinary magnesium (Mg2+) excretion in mice. We show here that variation in Oit3, a candidate gene for the locus associated with Mg2+ excretion in young mice, is unlikely to be involved as knockout of Oit3 did not affect Mg2+ excretion. Differences in the expression of the renal Mg2+ channel TRPM6 may contribute to the variation in urinary Mg2+ excretion in older mice.

01 Jul 2024·Nutrition, Metabolism and Cardiovascular Diseases

Identification of potential therapeutic targets for plaque vulnerability based on an integrated analysis

Article

Author: Yang, Zhi-Jie ; Liu, Yuan ; Qin, Yue-Ai ; Liu, Yan-Li ; Wei, Xin-Qiao ; Shi, Wan-Xin ; Miao, Liu

BACKGROUND AND AIMSThis study aimed to explore potential hub genes and pathways of plaque vulnerability and to investigate possible therapeutic targets for acute coronary syndrome (ACS).METHODS AND RESULTSFour microarray datasets were downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs), weighted gene coexpression networks (WGCNA) and immune cell inﬁltration analysis (IIA) were used to identify the genes for plaque vulnerability. Then, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, Disease Ontology, Gene Ontology annotation and protein-protein interaction (PPI) network analyses were performed to explore the hub genes. Random forest and artiﬁcial neural networks were constructed for validation. Furthermore, the CMap and Herb databases were employed to explore possible therapeutic targets. A total of 168 DEGs with an adjusted P < 0.05 and approximately 1974 IIA genes were identified in GSE62646. Three modules were detected and associated with CAD-Class, including 891 genes that can be found in GSE90074. After removing duplicates, 114 hub genes were used for functional analysis. GO functions identified 157 items, and 6 pathways were enriched for the KEGG pathway at adjusted P < 0.05 (false discovery rate, FDR set at < 0.05). Random forest and artificial neural network models were built based on the GSE48060 and GSE34822 datasets, respectively, to validate the previous hub genes. Five genes (GZMA, GZMB, KLRB1, KLRD1 and TRPM6) were selected, and only two of them (GZMA and GZMB) were screened as therapeutic targets in the CMap and Herb databases.CONCLUSIONWe performed a comprehensive analysis and validated GZMA and GZMB as a target for plaque vulnerability, which provides a therapeutic strategy for the prevention of ACS. However, whether it can be used as a predictor in blood samples requires further experimental verification.

01 May 2024·Pflügers Archiv - European Journal of Physiology

A novel mouse model for familial hypocalciuric hypercalcemia (FHH1) reveals PTH-dependent and independent CaSR defects

Article

Author: de Angelis, Martin Hrabĕ ; Rubio-Aliaga, Isabel ; Haykir, Betül ; Hernando, Nati ; Daryadel, Arezoo ; Fuente, Rocio ; Wagner, Carsten A ; Küng, Catharina J

AbstractThe Calcium-sensing receptor (CaSR) senses extracellular calcium, regulates parathyroid hormone (PTH) secretion, and has additional functions in various organs related to systemic and local calcium and mineral homeostasis. Familial hypocalciuric hypercalcemia type I (FHH1) is caused by heterozygous loss-of-function mutations in the CaSR gene, and is characterized by the combination of hypercalcemia, hypocalciuria, normal to elevated PTH, and facultatively hypermagnesemia and mild bone mineralization defects. To date, only heterozygous Casr null mice have been available as model for FHH1. Here we present a novel mouse FHH1 model identified in a large ENU-screen that carries an c.2579 T > A (p.Ile859Asn) variant in the Casr gene (CasrBCH002 mice). In order to dissect direct effects of the genetic variant from PTH-dependent effects, we crossed CasrBCH002 mice with PTH deficient mice. Heterozygous CasrBCH002 mice were fertile, had normal growth and body weight, were hypercalcemic and hypermagnesemic with inappropriately normal PTH levels and urinary calcium excretion replicating some features of FHH1. Hypercalcemia and hypermagnesemia were independent from PTH and correlated with higher expression of claudin 16 and 19 in kidneys. Likewise, reduced expression of the renal TRPM6 channel in CasrBCH002 mice was not dependent on PTH. In bone, mutations in Casr rescued the bone phenotype observed in Pth null mice by increasing osteoclast numbers and improving the columnar pattern of chondrocytes in the growth zone. In summary, CasrBCH002 mice represent a new model to study FHH1 and our results indicate that only a part of the phenotype is driven by PTH.

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TRPM6

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