Last update 01 Nov 2024

TRPM6

Last update 01 Nov 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

400

Literatures (Medical) associated with TRPM6

01 Dec 2024·International Immunopharmacology

Exploring therapeutic potential: Targeting TRPM7 in neurodegenerative diseases

Review

Author: Dhankhar, Sanchit ; Soni, Diksha ; Singh, Thakur Gurjeet ; Chauhan, Samrat ; Garg, Nitika ; Khan, Heena ; Kaur, Amarjot

The ions Ca²⁺ and Mg²⁺, which are both present in the body, have been demonstrated to be crucial in the control of a variety of neuronal processes. Transient melastatin-7 (TRPM7) channel plays an important role in controlling Ca²⁺ and Mg²⁺ homeostasis, which is crucial for biological processes. The review will also examine how changes in TRPM7 function or expression can lead to neurodegeneration.Even though eight different TRPM channels have been found so far, the channel properties, activation mechanisms, and physiological responses exhibited by these channels can vary greatly from one another. Only TRPM6 and TRPM7 out of the eight TRPM channels were found to have a high permeability to both Ca²⁺ and Mg²⁺. In contrast to TRPM6 channels, which are not highly expressed in neuronal cells, TRPM7 channels are widely distributed throughout the nervous system, so they will be the sole focus of this article. It is possible that, in the future, for the treatment of neurodegenerative disorder new therapeutic drug targets will be developed as a direct result of research into the specific roles played by TRPM7 channels in several different neurodegenerative conditions as well as the factors that are responsible for TRPM7 channel regulation.

01 Dec 2024·Journal of Trace Elements in Medicine and Biology

Effects of tauroursodeoxycholate on arsenic-induced hepatic injury in mice: A comparative transcriptomic analysis

Article

Author: Wang, Ningning ; Li, Haonan ; Wang, He ; Zheng, Xiujuan ; Li, Xuying ; Wang, Kewei ; Nian, Shijing ; Zhang, Hua ; Li, Mingqi ; Cao, Jianbin ; He, Rui ; Jin, Baiming ; Liu, Lele

BACKGROUNDProlonged exposure to excessive arsenic (As) and its compounds can cause damage to multiple systems, including respiratory, cardiovascular, immune, nervous, and endocrine systems. Manifestations include changes in skin pigmentation, excessive keratosis on palms and soles, gastrointestinal symptoms, and anemia. The liver as an important detoxification organ of the body, is a significant target organ for arsenic toxicity, and liver diseases are common. So far, the molecular mechanism has not been fully elucidated. Evidence suggests that taurodeoxycholic acid (TUDCA) has a protective role in arsenic-induced liver injury. This study aims to reveal potential target genes at the transcriptional level following TUDCA intervention, providing insights for the intervention of arsenic-induced liver injury.METHODSThe TUDCA intervention model of arsenic liver injury in C57BL/6 N mice was established. The experiment was divided into two phases and lasted for 24 weeks. The phase I trial (12 weeks) was divided into control, low, middle and high groups according to the dose of As. The phaseⅡtrial (12 weeks) was administered in combination with 10 mg/L sodium arsenite (the first stage high arsenic group) and TUDCA, so subsequent groups was named with H indicating high arsenic. Divide into four groups: control group(C), TUDCA solvent control group(H-Vehicle), TUDCA combined with As group(H-TUDCA), arsenic group (As). As was ingested through free water and TUDCA was administered to mice by gavage at a dose of 0.1 mL/10 g.b.w (100 mg/kg) once a day for 12 weeks. The differential expression gene (DEG) profile was obtained from the second batch of mouse liver tissues by RNA sequencing technology. Comparative transcriptomic analysis methods were used to identify co-varying DEGs between arsenic induction and TUDCA intervention, along with their associated pathways. QRT-PCR was utilized for validation.RESULTSTranscriptome results showed that 487 DEGs were identified after arsenic induction. TUDCA intervention identified 231 DEGs (p-values < 0.05 and | log2(fold change) | > 1). The comparison of "AS vs C" and "H_TUDCA vs AS" identified 65 covariant DEGs, and further screened the TUDCA pathways and related genes among these genes，six pathways and 11 genes (Ccl21a, Ccr7, Mdm2, Slc2a4, Akr1b7, Pnpla3, Dusp8, Hspa1a, Cyp7a1, Cybrd1, Trpm6) were obtained. Next, we screened for covariant DEGs among the top 50 potential hub genes in arsenic-induced DEGS, and obtained 7 (Hbb-bs, Hspa1a, Mdm2, Slc2a4, Ptk6, Egr1, and Dusp8). Finally, the intersection of Hub gene and pathway gene was selected as the target genes Dusp8, Hspa1a, Mdm2 and Slc2a4. The sequencing results showed that the mRNA expressions of Dusp8, Hspa1a and Mdm2 were significantly increased after arsenic induction, while the expression of Slc2a4 was significantly decreased (P<0.05). Conversely, TUDCA intervention reversed these DEGs changes, consistent with QRT-PCR validation results.CONCLUSIONThis study contributes to understanding the potential health effects of arsenic-induced liver injury, identifying new potential targets, and providing references for TUDCA intervention.

01 Sep 2024·Physiological Genomics

Genetic drivers of age-related changes in urinary magnesium excretion

Article

Author: van Megen, Wouter H. ; Hoenderop, Joost G J ; van Megen, Wouter H ; 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.

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TRPM6

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