TRPM6 (Chak2), antiserum, guinea pig, 100 ul.
- Known as:
- TRPM6 (Chak2), antibodies, guinea pig, 100 ul.
- Catalog number:
- GP14108-100
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- TRPM6 (Chak2) antiserum guinea pig 100 .
Related genes to: TRPM6 (Chak2), antiserum, guinea pig, 100 ul.
- Gene:
- TRPM6 NIH gene
- Name:
- transient receptor potential cation channel subfamily M member 6
- Previous symbol:
- HOMG, HSH
- Synonyms:
- CHAK2, FLJ22628
- Chromosome:
- 9q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-11
- Date modifiied:
- 2016-01-28
Related products to: TRPM6 (Chak2), antiserum, guinea pig, 100 ul.
Related articles to: TRPM6 (Chak2), antiserum, guinea pig, 100 ul.
- Transient receptor potential (TRP) ion channels of the melastatin family (TRPM) have eight members in mammals with a broad spectrum of functions. We investigated the evolution of this complex gene family across metazoans. The characteristic aminoterminal melastatin domain and the carboxyterminal NUDT9 homology domain with similarity to ADP-ribose pyrophosphatase were added to the common ancestor of TRPM and its sister channel TRPS. Gene duplications before the origin of bilaterians resulted in four TRPM genes: α, β, βlike and γ. The two latter were discovered in this study. All four and TRPS are present in extant mollusks, while differential losses occurred in the other animal lineages. TRPS, TRPMβlike and TRPMγ were lost in early chordates, meaning that the vertebrate ancestor started with TRPMα and β, both of which were duplicated before the first vertebrate tetraploidization 1R. The ancestor of the micro-RNA genes mir-211 and mir-204 was inserted in an intron of the ancestor of TRPM1/TRPM3. The TRPM6/TRPM7 ancestor acquired a kinase domain, probably a copy of the syntenic alpha protein kinase ALPK2/3 ancestor gene. Vertebrate 1R and gnathostome 2R together with local gene duplication and losses resulted in eight TRPM (TRPM1-8) in the gnathostome ancestor. In cyclostomes, extensive gene losses after the hexaploidization led to four TRPM. The teleost-specific tetraploidization 3R generated further TRPM ohnologs. The NUDT9 homology domain is retained in TRPM2 and TRPS but was lost repeatedly during TRPM evolution. Thus, the TRPM family displays considerable evolutionary variation with regard to gene and domain gains and losses. - Source: PubMed
Publication date: 2026/04/11
Morini MarinaBergqvist ChristinaAsturiano Juan FDufour SylvieLarhammar Dan - Transient receptor potential (TRP) channels comprise a superfamily of cation-permeable channels broadly expressed in the respiratory tract, playing essential roles in regulating epithelial integrity, mucus secretion, mechanotransduction, and innate immune responses. Increasing evidence suggests that dysregulation of TRP channels contributes to the pathogenesis of chronic obstructive pulmonary disease (COPD). - Source: PubMed
Publication date: 2026/03/30
Ye Yi-RanZhou Yu-YunQu SuZhou Wen-LiangChen LeiZhang Yi-Lin - Hypomagnesemia, defined as low serum/plasma magnesium concentration, is a highly prevalent yet underrecognized electrolyte disorder with extensive clinical, metabolic, and nutritional implications. This review provides an updated synthesis of magnesium physiology, dietary determinants, homeostatic regulation, diagnostic challenges, and therapeutic strategies, with particular emphasis on recent meta-analyses and large-scale epidemiological evidence linking hypomagnesemia to multisystem disease. - Source: PubMed
Publication date: 2026/03/24
Papagiannidou AnastasiaMitropoulou MariaPapantzikos KonstantinosPetropoulou DimitraTsilingiris DimitriosMagkos FaidonDalamaga Maria - Gitelman syndrome (GS) is a rare, autosomal recessive salt-losing tubulopathy caused by mutations in the gene. It involves dysfunction of the sodium-chloride cotransporter positioned on the apical membranes of the distal convoluted tubule cells, causing sodium shortage and mimicking the use of thiazide diuretics. Hyperaldosteronism secondary to sodium depletion and hypovolemia causes hypokalaemia and metabolic alkalosis. This is associated with inhibition of the Transient Receptor Potential Cation Channel, Subfamily M, Member 6 -TRPM6 channel, which leads to urinary magnesium leakage and hypomagnesemia, subsequently stopping PTH secretion and resulting in hypocalcemia and hypocalciuria. Gitelman syndrome frequently presents later in life, as the symptoms are usually not very threatening. However, early identification, diagnosis, and urgent intervention are essential to improve patient prognosis and quality of life. Importantly, both hypomagnesemia and hypokalaemia can impair insulin secretion and sensitivity. Furthermore, hyperaldosteronism caused by the secondary activation of the R-A-A system can also lead to these disorders. Glucose metabolism problems have been shown to prevail amongst GS patients and manifest more frequently in comparison to the general population. When it comes to the treatment used to reduce hyperglycemia in GS-related T2DM, we consider which of the available drugs are the best for those patients. The article analyses the association of Gitelman syndrome with diabetes mellitus based on the available medical literature-as there are no clinical trials or meta-analyses available for this group, it is presented as a narrative review. - Source: PubMed
Publication date: 2026/01/28
Szubert IzabelaCader-Ptak AleksandraKwiatkowska Ewa - Inflammatory bowel disease (IBD) is a chronic intestinal inflammatory condition driven by a combination of genetic, environmental, and immune factors. This review systematically explores the roles of selenium, copper, zinc, iron, and magnesium, five key trace elements, in the pathogenesis, disease progression, and potential treatment of IBD. These elements profoundly affect the pathological state of IBD by regulating oxidative stress, immune cell function (such as macrophage polarization, Th17/Treg balance), intestinal epithelial barrier integrity, and gut microbiota composition. For example, selenium deficiency exacerbates inflammation, while selenium supplementation can alleviate the condition; copper homeostasis imbalance participates in the disease through oxidative stress and the emerging "cuproptosis" pathway; zinc deficiency destroys the barrier and enhances the IL-23/Th17 axis to drive inflammation; iron metabolism disorder leads to anemia and regulates the ferroptosis process; magnesium maintains the barrier through the TRPM6 channel and affects the abundance of probiotics. In recent years, nanomaterials based on these elements (such as nanoselenium, copper/zinc complexes, iron-based nanoenzymes, .) have shown great potential as novel therapeutic strategies. They effectively alleviate colitis in preclinical models by enhancing targeting, improving bioavailability, and synergistically exerting antioxidant and anti-inflammatory effects. However, current research is mostly limited to the preclinical stage, and its clinical translation faces challenges such as optimal dosages, long-term safety, interactions between elements, and individual differences. In summary, restoring and maintaining trace element balance is a promising auxiliary strategy in the management of IBD. Future research should focus on developing intelligent delivery systems, combining personalized nutrition and medicine, to promote the transformation of trace elements from basic nutritional support to mechanism-driven, precise auxiliary treatment, ultimately improving the long-term prognosis of IBD patients. - Source: PubMed
Publication date: 2026/03/09
Yan YiDu RuiXia ChenglongDeng HuidanZhu YanqiuGuo Hongrui