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.
- The renal distal convoluted tubule (DCT) plays a key role in magnesium homeostasis with genetic and drug-induced causes of hypomagnesemia affecting this segment. The importance of the renal TRPM6 channel subunit of the TRPM6/7 magnesium channel in magnesium homeostasis is unclear due to discrepant findings in knockout mice. Furthermore, the apical potassium channel Kv1.1 has been proposed to drive magnesium entry through TRPM6/7 along DCT, with limited experimental evidence. To clarify the roles of TRPM6 and Kv1.1 we generated mice with inducible DCT-specific TRPM6 knockout (DCT-TRPM6 KO) or renal tubule Kv1.1 knockout (tubule-Kv1.1 KO). Using a newly generated antibody, we found that TRPM6 expression is restricted to early DCT (DCT1), consistent with single cell transcriptomic data. DCT-TRPM6 KO displayed lower plasma [Mg] on diets with normal (0.21% w/w) or reduced (0.08% w/w) magnesium content. In contrast, plasma [Mg] did not differ to controls in tubule-Kv1.1 KO mice on diets containing 0.08% w/w or 0.04% w/w magnesium. There were no differences in other blood chemistry values for either knockout. GFR, lithium clearance, and natriuretic responses to furosemide, hydrochlorothiazide, or amiloride did not differ in tubule-Kv1.1 KO mice. Immunofluorescence and single molecule fluorescent in situ hybridization revealed Kv1.1 expression in mouse and human in glomeruli and along the S3 segment of the proximal tubule, but not along DCT. In summary, renal TRPM6 plays a critical role in magnesium homeostasis under baseline conditions. Kv1.1 is not expressed along DCT and is not required for magnesium homeostasis or normal renal function at baseline. - Source: PubMed
Publication date: 2026/08/09
Thaitongsuk PoomipatGirardi Adriana C CMorrow AshleyMiyasako KishoSiliezar-Doyle JanelleHill Rose ZRunnels Loren Wde Baaij Jeroen HfHoenderop Joost G JMcCormick James A - Experimental and clinical evidence have demonstrated that Mg deficiency contributes to elevated blood pressure (BP), whereas Mg supplementation exerts modest but consistent antihypertensive effects. The systemic effects of Mg supplementation and/or deficiency on BP have been investigated in relation to vascular smooth muscle cells (VSMCs), the renin-angiotensin-aldosterone system (RAAS), endothelial function, the sympathetic nervous system, and inflammation associated with oxidative stress. Some of these mechanisms are supported by compelling evidence, whereas others remain controversial. In the kidney, following glomerular filtration, ~95% of filtered Mg is reabsorbed along the renal tubules. In the proximal tubule (PT), Mg reabsorption occurs mainly via a paracellular transport pathway driven by a negative transepithelial electrical gradient. In contrast, in the thick ascending limb of Henle's loop (TAL), Mg reabsorption is regulated by electrochemical gradients generated through the coordinated activity of transporters such as the Na-K-2Cl cotransporter (NKCC2) and Na-K-ATPase. In the distal convoluted tubule (DCT), transient receptor potential melastatin 6 and 7 (TRPM6/7) channels tightly regulate the transcellular Mg reabsorption pathway. Hypertension is associated with increased urinary Mg excretion, resulting in relative Mg deficiency. Accumulating evidence suggests that Mg deficiency contributes to the pathogenesis of salt-sensitive and/or implementation hypertension, presumably through mechanisms involving Mg, Na and K transporters, mainly in the TAL and DCT.In this review, we discuss both systemic and renal mechanisms linking Mg to BP regulation. A better understanding of the interactions among Mg, Na, and K transport may provide novel insights into the role of Mg in hypertension. Mg exerts both BP raising and lowering effects depending on the body Mg status. Mg deficiency is associated with increase in BP through the multifaceted systemic and renal mechanisms. Experimental studies have shown that Mg deficiency-induced hypertension can be salt-sensitive and may be associated with implementation hypertension. The pressure-natriuresis curve shifts rightward and downward as salt sensitivity develops, requiring a higher BP to achieve the same level of sodium excretion. - Source: PubMed
Publication date: 2026/08/04
Kuriyama Satoru - Conventional magnesium supplementation relies on passive diffusion in the small intestine, resulting in poor bioavailability. To address this, we developed an oxidized starch-chitosan-Mg2+ composite gel that directs more Mg2+ to the colon, where resistant polysaccharides are fermented to SCFAs that may actively enhance absorption. Mg2+ incorporation increased the gel's resistant component to 52.42 ± 0.63%. Increasing Mg2+ from 0.5% to 2% reduced cumulative upper gastrointestinal release from 70.61 ± 0.79% to 43.62 ± 1.01% (p < 0.05), with higher concentrations showing no further improvement. In Mg2+-deficient mice, the gel dose-dependently restored serum Mg2+ to healthy levels. Comparison at equal Mg2+ doses revealed that the polysaccharide carrier independently contributed to enhanced absorption. Mechanistically, resistant polysaccharides were associated with upregulation of SCFAs receptors (FFAR2/FFAR3/HCAR2) and Mg2+ transporters (TRPM6/TRPM7/CNNM4), with immunofluorescence indicating TRPM7 upregulation. This work provides proof-of-concept evidence for a paradigm shift from passive supplementation to active regulation via SCFAs-associated transporter modulation. - Source: PubMed
Guo QiyongCao WeihangChen Ling - The protective effect of Compound terminalia chebula extract (HL) against colonic injury induced by Porcine epidemic diarrhea virus (PEDV) infection in neonatal piglets remains unclear. This study aimed to evaluate the mitigating effects of HL on PEDV-induced colonic injury and elucidate the underlying mechanisms. Eighteen 7-day-old Duroc × Landrace × Large White piglets (2.58 ± 0.05 kg) were randomly assigned to three groups (n = 6/group): CON (blank control), PEDV (infected), and HL + PEDV (HL-supplemented + infected). The 11-day trial included 3 days of acclimatization (days 0-3) and an 8-day experimental period (days 4-11). HL (10 mg/kg BW) was orally administered daily to the HL + PEDV group. On day 8, PEDV and HL + PEDV groups were challenged with 3 mL PEDV (3 × 10 TCID/mL), while CON received Dulbecco's Modified Eagle Medium (DMEM). All piglets were euthanized on day 11 for colonic tissue collection. Results indicated that PEDV infection induced colonic injury, manifested by a significant increase in crypt depth and disruption of intestinal homeostasis. This was evidenced by impaired barrier integrity (upregulation of matrix metalloproteinase-7 gene [] and matrix metalloproteinase 13 gene [], mucus disorganization (elevation of mucin 5AC gene []), oxidative stress (reduced catalase [CAT] activity and increased malondialdehyde [MDA] levels in serum and colon), and inflammation (upregulation of regenerative islet-derived protein 3γ gene [], S100 calcium-binding protein A8/A9 gene [], and interleukin-1β gene []). Additionally, PEDV impaired colonic ion transport by downregulating calcium channel genes (Transient Receptor Potential Cation Channel Subfamily V Member 6 gene [], Transient Receptor Potential Cation Channel Subfamily M Member 6 gene []). Notably, HL supplementation effectively reversed these adverse effects. HL restored colonic morphology, increased CAT activity, reduced MDA accumulation, and suppressed inflammatory gene expression. Furthermore, HL modulated the expression of genes involved in water and ion transport upregulating Aquaporin 7 gene (), Chloride Channel Accessory 4 gene (), Sodium-Hydrogen Exchanger 3 gene (), Transient Receptor Potential Vanilloid 6 (), and Transient Receptor Potential Melastatin 6 gene () and significantly inhibited PEDV replication, as indicated by the downregulation of the transcription levels of PEDV membranegene (), nucleocapsid gene (), and spike gene (). Taken together, HL alleviates PEDV-triggered colonic tissue damage in suckling piglets via improving colonic antioxidant capacity, mitigating inflammatory response, partially regulating intestinal barrier and ion/water transport-related genes, and downregulating the transcription of PEDV structural genes at molecular and histological levels. - Source: PubMed
Publication date: 2026/07/06
Zhang YanyanGan LinglingLi MuziWang JiaxingLi ZongyunLi ZhonghuaWang LeiZhao DiWu TaoYi DanHou Yongqing - Age-related alterations in intracellular Mg homeostasis can influence cellular bioenergetics and stress responses, yet the epithelial mechanisms linking aging and cellular senescence to impaired magnesium handling remain incompletely defined. Frailty is an emerging public health challenge in aging societies, and age-related magnesium deficiency has been proposed as one contributing factor. We investigated whether aging and cellular senescence impair epithelial magnesium handling in the colon and whether Mallotus japonicus (M. japonicus) leaf extract ameliorates these alterations in mouse colonic epithelial MCE301 cells under senescence-inducing conditions. The mRNA levels of transient receptor potential melastatin 6 (TRPM6) magnesium channel were decreased in the intestines of middle-aged mice and in MCE301 cells after long-term culture or tenovin-6-induced senescence. TRPM6 knockdown, tenovin-6, an inducer of cellular senescence, and low-Mg medium each lowered intracellular free Mg concentration ([Mg]). Low-Mg medium also attenuated proliferation. Transcriptome profiling suggested mitochondrial involvement under Mg-limiting conditions, consistent with reduced mitochondrial membrane potential and ATP production as well as increased mitochondrial fragmentation. M. japonicus leaf extract restored TRPM6 expression and [Mg], improved mitochondrial function, and suppressed senescence-associated secretory phenotype-related gene expression. Among the tested components of M. japonicus leaf extract, geraniin showed the strongest activity and also reduced senescence-associated β-galactosidase-positive cells, whereas corilagin, mallotinic acid, and mallotusinic acid showed partial effects. We suggest that aging- and senescence-associated TRPM6 downregulation is linked to impaired magnesium homeostasis and mitochondrial dysfunction in colonic epithelial cells. M. japonicus leaf extract and selected ellagitannin-related polyphenols mitigate these senescence-associated alterations. - Source: PubMed
Publication date: 2026/06/26
Tanabe MikiMatsuda ShunsukeMorimoto KazushiYoshino YutaMitsui TaichiMaruyama HiroeKono HiroyukiTabuchi YoshiakiEndo SatoshiIkari Akira