SLC12A2 / NKCC1 Antibody
- Known as:
- SLC12A2 / NKCC1 Antibody
- Catalog number:
- 71-133
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- SLC12A2 / NKCC1 Antibody
Related genes to: SLC12A2 / NKCC1 Antibody
- Gene:
- SLC12A2 NIH gene
- Name:
- solute carrier family 12 member 2
- Previous symbol:
- -
- Synonyms:
- NKCC1, BSC, BSC2, PPP1R141
- Chromosome:
- 5q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-16
- Date modifiied:
- 2016-02-17
Related products to: SLC12A2 / NKCC1 Antibody
Related articles to: SLC12A2 / NKCC1 Antibody
- Abdominal pain is a hallmark symptom of both inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) and substantially impairs patients' quality of life. Relaxation response-based mind-body intervention (RR-MBI) has been reported to improve disease-specific outcomes and pain catastrophizing in both disorders, accompanied by whole-blood transcriptomic changes. However, the transcriptional features potentially relevant to abdominal pain before and after RR-MBI in IBS and IBD remain insufficiently explored. In this context, this study aimed to analyze these transcriptional changes and prioritize putative abdominal pain-relevant candidate genes from exploratory differentially expressed gene (DEG) sets. - Source: PubMed
Publication date: 2026/06/10
Lin ZhongyuanMo GuohuiWang YiminLin ShiqingGuo Qianqian - Both hypertensive and breast diseases impose a significant societal burden. However, the correlation between antihypertensive drug use and breast cancer remains controversial. We aimed to determine their potential correlations and explore their possible mechanisms. We performed summary data-based Mendelian Randomization (SMR) analysis of expression quantitative trait loci (eQTL) data from the blood of patients with breast diseases. We then performed drug-targeting Mendelian Randomization (MR) analysis using blood pressure-related single nucleotide polymorphism (SNPs) as instrumental variables (IVs). False discovery rate (FDR) correction was performed for reliable results, and colocalization analysis was performed to clarify shared gene variants. Mediation MR methods were used to investigate the mechanistic pathways involved in this association. Combined with the results of SMR analysis and drug-targeting MR analysis, loop diuretics aggravated overall breast cancer (OR_SMR = 0.842, 95% CI_SMR: 0.778-0.911, P_SMR_FDR = 0.008) and ER + breast cancer (OR_SMR = 0.854, 95% CI_SMR: 0.778-0.937, P_SMR_FDR = 0.008) within SLC12A2 gene loci. Colocalization analysis showed that SLC12A2-targeted drugs share a common variant site with breast cancer. Mediation analyses suggested that the pathway related to intestinal ischemia mediated 73.711% of the total effect on over breast cancer risk in the SLC12A2 gene loci. Antihypertensive drugs increase the overall risk of breast cancer and ER + breast cancer within the SLC12A2 gene. And overall breast cancer risk which may result from intestinal ischemia. Given the long-term safety of antihypertensive drugs, significance should be attached to the prevention and early detection of breast cancer in patients taking loop diuretics. - Source: PubMed
Li JiaxuanMa YiqunZhang Kaili - Gamma-aminobutyric acid (GABA), acting through its receptors, is the principal inhibitory neurotransmitter in the brain. It plays a vital role in maintaining neuronal chloride balance by interacting with chloride co-transporters, mainly NKCC1 and KCC2. In addition to the neurons, GABA receptors and chloride co-transporters are found to be expressed by the immune cells also. This present work aimed to study the gene expression patterns of GABA receptors and chloride co-transporters (NKCC1 and KCC2) in the autism-affected children of West Bengal using peripheral blood as model. - Source: PubMed
Publication date: 2026/06/04
Adak PallabiChakraborty Samidh SankarBandyopadhyay Apurba KumarSinha SwagataBanerjee Nilanjana - The WNK3-SPAK-NKCC1 signaling pathway has been implicated in the pathogenesis of brain injury. The aim of this study is to examine the involvement of this pathway in intracerebral hemorrhage (ICH) and evaluate the therapeutic potential of acupuncture in modulating its activity. A total of 210 Sprague Dawley rats were randomly assigned to experimental groups. ICH was induced in all groups except the sham group via autologous blood injection. Point-through-point acupuncture was administered on the Baihui (GV20) and Qubin (GB7) acupoints. Protein expression levels within the WNK3-SPAK-NKCC1 pathway, as well as inflammatory and apoptotic markers in the perihematomal region, were assessed using western blotting, immunohistochemistry, immunofluorescence co-localization, and enzyme-linked immunosorbent assay. Brain water content, hematoxylin-eosin staining, and neurological function scoring were used to evaluate histopathological changes and functional outcomes. Acupuncture significantly improved neurological function, alleviated cerebral edema, and reduced perihematomal pathological injury in ICH rats at all observed time points. Notably, the therapeutic effect was most pronounced after seven consecutive acupuncture treatments. Time-course analysis of WNK3 and cleaved caspase-3 expression, together with correlation analysis, revealed that the neuroprotective effects of acupuncture were potentially associated with WNK3-mediated apoptotic mechanisms. Based on these findings, day 7 was identified as the optimal time point for further mechanistic investigation. At this time point, continuous acupuncture treatment significantly improved neurological function and decreased brain water content. In addition, the expression levels of WNK3, phosphorylated SPAK and NKCC1, TNF-α, and cleaved caspase-3 were significantly reduced, accompanied by decreased NeuN/TUNEL co-localization (p < 0.05), suggesting that acupuncture may exert neuroprotective effects partly through inhibition of the WNK3-SPAK-NKCC1 signaling pathway. Acupuncture may alleviate brain injury following ICH by suppressing activation of the WNK3-SPAK-NKCC1 signaling pathway, thereby decreasing cerebral edema, inflammatory responses, and neuronal apoptosis. - Source: PubMed
Publication date: 2026/05/25
Zhang Bai-WenZheng LeiKuang Bing-LinZheng JiaYu Xue-PingDai Xiao-HongZou Wei - Early postnatal development is a sensitive period for inhibitory maturation, during which GABAergic signaling shifts from depolarizing to hyperpolarizing as a function of the chloride cotransporters KCC2 and NKCC1. Although these cotransporters are key to inhibitory development, little is known about how early caregiving influences their maturation in cortical circuits supporting attachment learning. We characterized KCC2 and NKCC1 expression in the piriform cortex (PC) of male and female rats from postnatal (P) Day 5 to 22 and assessed their sensitivity to altered caregiving using the limited bedding and nesting (LBN) paradigm (P2-P9). Both cotransporters showed robust postnatal protein upregulation, with sex-specific transcriptional differences for KCC2. At P15, LBN induced sex- and region-dependent changes. KCC2 transcription decreased in the anterior PC of males but increased in females in the posterior PC. NKCC1 protein was reduced in both sexes with distinct anterior-posterior patterns. Using a single-neuron Hodgkin-Huxley model with dynamic ion concentrations incorporating the measured cotransporter profiles, simulations indicated that these differences were sufficient to modify chloride homeostasis and shift GABAergic control of excitability. This multiscale approach links early alterations in caregiving to predicted functional consequences for inhibitory maturation in the PC. - Source: PubMed
Becerra-Flores ChristellOruro Enver MMedina-Saldivar CarlosPacheco-Otálora Luis FPardo Grace E