Ask about this productRelated genes to: SLC12A4 antibody
- Gene:
- SLC12A4 NIH gene
- Name:
- solute carrier family 12 member 4
- Previous symbol:
- -
- Synonyms:
- KCC1
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-15
- Date modifiied:
- 2016-02-17
Related products to: SLC12A4 antibody
Related articles to: SLC12A4 antibody
- Cytolethal Distending Toxin (CDT) is the only exotoxin that () can secrete. CDT (CDT) triggers DNA damage responses, leading to irreversible cell cycle arrest and apoptosis, playing an important role in the pathogenic process of . Currently, research on the host cell receptors of CDT remains limited. Screening and identification of host cell receptors that interact with CDT are crucial for systematically elucidating the cytotoxic mechanisms induced by this toxin. - Source: PubMed
Publication date: 2026/03/19
Lei LiXu ShiyuYang ZhenPan XingyuXu JialiDu SenyanZhao QinHuang XiaoboCao SanjieWu RuiWang YipingYan QiguiWen Yiping - Diabetic retinopathy (DR) is a common microvascular complication that leads to vision loss in patients with diabetes. The SLC12A2/SLC12A4 inhibitor, bumetanide, has been reported to alleviate hypoxia‑induced retinopathy. It was hypothesized that it may exert the same effect in DR. DR cell types and SLC12A2/SLC12A4 expression at the cell level were analyzed using single cell RNA‑sequencing (scRNA‑seq) data. Next, cell [high glucose (HG) stimulation] and animal (mice injected with streptozotocin) DR models were constructed. The protective effects and possible mechanisms of bumetanide and SLC12A2 were investigated through a series of experiments, including Cell Counting Kit‑8, TUNEL, Transwell, tube formation, ELISA, immunofluorescence staining, western blot and reverse transcription‑quantitative PCR assays. Bumetanide reduced HG‑induced cell apoptosis by suppressing the expression of SLC12A2 and SLC12A4. Second, scRNA‑seq analysis revealed that SLC12A2 was predominantly expressed in endothelial cells, which are the main targets of hyperglycemic damage. Endothelial cell‑related markers were involved in angiogenesis and adhesion molecule‑related pathways. Third, in HG‑stimulated cells, SLC12A2 knockdown efficiently reduced the inflammatory response and angiogenesis, while maintaining endothelial barrier integrity. This protective process involved reduced release of inflammatory factors (IL‑1β and IL‑6) and growth factors (vascular endothelial growth factor), suppression of adhesion molecule expression (VCAM1, ICAM1, E‑Selectin and P‑Selectin), activation of tight junction protein (ZO‑1), and decreased matrix metalloproteinases (MMP2 and MMP9). Furthermore, SLC12A2 deficiency ameliorated DR progression in streptozotocin‑induced diabetic mice by improving retinal thickness and pathological changes. The present study elucidates the crucial role of bumetanide in DR treatment and suggests that targeting SLC12A2 may represent a novel therapeutic strategy for the prevention of DR. - Source: PubMed
Publication date: 2026/03/06
Zhang YutingWang XiuliXie QinyueHuang YueHuang DongjiaLiu ZiqingXu TongNi ManYang Hongwei - The plasma membrane (PM) is a dynamic interface that integrates environmental cues with cellular responses. Insulin is known to remodel the PM primarily by stimulating the translocation of glucose transporter GLUT4, but the full scope of insulin's PM remodeling remains poorly defined. Here, we performed a meta-analysis of insulin-regulated PM proteins in adipocytes by integrating nine independent proteomic datasets generated using complementary PM enrichment strategies. The meta-analysis identified 37 insulin-regulated candidates detected in at least three datasets, including 30 proteins not previously implicated in insulin action. Among these, we experimentally characterized the insulin-stimulated translocation of two transporters: potassium-chloride cotransporter 1 KCC1 (SLC12A4) and sodium-dependent phosphate transporter PIT2 (SLC20A2), which showed robust and reproducible recruitment to the PM in response to insulin. siRNA-mediated knockdown of KCC1 or PIT2 impaired insulin-stimulated glucose transport, suggesting a role for these transporters in insulin action. Live-cell and fixed-cell imaging revealed that both proteins localize across multiple endosomal compartments, undergo insulin dose-dependent trafficking to the PM, and require PI3K-AKT signaling for their mobilization. Strikingly, insulin-induced translocation of KCC1 and PIT2 to the PM was impaired in adipocytes rendered insulin resistant by chronic hyperinsulinemia, accompanied by increased perinuclear retention under basal conditions. Together, our work provides a valuable resource for understanding insulin-regulated PM remodeling in adipocytes, establishes KCC1 and PIT2 as novel insulin-responsive transporters, and supports the idea that insulin resistance involves defects in cell-surface delivery that extend beyond GLUT4. - Source: PubMed
Publication date: 2026/02/12
Zhang YijuCooke Kristen CScavuzzo JonathanCutler Harry BMadsen SørenKearney Alison LConway Olivia JHawkins Bethan LMenon DilipHumphrey Sean JKoumanov FrançoiseStöckli JacquelineGeddes Thomas AFazakerley Daniel JDiaz-Vegas AlexisBurchfield James GJames David E - The potassium chloride cotransporter 1 (KCC1) is ubiquitously expressed and essential for regulating cellular fluid balance. We identified a patient carrying a genetic variant (E1065K) in the KCC1 coding gene SLC12A4. This study explored the impact of the variant in ectopic cell systems and enhanced the understanding of cell biological properties of the KCC1 protein. KCC1 WT and E1065K DNA expression constructs were transfected in HEK293T, EPI7 or COS7 cells. KCC1 protein expression levels, glycosylation, intracellular trafficking, half-life and protein localization were determined with western blot and immunofluorescence microscopy. Molecular docking investigated interactions within the cotransporter. Cotransporter activity was tested with NH flux measurements. The variant reduces interactions within the cotransporter and functional activation decreases in hypotonic conditions. Other cell biology characteristics with respect to protein expression level, half-life or subcellular localization did not show any statistical difference between KCC1 WT and E1065K. However, this data provided new characteristics of KCC1 protein. Altogether, these findings are the first description of a potential pathogenic human variant in the KCC1 protein. - Source: PubMed
Bloothooft MeyeHuang JiahuiHamze MiraHoutman Marien J Cde Boer Teun Pvan Hasselt Peter MEcker Gerhard FPorcher ChristopheMedina Igorvan der Heyden Marcel A G - As a global pest, causes significant economic losses annually, making it imperative to investigate its metabolic detoxification mechanisms. The solute carrier (SLC) gene constitutes a superfamily of genes that can directly or indirectly influence the metabolic detoxification functions of insects. In this study, 108 SLC genes were identified via the genome database (ASM270686v3), and their expression patterns were analyzed through transcriptome analysis. Three candidate SLC genes with inducible expression characteristics in different tissues, namely, , , and , were selected for further experimental studies. The quantitative real-time polymerase chain reaction results indicated that following exposure to xenobiotics, was expressed in both the midgut and Malpighian tubules, expression was induced in the Malpighian tubules, and was expressed in the midgut. Overexpression of , , and in transgenic conferred tolerance to xenobiotics. Furthermore, following the knockdown of via RNA interference, the tolerance of to both cyantraniliprole and chlorantraniliprole significantly decreased. These results suggest that SLC genes may play roles in driving the development of xenobiotic tolerance in . - Source: PubMed
Publication date: 2025/11/21
Jin LongFan ChengchengXun PengjunZhang ZhixinKong HaoranZhao HaizhengPan YiouShang Qingli