KCNN4 antibody
- Known as:
- KCNN4 (anti-)
- Catalog number:
- orb101130
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- KCNN4 antibody
Related genes to: KCNN4 antibody
- Gene:
- KCNN4 NIH gene
- Name:
- potassium calcium-activated channel subfamily N member 4
- Previous symbol:
- -
- Synonyms:
- KCa3.1, hSK4, hKCa4, hIKCa1, IK
- Chromosome:
- 19q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-07
- Date modifiied:
- 2019-04-23
Related products to: KCNN4 antibody
Related articles to: KCNN4 antibody
- Pancreatic cancer (PC) is one of the leading causes of cancer-related death worldwide. The lack of effective diagnostic biomarkers and therapeutic targets makes PC difficult to screen and treat. The aim of this study was to develop a diagnostic and survival-related gene signature for PC to construct a prognostic model. - Source: PubMed
Publication date: 2026/06/22
Liu ChangQian DanTian YeYang YingLi MengluYou YiqinZhang Liqun - Cancer cells can acquire neuron-like characteristics ("neural mimicry") to promote progression. However, the role of specific ion channel genes in Papillary Thyroid Carcinoma (PTC) and their clinical significance remains unclear. - Source: PubMed
Publication date: 2026/06/22
Liu XinyuMei ChengjinTan JifengLiu YanlanLiu YuyaoZhou ZhigangZhao Jianfu - GABA binding to GABA receptors induces transient elevation in intracellular Ca concentrations in activated human CD4 T cells. Here we examined the Ca response evoked by the GABA receptor agonists THIP, muscimol, isoguvacine, and TACA and further, effects of K1.3 and KCa3.1 channel blockers on the GABA-evoked Ca signal. The cells were activated by anti-CD3 antibody and cultured for 72 h before the effects of agonists and antagonists on intracellular Ca levels were examined by Ca imaging. mRNA sequencing, qPCR, and immunofluorescence imaging identified the GABA subunits expressed. Both the half-maximal concentration for activation (the apparent affinity (EC)) and the evoked, peak cellular Ca response varied among the agonists. The agonists EC values varied more than 1,000-fold, but the compounds can, nevertheless, all be classified as high-affinity agonists (EC < 1 μM). The EC sequence was as follows: GABA (0.005 nM) ≈ THIP (0.005 nM) < muscimol (0.162 nM) < TACA (2.2 nM) < isoguvacine (54.4 nM). In contrast, the peak increase in the cellular Ca signal followed the sequence: GABA >> THIP > muscimol > isoguvacine > TACA. For all agonists, the transient Ca signal was attenuated at micromolar concentrations. ShK-Dap22 and TRAM-34 that block K1.3 and KCa3.1 channels, respectively, inhibited the GABA-activated Ca response. The CRAC channel inhibitor YM58483 reduced the Ca current by 40%. The pharmacology is consistent with the ρ2 GABA receptor subunit being a part of the high-affinity GABA receptors expressed in human CD4 T cells. The agonists at the ρ2-containing GABA receptors induced intracellular Ca signals in human CD4 T cells that were related to the agonist concentration. All tested agonists have a high apparent affinity but differ in efficacy at the receptors. Ca signaling enables high-throughput assays for fast screening of potential drugs aimed at GABA receptors regulating the T cell functions. - Source: PubMed
Publication date: 2026/05/08
Korol Sergiy VJin ZheBhandage Amol KHammoud HaymaBirnir Bryndis - Silver nanoparticles (AgNPs) have emerged as a promising therapeutic tool for managing glioblastoma (GB), particularly in radiosensitisation. However, their mechanisms of action are not yet fully understood. Since ion channel activity is implicated in various aspects of radioresistance, we investigated the electrophysiological effects of AgNPs on GB cells. In the U251 human GB cell line, the acute application of AgNPs induced the activation of a cationic nonselective current in a dose-dependent manner, which was not affected by ACA (TRPM2 blocker). In addition, AgNPs increased intracellular calcium concentration, caused depolarisation of the mitochondrial inner membrane, and promoted membrane blebbing. The investigation revealed that calcium influx is a critical step in the AgNPs-induced effects. Thiol reagents such as cysteine are known silver chelating agents and their application prevented the activation of cationic currents, intracellular calcium increases, and membrane blebbing formation induced by AgNPs. This finding suggested Ag are the active species responsible for these effects, acting through IAg current previously characterized in our laboratory. Intracellular calcium influx induced by AgNPs activated intermediate-conductance calcium-activated potassium currents. This activation was accordingly blocked by TRAM-34, a selective inhibitor of KCa3.1 channels. Finally, AgNPs were found to reduce U251-GB cell viability in a dose-dependent manner and to increase G2/M phase accumulation following sublethal irradiation. In the presence of TRAM-34 the G2/M phase accumulation induced by the combined treatment with AgNPs and irradiation was reduced, suggesting the involvement of radioresistance-associated KCa3.1 currents. These results provide new insights into optimizing the use of AgNPs as radiosensitizing agents in GB therapy. - Source: PubMed
Publication date: 2026/05/20
Ragonese FrancescoBiagini AndreaSallicandro LuanaMirarchi AlessandraReali GianmarcoDe Luca AntonellaArcuri CataldoFlamini SaraBereshchenko OxanaCogliati PaoloSpogli RobertoSabbatini PaolaBruscoli StefanoSportoletti PaoloFioretti Bernard - Genetically modified chimeric antigen receptor (CAR) T cells eliminate tumors by recognizing specific antigens on the cell surface. T cell ion channels (e.g. Kv1.3, KCa3.1) influence activation, proliferation, and effector functions such as target cell killing, through the regulation of Ca2+ signaling. We showed that CAR-expressing cells (Jurkat) specifically eliminate tumor cells (Raji B cells) in monolayer culture and inhibition of KCa3.1 by TRAM34 increased the tumor cell-killing ability of KCa3.1+ Jurkat CARs. Blockage of KCa3.1 facilitated the migration of KCa3.1+ Jurkat CARs (mean speed, displacement and distance). The application of TRAM34 lowered the baseline Ca2+ level in mCherry-KCa3.1+ Jurkat CARs. Finally, TRAM34 significantly reduced the time needed to eliminate tumor cells. We concluded that expression and modification of KCa3.1 ion channels shifts the intracellular Ca2+ concentration into the range where cytotoxicity dominates. Hence, modification of KCa3.1 channels could contribute to a more effective anticancer immunotherapy. - Source: PubMed
Jusztus VivienHajdu MártonHorváth PéterPanyi GyörgyHajdu Péter