Recombinant Human Intermediate conductance calcium-activated potassium channel protein 4 (KCNN4)

Code CSB-CF012086HU
Size $1620
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
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Product Details

Greater than 85% as determined by SDS-PAGE.
Target Names
Uniprot No.
Research Area
Cell Biology
Alternative Names
KCNN4; IK1; IKCA1; KCA4; SK4; Intermediate conductance calcium-activated potassium channel protein 4; SKCa 4; SKCa4; IKCa1; KCa3.1; KCa4; Putative Gardos channel
Homo sapiens (Human)
in vitro E.coli expression system
Expression Region
1-427 aa
Target Protein Sequence
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight
53.7 kDa
Protein Length
Full Length
Tag Info
N-terminal 10xHis-tagged
Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol.
Note: If you have any special requirement for the glycerol content, please remark when you place the order.
If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA
Please contact us to get it.

This recombinant HumanKCNN4 protein is an in vitro E.coli (cell-free) expressed Full Length protein. Its purity is 85%+ determined by SDS-PAGE. Cell-free protein expression is the in vitro synthesis of a protein using translation-compatible extracts of whole cells. In principle, whole-cell extracts contain all the macromolecules and components needed for transcription, translation, and even post-translational modification. These components include RNA polymerase, regulatory protein factors, transcription factors, ribosomes, and tRNA. When supplemented with cofactors, nucleotides, and the specific gene template, these extracts can synthesize proteins of interest in a few hours.

The KCNN4 is the encoding gene for the KCa3.1/SK4, which plays a critical role in calcium-activated anion secretion in mice and humans. It is abundantly expressed in non-excitable cells such as erythrocytes, lymphocytes, and placenta cells. The KCa3.1 has been found to participate in the pacemaker activity of cardiomyocytes sourcing from human embryonic stem cells (hESC-CMs). It is involved in cancer progression, including cell proliferation, apoptosis, epithelial-mesenchymal transition (EMT), and metastasis.

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Target Background

Forms a voltage-independent potassium channel that is activated by intracellular calcium. Activation is followed by membrane hyperpolarization which promotes calcium influx. Required for maximal calcium influx and proliferation during the reactivation of naive T-cells. Plays a role in the late stages of EGF-induced macropinocytosis.
Gene References into Functions
  1. These results suggest that His358, the inhibitory histidine in KCa3.1, might coordinate a copper ion through a similar binding mode. PMID: 29953543
  2. present study was designed to evaluate in hereditary xerocytosis the functional link between mutated Piezo1 and KCNN4 PMID: 28619848
  3. this study reports cryo-electron microscopy (cryo-EM) structures of a human SK4-CaM channel complex in closed and activated states at 3.4- and 3.5-angstrom resolution, respectively. PMID: 29724949
  4. Expression of intermediate-conductance calmodulin/calcium-activated K+ channels 3.1 (KCa3.1) mRNA and protein was detected in all three layers of the human cornea. PMID: 29554088
  5. KCa3.1 channels are important modulators in hepatocellular homeostasis. PMID: 27354175
  6. Tumor suppressor miR-497-5p down-regulates KCa3.1 expression and contributes to the inhibition of angiosarcoma malignancy development. PMID: 27531900
  7. We identified a two-gene signature including KCNN4 and S100A14 which was related to recurrence in optimally debulked serous ovarian carcinoma patients PMID: 27270322
  8. Human arrhythmogenic calmodulin mutations impede the activation of SK2 channels in human embryonic kidney 293 cells. PMID: 27165696
  9. This study found a very substantial functional expression of KCa3.1 channels in microglia from adult epilepsy patients. PMID: 27470924
  10. Data show that RNAi-mediated knockdown of KCa3.1 and/or TRPC1 leads to a significant decrease in cell proliferation due to cell cycle arrest in the G1 phase. PMID: 27183905
  11. Higher epithelial KCNN4 expression was closely correlated with advanced TNM stages and predicted a poor prognosis in patients with pancreatic ductal adenocarcinoma. PMID: 29050937
  12. Here, the authors demonstrate that phosphorylation of His358 activates KCa3.1 by antagonizing copper-mediated inhibition of the channel. PMID: 27542194
  13. This work demonstrates the critical role of SK4 Ca(2+)-activated K(+) channels in adult pacemaker function. PMID: 28219898
  14. Blocking KCa3.1 suppresses plaque instability in advanced stages of atherosclerosis by inhibiting macrophage polarization toward an M1 phenotype. PMID: 28062499
  15. IKCa1 is overexpressed in cervical cancer tissues, and IKCa1 upregulation in cervical cancer cell linea enhances cell proliferation, partly by reducing the proportion of apoptotic cells. PMID: 28280257
  16. Findings suggest that SK4 channels are expressed in triple-negative breast cancer (TNBC) cells and are involved in the proliferation, apoptosis, migration and epithelial-mesenchymal transition processes of TNBC cells. PMID: 27124117
  17. KCa3.1 blockade protects against cisplatin-induced acute kidney injury through the attenuation of apoptosis by interference with intrinsic apoptotic and endoplasmic reticulum stress-related mediators. PMID: 26438401
  18. KCa3.1 in human immature dendritic cells play a major role in their migration and constitute an attractive target for the cell therapy optimization PMID: 27020659
  19. The results suggest that KCa3.1 activation contributes to dysfunctional tubular autophagy in diabetic nephropathy through PI3K/Akt/mTOR signaling pathways. PMID: 27029904
  20. that KCa3.1 channels are key actors in the migration capacity of neutrophils, and its inhibition did not affect other relevant cellular functions PMID: 26138196
  21. KCa3.1 and CFTR colocalize at the plasma membrane. PMID: 27092946
  22. KCNN4 inhibition differentially regulates migration of intestinal epithelial cells in inflamed vs. non-inflamed conditions in a PI3K/Akt-mediated manner. PMID: 26824610
  23. KCa3.1 protein expression was increased in asthmatic compared to healthy airway epithelium in situ, and KCa3.1 currents were larger in asthmatic compared to healthy HBECs cultured in vitro PMID: 26689552
  24. Data show that calcium-dependent potassium channel KCa3.1 operates as a positive feedback mechanism for intracellular Ca2+ increase. PMID: 26418693
  25. high KCa3.1-mRNA expression levels were indicative of low disease specific survival of ccRCC patients, short progression-free survival, and a high metastatic potential. Therefore, KCa3.1 is of prognostic value in ccRCC PMID: 25848765
  26. KCa3.1 activation in human lung mast cells is highly dependent on Ca(2+) influx through Orai1 channels, mediated via a close spatiotemporal interaction between the two channels. PMID: 26177720
  27. Novel Gardos channel mutations linked to dehydrated hereditary stomatocytosis (xerocytosis). PMID: 26178367
  28. describes patients from 2 well-phenotyped hereditary xerocytosis (HX) kindreds, including from one of the first HX kindreds described, who lack predicted heterozygous PIEZO1-linked variants PMID: 26198474
  29. identification of a dominantly inherited missense mutation in the Gardos channel in 2 unrelated families and its association with chronic hemolysis and dehydrated cells, also referred to as hereditary xerocytosis PMID: 26148990
  30. Inhibition of K(Ca)3.1 by EETs (14,15-EET), 20-HETE, and omega3 critically depended on the presence of electron double bonds and hydrophobicity within the 10 carbons preceding the carboxyl-head of the molecules. PMID: 25372486
  31. Ca2+- and KCa3.1-dependent processes facilitate "constitutive" alpha smooth muscle actin expression and Smad2/3 signalling in IPF-derived fibroblasts, and thus promote fibroblast to myofibroblast differentiation. PMID: 25476248
  32. The role and mechanisms of KCa3.1 in progressive diabetic chronic kidney disease are reviewed. PMID: 25415613
  33. The present study shows that KCNN4 is expressed at the mRNA and protein level in RA-SFs, is functionally active, and has a regulatory impact on cell proliferation and secretion of pro-inflammatory and pro-destructive mediators. PMID: 25545021
  34. Overexpression of CCL20 in human proximal tubular cells is inhibited by blockade of KCa3.1 under diabetic conditions through inhibition of the NF-kappaB pathway. PMID: 24733189
  35. Blood brain barrier endothelial cells exhibit KCa3.1 protein and activity. PMID: 25477223
  36. These data suggest that NO activates KCNN4 channels through the PKG but not the PKA pathways. PMID: 24826782
  37. Mg(2+) inhibits KCa3.1 via a rapid, voltage-dependent mechanism that leads to a reduction of the channel's unitary current and by reducing the open probability of the channel PMID: 24193405
  38. Tumor-associated macrophages participate in the metastasis of CRC induced by PRL-3 through secretion of IL-6 and IL-8 in a KCNN4 dependent manner. PMID: 24885636
  39. KCa3.1 confers an invasive phenotype that significantly worsens a patient's outlook with malignant glioma. PMID: 24585442
  40. These findings highlight a novel role for the KCa3.1 channel in human BSM cell phenotypic modulation. PMID: 24055799
  41. blockade of KCa3.1 attenuates diabetic renal interstitial fibrogenesis through inhibiting activation of fibroblasts PMID: 24166472
  42. The channel gating process for KCa3.1 and the S5 transmembrane segment is controlled by aromatic-aromatic interactions involving the pore helix. PMID: 24470490
  43. KCa3.1 has a role in diabetic nephropathy. (review) PMID: 24963668
  44. Our findings suggest that KCa3.1 channels play an important role in the pathogenesis of chronic AV and constitute an attractive target for the prevention of arteriopathy. PMID: 24312257
  45. Our results suggested that IKCa1 may play a role in the proliferation of human HCC, and IKCa1 blockers may represent a potential therapeutic strategy for HCC. PMID: 23392713
  46. KCa3.1 pharmacological blockade attenuated human myofibroblast proliferation, wound healing, collagen secretion and contractility in vitro, and this was associated with inhibition of TGFbeta1-dependent increases in intracellular free Ca2+. PMID: 24392001
  47. blocking KCa3.1 increases the degranulation and cytotoxicity of adherent Natural killer cells, but not of non-adherent-Natural killer cells. PMID: 24146918
  48. This study provides insight into the key molecular determinants for the high-affinity binding of peptide toxins to KCa3.1. PMID: 24138859
  49. KCa3.1 activity has an important role in glioblastoma invasiveness. PMID: 23949222
  50. Globotriaosylceramide accelerates the endocytosis and lysosomal degradation of endothelial KCa3.1 via a clathrin-dependent process, leading to endothelial dysfunction in Fabry disease. PMID: 24158513

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Involvement in disease
Dehydrated hereditary stomatocytosis 2 (DHS2)
Subcellular Location
Cell membrane; Multi-pass membrane protein.
Protein Families
Potassium channel KCNN family, KCa3.1/KCNN4 subfamily
Tissue Specificity
Widely expressed in non-excitable tissues.
Database Links

HGNC: 6293

OMIM: 602754

KEGG: hsa:3783

STRING: 9606.ENSP00000262888

UniGene: Hs.10082

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