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  4. Recombinant Mouse Intermediate conductance calcium-activated potassium channel protein 4 (Kcnn4)

Recombinant Mouse Intermediate conductance calcium-activated potassium channel protein 4 (Kcnn4)

  • 货号：
    CSB-CF012086MO
  • 规格：
  • 来源：
    in vitro E.coli expression system
  • 其他：

产品详情

  • 基因名：
  • Uniprot No.：
  • 别名：
    Kcnn4; Intermediate conductance calcium-activated potassium channel protein 4; SK4; SKCa 4; SKCa4; IK1; KCa3.1; KCa4
  • 种属：
    Mus musculus (Mouse)
  • 蛋白长度：
    Full length protein
  • 表达区域：
    1-425
  • 氨基酸序列
    MGGELVTGLGALRRRKRLLEQEKRVAGWALVLAGTGIGLMVLHAEMLWFLGCKWVLYLLL VKCLITLSTAFLLCLIVVFHAKEVQLFMTDNGLRDWRVALTRRQVAQILLELLVCGVHPV PLRSPHCALAGEATDAQPWPGFLGEGEALLSLAMLLRLYLVPRAVLLRSGVLLNASYRSI GALNQVRFRHWFVAKLYMNTHPGRLLLGLTLGLWLTTAWVLSVAERQAVNATGHLTDTLW LIPITFLTIGYGDVVPGTMWGKIVCLCTGVMGVCCTALLVAVVARKLEFNKAEKHVHNFM MDIHYAKEMKESAARLLQEAWMYYKHTRRKDSRAARRHQRKMLAAIHTFRQVRLKHRKLR EQVNSMVDISKMHMILCDLQLGLSSSHRALEKRIDGLAGKLDALTELLGTALQQQQLPEP SQEAT
    Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
  • 蛋白标签：
    N-terminal 10xHis-tagged
  • 产品提供形式：
    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.
  • 缓冲液：
    Lyophilized from Tris/PBS-based buffer, 6% Trehalose, pH 8.0
  • 储存条件：
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保质期：
    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.
  • 货期：
    Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
    Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
  • 注意事项：
    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.

产品评价

靶点详情

  • 功能：
    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.
  • 基因功能参考文献：
    1. KCa3.1 channel is likely to be a critical target on the oxidative stress. PMID: 28455747
    2. Diet-induced hyperhomocysteinemia enhanced myoendothelial feedback, and increased Cx37 and IK1 expression may contribute. nNOS or iNOS did not upregulate to compensate for decreased eNOS, and they had little involvement in vasomotor function. PMID: 28857417
    3. The Intermediate-conductance calmodulin/calcium-activated K+ channels 3.1 (KCa3.1-/- knockout mice) significantly reduced corneal fibrosis and expression of pro-fibrotic marker genes, suggesting that KCa3.1 plays an important role corneal wound healing in vivo. PMID: 29554088
    4. KCa3.1(-/-) mice exhibited significantly smaller infarct areas in a model of ischemic stroke. PMID: 29037241
    5. KCa3.1(-/-) mice demonstrated normal behavioral responses in models of acute nociceptive, persistent inflammatory, and persistent neuropathic pain. However, their behavioral responses to noxious chemical stimuli such as formalin and capsaicin were increased. Accordingly, formalin-induced nociceptive behavior was increased in wild-type mice after administration of the KCa3.1 inhibitor TRAM-34. PMID: 28823609
    6. SK4 activity is crucial for cell cycle control. PMID: 28557306
    7. Deletion of KCa3.1 reduced astrogliosis and rescued memory loss induced by intrahippocampal Abeta1-42 peptide injection. PMID: 27567685
    8. Blocking KCa3.1 suppresses plaque instability in advanced stages of atherosclerosis by inhibiting macrophage polarization toward an M1 phenotype. PMID: 28062499
    9. enhanced KCa 3.1 activity may compensate for decreased nitric oxide signaling during vascular aging. PMID: 27363720
    10. Findings highlight a novel role for intermediate-conductance calcium-activated potassium channel (KCa3.1) in phenotypic modulation of reactive astrocytes and in astrocyte mobilization in response to mechanical stress, providing a potential target for therapeutic intervention in brain injuries. PMID: 27163196
    11. alpha1D Ca and SK4 channels are coupled in the atria, and deletion of alpha1D leads to decreased SK4 mRNA and BNP secretion providing evidence for a novel role of alpha1D in atrial endocrine function PMID: 27884747
    12. 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
    13. The results suggest that KCa3.1 activation contributes to dysfunctional tubular autophagy in diabetic nephropathy through PI3K/Akt/mTOR signaling pathways. PMID: 27029904
    14. These results indicate that IK1 channels do not mediate the a slow afterhyperpolarization in pyramidal neurons. PMID: 26765773
    15. KCa3.1 is a possible marker of M/MPhi in the protumor state and a potential therapeutic target to induce glioma-associated microglia/macrophages to re-acquire a pro-inflammatory, antitumor activity. PMID: 27054329
    16. 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
    17. Modulation of PKA and PI3KC2beta activity to control of KCa3.1 channel expression can be an alternative important target to attenuate ascending thoracic aortic aneurysms in Fabry disease. PMID: 26820527
    18. These findings suggest that the KCa3.1 channel can serve as a new target to attenuate and prevent development of ascending thoracic aortic aneurysm in Fabry disease. PMID: 26592662
    19. 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
    20. NDPKB/SK4 signaling is required for neointima formation in injured carotid arteries. PMID: 26088577
    21. KCa 3.1 blockade strongly reduced the growth of xenografted NSCLC cells. PMID: 25704182
    22. The data suggest that the P2Y2/4 receptor activation elicits blood pressure responses via distinct mechanisms involving KCa3.1 and Cx37. PMID: 25545736
    23. 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
    24. Studies suggest an important modulatory role for KCa3.1 in adult neuroblast migration that could be capitalized on in future attempts to alter the intrinsic repair response of the brain using neuronal precursor cells PMID: 23585521
    25. Role of the K(Ca)3.1 K+ channel in auricular lymph node CD4+ T-lymphocyte function of the delayed-type hypersensitivity model PMID: 23594188
    26. Pulmonary hypertension in wild type mice and animals with genetic deficit in KCa2.3 and KCa3.1 channels PMID: 24858807
    27. blockade of KCa3.1 attenuates diabetic renal interstitial fibrogenesis through inhibiting activation of fibroblasts PMID: 24166472
    28. Targeted inhibition of KCa3.1 reduces reactive gliosis in cultured astrocytes. PMID: 24606313
    29. increase in KCa3.1 activity induced by the upregulation of KCa3.1a and NDPK-B may be involved in the pathogenesis of IBD by mediating the enhancement of the proliferative response in MLN CD4(+) T lymphocyte. PMID: 24674776
    30. 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
    31. IK1, and to some extent SK3, channels exert a substantial positive feedback influence on endothelial Ca(2+) dynamics in agonist stimulated mesenteric arteries. PMID: 24177326
    32. Blockade of KCa3.1 with potassium channel blockers prevented airway remodeling in allergic asthma. PMID: 23492185
    33. The inhibition of KCa3.1 channels activity reduces cell motility in glioblastoma derived cancer stem cells. PMID: 23110108
    34. Genetic KCa3.1-deficiency causes locomotor hyperactivity and altered monoamine levels in selected brain regions PMID: 23077667
    35. KCa3.1 channels are involved in the pathogenesis of obliterative airway disease (OAD). KCa3.1 blockade holds promise to reduce OAD development. PMID: 23325003
    36. Modafinil inhibits K(Ca)3.1 channels and vascular smooth muscle contraction by cAMP-dependent phosphorylation. PMID: 22414869
    37. KCa3.1 expression in lung dendritic cells was up-regulated by ovalbumin sensitization. KCa3.1 was involved in the migration of lung dendritic cells to lymphatic chemokines. PMID: 21493782
    38. Ca2+ activated K+ channel Kca3.1 plays a central role in gastric acid secretion. PMID: 21691077
    39. the N-terminal domain of K(Ca)3.1 is critical for channel trafficking to the plasma membrane PMID: 21345794
    40. Globotriaosylceramide evokes K(Ca)3.1 channel dysfunction, and the channel dysfunction in vascular endothelial cells may contribute to vasculopathy in Fabry disease. PMID: 20971723
    41. The SK4 component of the Kslow current can trigger oscillations in mice without functioning KATP channels. PMID: 21099262
    42. Kcnn4 is crucially involved in cardiac and cardiac pacemaker cell differentiation of embryonic stem cells PMID: 20956206
    43. K(Ca)3.1 channel activity and Gardos effect counteract hemolysis of injured erythrocytes, thus decreasing hemoglobin release into circulating blood. PMID: 20857305
    44. Nucleoside diphosphate kinase B knock-out mice have impaired activation of the K+ channel KCa3.1, resulting in defective T cell activation PMID: 20884616
    45. found that inhibition of KCa3.1(-/-) protected mice from developing severe colitis in mouse models of inflammatory bowel disease. PMID: 20080610
    46. Selective blockade of T-lymphocyte K(Ca)3.1 and K(v)1.3 channels may represent a novel alternative therapy for prevention of kidney allograft rejection. PMID: 19715983
    47. SK1, -2, -3, and IK1 (SK4) are expressed in islet cells and insulin-secreting cells and are able to influence glucose-induced calcium responses, thereby regulating insulin secretion. PMID: 12882916
    48. Results confirm that IK channels in red blood cells, T lymphocytes, and parotid acinar cells are indeed encoded by the Kcnn4 gene. PMID: 15347667
    49. cardiac Ang II overproduction leads to the emergence of a long QT syndrome resulting from an IK1-dependent prolongation of the action potential duration through modulation of channel subunit expression. PMID: 17070838
    50. Submandibular acinar cell function relies on KCNN4 channel activity. PMID: 17379640

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  • 亚细胞定位：
    Cell membrane; Multi-pass membrane protein.
  • 蛋白家族：
    Potassium channel KCNN family, KCa3.1/KCNN4 subfamily
  • 数据库链接：

    KEGG: mmu:16534

    STRING: 10090.ENSMUSP00000133065

    UniGene: Mm.9911