| Structural highlights
Disease
KCNN4_HUMAN The disease is caused by mutations affecting the gene represented in this entry.
Function
KCNN2_HUMAN Forms a voltage-independent potassium channel activated by intracellular calcium. Activation is followed by membrane hyperpolarization. Thought to regulate neuronal excitability by contributing to the slow component of synaptic afterhyperpolarization. The channel is blocked by apamin.KCNN4_HUMAN Forms a voltage-independent potassium channel that is activated by intracellular calcium (PubMed:26148990). Activation is followed by membrane hyperpolarization which promotes calcium influx. Required for maximal calcium influx and proliferation during the reactivation of naive T-cells. The channel is blocked by clotrimazole and charybdotoxin but is insensitive to apamin (PubMed:17157250, PubMed:18796614).[1] [2] [3]
References
- ↑ Srivastava S, Li Z, Ko K, Choudhury P, Albaqumi M, Johnson AK, Yan Y, Backer JM, Unutmaz D, Coetzee WA, Skolnik EY. Histidine phosphorylation of the potassium channel KCa3.1 by nucleoside diphosphate kinase B is required for activation of KCa3.1 and CD4 T cells. Mol Cell. 2006 Dec 8;24(5):665-675. doi: 10.1016/j.molcel.2006.11.012. PMID:17157250 doi:https://dx.doi.org/10.1016/j.molcel.2006.11.012
- ↑ Srivastava S, Zhdanova O, Di L, Li Z, Albaqumi M, Wulff H, Skolnik EY. Protein histidine phosphatase 1 negatively regulates CD4 T cells by inhibiting the K+ channel KCa3.1. Proc Natl Acad Sci U S A. 2008 Sep 23;105(38):14442-6. doi:, 10.1073/pnas.0803678105. Epub 2008 Sep 16. PMID:18796614 doi:https://dx.doi.org/10.1073/pnas.0803678105
- ↑ Rapetti-Mauss R, Lacoste C, Picard V, Guitton C, Lombard E, Loosveld M, Nivaggioni V, Dasilva N, Salgado D, Desvignes JP, Beroud C, Viout P, Bernard M, Soriani O, Vinti H, Lacroze V, Feneant-Thibault M, Thuret I, Guizouarn H, Badens C. A mutation in the Gardos channel is associated with hereditary xerocytosis. Blood. 2015 Sep 10;126(11):1273-80. doi: 10.1182/blood-2015-04-642496. Epub 2015 , Jul 6. PMID:26148990 doi:https://dx.doi.org/10.1182/blood-2015-04-642496
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