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KCNK17 Membrane Protein Introduction

Introduction of KCNK17

KCNK17, the full name is potassium channel subfamily K member 17, also known as 2P domain potassium channel Talk-2, Acid-sensitive potassium channel protein TASK-4, TWIK-related acid-sensitive K(+) channel 4, TWIK-related alkaline pH-activated K(+) channel 2 (TALK-2). TASK-4 is a member of the acid-sensitive subfamily of tandem K+ channels. TASK-4 transcripts are widely expressed in humans and have the highest levels in the liver, lung, pancreas, placenta, aorta, and heart.

Basic Information of KCNK17
Protein Name Potassium channel subfamily K member 17
Gene Name KCNK17
Aliases 2P domain potassium channel Talk-2, Acid-sensitive potassium channel protein TASK-4, TWIK-related acid-sensitive K(+) channel 4, TWIK-related alkaline pH-activated K(+) channel 2 (TALK-2)
Organism Homo sapiens (Human)
UniProt ID Q96T54
Transmembrane Times 4
Length (aa) 332
Sequence MYRPRARAAPEGRVRGCAVPSTVLLLLAYLAYLALGTGVFWTLEGRAAQDSSRSFQRDKWELLQNFTCLDRPALDSLIRDVVQAYKNGASLLSNTTSMGRWELVGSFFFSVSTITTIGYGNLSPNTMAARLFCIFFALVGIPLNLVVLNRLGHLMQQGVNHWASRLGGTWQDPDKARWLAGSGALLSGLLLFLLLPPLLFSHMEGWSYTEGFYFAFITLSTVGFGDYVIGMNPSQRYPLWYKNMVSLWILFGMAWLALIIKLILSQLETPGRVCSCCHHSSKEDFKSQSWRQGPDREPESHSPQQGCYPEGPMGIIQHLEPSAHAAGCGKDS

Function of KCNK17 Membrane Protein

KCNK17 generated K+ currents displaying a marked outward rectification which is lost by elevation of extracellular K+. KCNK17 is sensitive to extracellular pH, but in contrast to other TASK channels, pH sensitivity was shifted to more alkaline pH. The IC50 of KCNK17 is pH 8.8. Thus, KCNK17 synergizes with other TASK channels to modulate cell membrane potential over a wide range of extracellular pH. The KCNK17 channel is a new gene involved in progressive cardiac conduction disorder (PCCD), a disease with a wide range of unknown genetic origins.

TASK-4 pore homology model based on the crystal structure of TWIK-1. Fig.1 TASK-4 pore homology model based on the crystal structure of TWIK-1. (Friedrich, 2014)

Application of KCNK17 Membrane Protein in Literature

  1. Suzuki Y., et al. Heterodimerization of two pore domain K+ channel TASK1 and TALK2 in living heterologous expression systems. PLoS One. 2017, 12(10):e0186252. PubMed ID: 29016681

    The results indicated that heterodimerization of TASK1 and TALK2 conferred the ability of cells to produce multiple responses to a variety of physiological and pharmacological stimuli.

  2. He L., et al. Association of variants in KCNK17 gene with ischemic stroke and cerebral hemorrhage in a Chinese population. J Stroke Cerebrovasc Dis. 2014, 23(9):2322-7. PubMed ID: 25179130

    KCNK17 may play an important role in the pathogenesis of cerebral hemorrhage.

  3. Friedrich C., et al. Gain-of-function mutation in TASK-4 channels and severe cardiac conduction disorder. EMBO Mol Med. 2014, 6(7):937-51. PubMed ID: 24972929

    This study identified KCNK17 as a novel arrhythmia gene.

  4. Domingues-Montanari S., et al. KCNK17 genetic variants in ischemic stroke. Atherosclerosis. 2010, 208(1):203-9. PubMed ID: 19647252

    The A allele of the rs10947803 variant of KCNK17 was associated with increased risk of ischemic stroke (IS) and increased levels of KCNK17 gene expression.

  5. Ma Q., et al. The rs10947803 SNP of KCNK17 is associated with cerebral hemorrhage but not ischemic stroke in a Chinese population. Neurosci Lett. 2013, 539:82-5. PubMed ID: 23391755

    The rs10947803 SNP (A allele) in KCNK17 increased the risk of cerebral hemorrhage but not ischemic stroke in the Chinese population.

KCNK17 Preparation Options

Membrane protein studies have advanced significantly over the past few years. Based on our versatile Magic™ membrane protein production platform, we could offer a series of membrane protein preparation services for worldwide customers in reconstitution forms or membrane protein mutants. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-KCNK17 antibody development services.


During the past years, Creative Biolabs has successfully generated many functional membrane proteins for our global customers. We are happy to accelerate the development of our clients’ programs with our one-stop, custom-oriented service. For more detailed information, please feel free to contact us.

Reference

  1. Friedrich C, et al. (2014). Gain-of-function mutation in TASK-4 channels and severe cardiac conduction disorder. EMBO Mol Med. 6(7):937-51.

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