KCNK2 potassium two pore domain channel subfamily K member 2 [Bos taurus (domestic cattle)] - Gene

Summary

Official Symbol: KCNK2provided by VGNC
Official Full Name: potassium two pore domain channel subfamily K member 2provided by VGNC
Primary source: VGNC:VGNC:30472
See related: BGD:BT21159; Ensembl:ENSBTAG00000004407
Gene type: protein coding
RefSeq status: PROVISIONAL
Organism: Bos taurus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Laurasiatheria; Artiodactyla; Ruminantia; Pecora; Bovidae; Bovinae; Bos
Orthologs: human mouse all
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Genomic context

Location:: chromosome: 16

Exon count:: 10

Annotation release	Status	Assembly	Chr	Location
RS_2024_12	current	ARS-UCD2.0 (GCF_002263795.3)	16	NC_037343.1 (68370668..68595838, complement)

Chromosome 16 - NC_037343.1 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Go to reference sequence details

Genomic Sequence:: NC_037343.1 Chromosome 16 Reference ARS-UCD2.0 Primary Assembly

Go to nucleotide: Graphics FASTA GenBank

Expression

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See details

Project title: Dominette sequence data
BioProject: PRJNA294306
Analysis date: Tue Dec 17 08:57:05 2024

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

ANG II inhibits bTREK-1 K(+) channels by a Ca(2+)-dependent mechanism that does not require the depletion of membrane-associated PIP(2).
Title: Calcium-dependent inhibition of adrenal TREK-1 channels by angiotensin II and ionomycin.
Metabolites of cAMP stimulate TREK-1 expression in adrenal cortex cells by activation of a novel cAMP-independent mechanism.
Title: cAMP analogs and their metabolites enhance TREK-1 mRNA and K+ current expression in adrenocortical cells.
These findings demonstrate that, in addition to the well-described PKA-dependent TREK-1 inhibition, ACTH, NPS-ACTH, forskolin, and 8-pCPT-2'-O-Me-cAMP also inhibit these K(+) channels by a PKA-independent signaling pathway.
Title: ACTH inhibits bTREK-1 K+ channels through multiple cAMP-dependent signaling pathways.
Angiotensin II (ANGII) inhibits adrenocortical cell KCNK2 in an ATP dependent, PLC/PKC independent manner.
Title: Angiotensin II inhibits native bTREK-1 K+ channels through a PLC-, kinase C-, and PIP2-independent pathway requiring ATP hydrolysis.
These results identify bTREK-1 K(+) channels as a pivotal control point where ANG II receptor activation is transduced to depolarization-dependent Ca(2+) entry and aldosterone secretion.
Title: TREK-1 K+ channels couple angiotensin II receptors to membrane depolarization and aldosterone secretion in bovine adrenal glomerulosa cells.
Data show that angiotensin II and paracrine factors that act through phospholipase C inhibit bTREK-1 in adrenocortical cells through simultaneous activation of separate Ca2+- and ATP hydrolysis-dependent signaling pathways.
Title: Angiotensin II inhibits bTREK-1 K+ channels in adrenocortical cells by separate Ca2+- and ATP hydrolysis-dependent mechanisms.
TREK-1 channels may function as sensors that couple the metabolic state of the cell to membrane potential, perhaps through an associated ATP-binding protein
Title: An ACTH- and ATP-regulated background K+ channel in adrenocortical cells is TREK-1.

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General gene information

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Gene Ontology Provided by RefSeq

Function	Evidence Code	Pubs
enables outward rectifier potassium channel activity	IEA Inferred from Electronic Annotation more info	PubMed
enables potassium ion leak channel activity	IEA Inferred from Electronic Annotation more info	PubMed

Process	Evidence Code	Pubs
involved_in potassium ion transmembrane transport	IEA Inferred from Electronic Annotation more info	PubMed
involved_in stabilization of membrane potential	IEA Inferred from Electronic Annotation more info	PubMed

Component	Evidence Code	Pubs
located_in plasma membrane	IEA Inferred from Electronic Annotation more info	PubMed

General protein information

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Preferred Names: potassium channel subfamily K member 2

Names: potassium channel, subfamily K, member 2

NCBI Reference Sequences (RefSeq)

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RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above.