Kcnj13 potassium inwardly-rectifying channel, subfamily J, member 13 [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Kcnj13provided by MGI
Official Full Name: potassium inwardly-rectifying channel, subfamily J, member 13provided by MGI
Primary source: MGI:MGI:3781032
See related: Ensembl:ENSMUSG00000079436 AllianceGenome:MGI:3781032
Gene type: protein coding
RefSeq status: VALIDATED
Organism: Mus musculus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus
Also known as: Kir7.1
Summary: Predicted to enable inward rectifier potassium channel activity. Predicted to be involved in potassium ion import across plasma membrane and regulation of ion transmembrane transport. Predicted to act upstream of or within potassium ion transport. Predicted to be located in membrane. Predicted to be integral component of membrane. Predicted to be active in plasma membrane. Is expressed in brain; male reproductive gland or organ; metanephros; and respiratory system. Human ortholog(s) of this gene implicated in Leber congenital amaurosis 16 and snowflake vitreoretinal degeneration. Orthologous to human KCNJ13 (potassium inwardly rectifying channel subfamily J member 13). [provided by Alliance of Genome Resources, Apr 2022]
Expression: Biased expression in lung adult (RPKM 2.1), large intestine adult (RPKM 1.8) and 14 other tissues See more
Orthologs: human all
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Genomic context

Location:: 1 D; 1 44.3 cM

Exon count:: 3

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	1	NC_000067.7 (87312299..87322451, complement)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	1	NC_000067.6 (87384577..87394729, complement)

Chromosome 1 - NC_000067.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

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Expression

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See details

Project title: Mouse ENCODE transcriptome data
Description: RNA profiling data sets generated by the Mouse ENCODE project.
BioProject: PRJNA66167
Publication: PMID 25409824
Analysis date: n/a

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

A critical role for the inward rectifying potassium channel Kir7.1 in oligodendrocytes of the mouse optic nerve.
Title: A critical role for the inward rectifying potassium channel Kir7.1 in oligodendrocytes of the mouse optic nerve.
Glial and neuronal expression of the Inward Rectifying Potassium Channel Kir7.1 in the adult mouse brain.
Title: Glial and neuronal expression of the Inward Rectifying Potassium Channel Kir7.1 in the adult mouse brain.
the presence of a novel splice variant of Kir7.1 in mouse tissues including kidney, lung, choroid plexus and retinal pigment epithelium, is reported.
Title: A novel Kir7.1 splice variant expressed in various mouse tissues shares organisational and functional properties with human Leber amaurosis-causing mutations of this K(+) channel.
Late onset obesity in mice with targeted deletion of potassium inward rectifier Kir7.1 from cells expressing the melanocortin-4 receptor.
Title: Late onset obesity in mice with targeted deletion of potassium inward rectifier Kir7.1 from cells expressing the melanocortin-4 receptor.
Kcnj13 mutants exhibit a shorter trachea as well as defective smooth muscle cell alignment and polarity. Kcnj13 is essential to maintain ion homeostasis in tracheal smooth cells, which is required for actin polymerization and is mediated, at least in part, through activation of the actin regulator, AKT.
Title: The potassium channel KCNJ13 is essential for smooth muscle cytoskeletal organization during mouse tracheal tubulogenesis.
These results suggest that KCNJ13 expression is required for RPE cells to maintain photoreceptor survival.
Title: CRISPR-engineered mosaicism rapidly reveals that loss of Kcnj13 function in mice mimics human disease phenotypes.
Kir7.1 regulates the transition from quiescence to contractions in the pregnant uterus.
Title: The inwardly rectifying K+ channel KIR7.1 controls uterine excitability throughout pregnancy.
Coupling of MC4R to Kir7.1 may explain unusual aspects of the control of energy homeostasis by melanocortin signalling, including the gene dosage effect of MC4R and the sustained effects of AgRP on food intake.
Title: G-protein-independent coupling of MC4R to Kir7.1 in hypothalamic neurons.

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Variation

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Alleles

Alleles of this type are documented at Mouse Genome Informatics (MGI)

Targeted (6) 1 citation
Endonuclease-mediated (10) 1 citation

General gene information

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Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables inward rectifier potassium channel activity	IBA Inferred from Biological aspect of Ancestor more info

Process	Evidence Code	Pubs
acts_upstream_of_or_within monoatomic ion transmembrane transport	IEA Inferred from Electronic Annotation more info
acts_upstream_of_or_within monoatomic ion transport	IEA Inferred from Electronic Annotation more info
involved_in potassium ion import across plasma membrane	IBA Inferred from Biological aspect of Ancestor more info
acts_upstream_of_or_within potassium ion transport	IEA Inferred from Electronic Annotation more info
involved_in potassium ion transport	IEA Inferred from Electronic Annotation more info
involved_in regulation of monoatomic ion transmembrane transport	IBA Inferred from Biological aspect of Ancestor more info

Component	Evidence Code	Pubs
located_in membrane	IEA Inferred from Electronic Annotation more info
part_of monoatomic ion channel complex	IEA Inferred from Electronic Annotation more info
is_active_in plasma membrane	IBA Inferred from Biological aspect of Ancestor more info

General protein information

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Preferred Names: inward rectifier potassium channel 13

Names: inward rectifier K(+) channel Kir7.1

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.