Channelpedia

Kir7.1

Description: potassium inwardly-rectifying channel, subfamily J, member 13
Gene: Kcnj13
Alias: Kir7.1, kcnj13

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Introduction

A large variety of potassium channels have been recognized to be of physiological importance in the kidney. Several of those belong to the family of inward rectifier K+ channels (Kir channels) that has been classified into seven subgroups (Kir1–7) (Reimann [1069]). A renal member of this family is the Kir7.1 channel.

The gene KCNJ13 (also known as SVD; KIR1.4; KIR7.1; MGC33328) encodes Kir7.1, a member of the inwardly rectifying potassium channel family, subfamily J, member 13. Members of this family form ion channel pores that allow potassium ions to pass into a cell. The encoded protein belongs to a subfamily of low signal channel conductance proteins that have a low dependence on potassium concentration. Mutations in this gene are associated with snowflake vitreoretinal degeneration. Alternate splicing results in multiple transcript variants.

http://www.ncbi.nlm.nih.gov/gene/3769


Experimental data

Rat Kir7.1 gene in CHO host cells
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Gene

Species NCBI gene ID Chromosome Position
Human 3769 2 10763
Mouse 100040591 1 13318
Rat 94341 9 8109

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Transcript

Species NCBI accession Length (nt)
Human NM_002242.4 3609
Mouse NM_001110227.2 3056
Rat NM_053608.2 1268

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Protein Isoforms

Species Uniprot ID Length (aa)
Human O60928 360
Mouse P86046 360
Rat O70617 360

Isoforms

Transcript
Length (nt)
Protein
Length (aa)
Variant
Isoform

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Post-Translational Modifications

PTM
Position
Type

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Structure

Kir7.1 predicted AlphaFold size

Species Area (Å2) Reference
Human 2923.04 source
Mouse 3891.14 source
Rat 2310.77 source

Methodology for AlphaFold size prediction and disclaimer are available here


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Kinetics

Kir7.1 displays unique biophysical characteristics, particularly a very weak inward rectification and a lack of major influence of external K+ on channel conductance, both being markedly different from other members of Kir channels (Derst [1070]).


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Expression and Distribution

Kir7.1 is located predominantly in the basolateral membrane of the proximal tubule (PT), the thick ascending limb (TAL) (Derst [1070]) and the cortical collecting duct (CCD) principal cells (Ookata[1071]).

The expression of Kir7.1 in the brain appears to be restricted to the epithelial cells of the choroid plexus (Doring [1042], Nakamura [1073]). It is also strongly expressed in various other epithelial cells, for example, in small intestine or in follicular cells of the thyroid gland. Significant expression of gpKir7.1 was found in brain, kidney, and lung, but not in heart, skeletal muscle, liver, or spleen. (Derst [1070])


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CNS Sub-cellular Distribution

Immunocytochemical detection in guinea pig identified the gpKir7.1 protein in the basolateral membrane of epithelial cells of the proximal tubule. RT-PCR analysis identified strong gpKir7.1 expression in the proximal tubule and weak expression in glomeruli and thick ascending limb. In isolated human tubule fragments, RT-PCR showed expression in proximal tubule and thick ascending limb. (Derst [1070])


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Function

Kir7.1 it has been proposed to contribute to tubular K+ recycling and secretion (Derst [1070], Ookata [1071], Doring [1072]). The evidence that expression of Kir7.1 is upregulated under dietary potassium overload also supports a functional significance for K+ secretion (Ookata [1071]).


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Interaction

the dual regulation of Kir7.1 channel function by protein kinase A (PKA) and protein kinase C (PKC). Structurally, these regulations depend on two key residues in the C-terminal channel domain (Ser201 for PKC and Ser287 for PKA). (Zahng [1067])

Low micromolar concentrations of the small molecule VU590 inhibit Kir7.1, as an intracellular pore blocker. (Lewis [1068])

The expression of gpKir7.1 in Xenopus laevis oocytes revealed inwardly rectifying K+ currents. The reversal potential was strongly dependent on the extracellular K+ concentration, shifting from -14 mV at 96 mmol/L K+ to -90 mV at 1 mmol/L K+. gpKir7.1 showed a low affinity for Ba2+. (Derst [1070])


References


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Credits

To cite this page: [Contributors] Channelpedia https://channelpedia.epfl.ch/wikipages/55/ , accessed on 2024 Dec 03



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