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KCNJ5 (Potassium voltage-gated channel subfamily J member 5)

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Summary of KCNJ5

The gene codes for a protein, potassium voltage-gated channel subfamily J member 5. It is controlled by G-proteins [R].

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The Function of KCNJ5

This potassium channel is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by external barium.

Protein names

Recommended name:

G protein-activated inward rectifier potassium channel 4

Short name:

CIR

Alternative name(s):

GIRK-4
Cardiac inward rectifier
Heart KATP channel
Inward rectifier K(+
IRK-4
KATP-1
Potassium channel, inwardly rectifying subfamily J member 5

KCNJ5 SNPs

    To see your genotype, you should be logged in and have a file with your genotype uploaded.

  1. RS6590357 (KCNJ5) ??
  2. RS7118824 (KCNJ5) ??

Top Gene-Substance Interactions

Substances That Increase KCNJ5

Substances Interaction Organism Category

Substances That Decrease KCNJ5

Substances Interaction Organism Category

Advanced Summary

     familial hyperaldosteronism At least four KCNJ5 gene mutations have been identified in people with familial hyperaldosteronism type III. Familial hyperaldosteronism is a disorder that causes high blood pressure (hypertension). Mutations in the KCNJ5 gene are thought to result in the production of potassium channels that are less selective, allowing other ions (predominantly sodium) to pass as well. The flow of sodium ions into adrenal gland cells affects the electrical charge across the cell membrane, activating another type of channel that allows calcium ions to enter. The influx of calcium ions overactivates a process called the calcium/calmodulin pathway that increases aldosterone production, resulting in excess aldosterone and the hypertension associated with familial hyperaldosteronism type III. other disorders Some gene mutations are acquired during a person's lifetime and are present only in certain cells. These changes, which are called somatic mutations, are not inherited. Somatic mutations in the KCNJ5 gene have been identified in approximately 40 percent of nonhereditary (sporadic) tumors of the adrenal glands called aldosterone-producing adenomas. These noncancerous (benign) tumors cause hypertension that gets worse over time. As in familial hyperaldosteronism (described above), KCNJ5 gene mutations in cells of the adrenal gland result in increased aldosterone production, leading to hypertension.

     The KCNJ5 gene provides instructions for making a protein that functions as a potassium channel, which means that it transports positively charged atoms (ions) of potassium into and out of cells. Potassium channels produced from the KCNJ5 gene are thought to help regulate production of the hormone aldosterone. In the adrenal glands, which are small hormone-producing glands located on top of each kidney, the channels control the flow of ions into the cell. The flow of ions creates an electrical charge across the cell membrane, which affects the triggering of certain biochemical processes (pathways) that regulate aldosterone production. Aldosterone helps control blood pressure by maintaining proper salt and fluid levels in the body.

Conditions with Increased Gene Activity

Condition Change (log2fold) Comparison Species Experimental variables Experiment name

Conditions with Decreased Gene Activity

Condition Change (log2fold) Comparison Species Experimental variables Experiment name

Technical

The following transcription factors affect gene expression:

  • STAT3

Tissue specificity:

Islets, exocrine pancreas and heart. Expressed in the adrenal cortex, particularly the zona glomerulosa.

Gene Pathways:

  • Neuronal System

Molecular Function:

  • G-Protein Activated Inward Rectifier Potassium Channel Activity

Biological Processes:

  • Potassium Ion Import
  • Potassium Ion Transport

Drug Bank:

  • Glyburide
  • Ethanol
*synonyms

Synonyms/Aliases/Alternative Names of the Gene:

hypothetical protein| CIR| AS27_01293| AS28_05408| cardiac ATP-sensitive potassium channel| cardiac inward rectifier| CB1_000568031| EH28_10938| girk4| GIRK-4| G protein-activated inward rectifier potassium channel 4| GW7_05537| H920_20436| heart KATP channel| inward rectifier K(+) channel Kir3.4| inward rectifier K+ channel KIR3.4| inward rectifying K channel| IRK-4| katp1| KATP-1| kcnj6| KIR3.4| LQT13| M91_11184| M959_07659| N300_07170| N301_15871| N302_11047| N303_10835| N305_02044| N306_01844| N307_02618| N308_10470| N309_07482| N310_12861| N312_08351| N321_04811| N322_06758| N324_08295| N326_05242| N327_02467| N328_01931| N329_09740| N330_03353| N331_04378| N332_01877| N333_00593| N334_02537| N336_06832| N339_09779| N340_05261| PAL_GLEAN10007617| PANDA_000483| potassium channel, inwardly rectifying subfamily J member 5| potassium channel, inwardly rectifying subfamily J, member 5| potassium inwardly-rectifying channel J5| potassium inwardly-rectifying channel, subfamily J, member 5| potassium inwardly-rectifying channel, subfamily J, member 6| TREES_T100014939| UY3_13255| Y1Q_025988| Y956_07358| Z169_04236| kcnj5

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