HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

G Protein-Coupled Inwardly-Rectifying Potassium Channels

A family of inwardly-rectifying potassium channels that are activated by PERTUSSIS TOXIN sensitive G-PROTEIN-COUPLED RECEPTORS. GIRK potassium channels are primarily activated by the complex of GTP-BINDING PROTEIN BETA SUBUNITS and GTP-BINDING PROTEIN GAMMA SUBUNITS.
Also Known As:
G Protein-Activated Potassium Channels; G Protein-Coupled Inwardly-Rectifying Potassium Channel 1; G Protein-Coupled Inwardly-Rectifying Potassium Channel 2; G Protein-Coupled Inwardly-Rectifying Potassium Channel 3; G Protein-Coupled Inwardly-Rectifying Potassium Channel 4; GIRK Potassium Channels; GIRK1 Potassium Channel; GIRK2 Potassium Channel; GIRK3 Potassium Channel; GIRK4 Potassium Channel; Kir3 Potassium Channels; Kir3.1 Potassium Channel; Kir3.2 Potassium Channel; Kir3.3 Potassium Channel; Kir3.4 Potassium Channel; G Protein Activated Potassium Channels; G Protein Coupled Inwardly Rectifying Potassium Channel 1; G Protein Coupled Inwardly Rectifying Potassium Channel 2; G Protein Coupled Inwardly Rectifying Potassium Channel 3; G Protein Coupled Inwardly Rectifying Potassium Channel 4; G Protein Coupled Inwardly Rectifying Potassium Channels; Potassium Channel, GIRK1; Potassium Channel, GIRK2; Potassium Channel, GIRK3; Potassium Channel, GIRK4; Potassium Channel, Kir3.1; Potassium Channel, Kir3.2; Potassium Channel, Kir3.3; Potassium Channel, Kir3.4; Potassium Channels, GIRK; Potassium Channels, Kir3
Networked: 11 relevant articles (0 outcomes, 1 trials/studies)

Bio-Agent Context: Research Results

Experts

1. Boulkroun, Sheerazed: 2 articles (07/2013 - 05/2013)
2. Rickard, Amanda Jane: 2 articles (07/2013 - 05/2013)
3. Zennaro, Maria-Christina: 2 articles (07/2013 - 05/2013)
4. Kurata, Shinji: 1 article (07/2022)
5. Mori, Tomohisa: 1 article (07/2022)
6. Saeki, Tomoya: 1 article (07/2022)
7. Sudo, Yuka: 1 article (07/2022)
8. Suzuki, Tsutomu: 1 article (07/2022)
9. Takemura, Yoshinori: 1 article (07/2022)
10. Uezono, Yasuhito: 1 article (07/2022)

Related Diseases

1. Neuralgia (Stump Neuralgia)
2. Adenoma (Adenomas)
12/01/2015 - "Somatic mutations have been identified in the KCNJ5 gene (encoding the potassium channel GIRK4) in aldosterone-producing adenomas (APA). "
05/22/2013 - "Somatic mutations of KCNJ5, coding for the potassium channel GIRK4, have recently been implicated in the formation of aldosterone producing adenoma (APA). "
12/01/2017 - "Aldosterone-producing adenoma (APA), a major subtype of primary hyperaldosteronism, the main curable cause of human endocrine hypertension, involves somatic mutations in the potassium channel Kir3.4 (KCNJ5) in 30% to 70% of cases, typically the more florid phenotypes. "
07/01/2013 - "Although genetic causes underlying glucocorticoid-remediable aldosteronism, one of the three Mendelian forms of PA, were established some time ago, somatic and inherited mutations in the potassium channel GIRK4 have only recently been implicated in the formation of aldosterone-producing adenoma (APA) and in familial hyperaldosteronism type 3. Moreover, recent findings have shown somatic mutations in two additional genes, involved in maintaining intracellular ionic homeostasis and cell membrane potential, in a subset of APAs. "
01/01/2014 - "Aldosterone-producing adenomas (APAs) are responsible for half the cases of primary aldosteronism, and about half have mutations of the G protein-activated inward rectifying potassium channel Kir3.4. Under basal conditions, the adrenal zona glomerulosa cells are hyperpolarized with negative resting potentials determined by membrane permeability to K(+) mediated through various K(+) channels, including the leak K(+) channels TASK-1, TASK-3, and Twik-Related Potassium Channel 1, and G protein inward rectifying potassium channel Kir3.4. Angiotensin II decreases the activity of the leak K(+) channels and Kir3.4 channel and decreases the expression of the Kir3.4 channel, resulting in membrane depolarization, increased intracellular calcium, calcium-calmodulin pathway activation, and increased expression of cytochrome P450 aldosterone synthase (CYP11B2), the last enzyme for aldosterone production. "
3. Hyperaldosteronism (Conn Syndrome)
4. Familial Hyperaldosteronism
5. Infarction (Infarctions)

Related Drugs and Biologics

1. Opioid Receptors (Opioid Receptor)
2. Cannabinoid Receptors (Cannabinoid Receptor)
3. Aldosterone
4. GTP-Binding Proteins (G-Protein)
5. L-Type Calcium Channels (Dihydropyridine Receptor)
6. Cytochrome P-450 CYP11B2 (CYP11B2)
7. Potassium Channels (Potassium Channel)
8. Enzymes
9. Cytochrome P-450 Enzyme System (Cytochrome P450)
10. Calmodulin (Calcium-Dependent Activator Protein)