G Protein-Coupled Inwardly-Rectifying Potassium Channels
"G Protein-Coupled Inwardly-Rectifying Potassium Channels" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
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.
MeSH Number(s)
D12.776.157.530.400.600.450.500
D12.776.543.550.425.750.450.500
D12.776.543.585.400.750.450.500
Concept/Terms
G Protein-Coupled Inwardly-Rectifying Potassium Channels- G Protein-Coupled Inwardly-Rectifying Potassium Channels
- G Protein Coupled Inwardly Rectifying Potassium Channels
- GIRK Potassium Channels
- Potassium Channels, GIRK
- Kir3 Potassium Channels
- Potassium Channels, Kir3
- G Protein-Activated Potassium Channels
- G Protein Activated Potassium Channels
Below are MeSH descriptors whose meaning is more general than "G Protein-Coupled Inwardly-Rectifying Potassium Channels".
Below are MeSH descriptors whose meaning is more specific than "G Protein-Coupled Inwardly-Rectifying Potassium Channels".
This graph shows the total number of publications written about "G Protein-Coupled Inwardly-Rectifying Potassium Channels" by people in Harvard Catalyst Profiles by year, and whether "G Protein-Coupled Inwardly-Rectifying Potassium Channels" was a major or minor topic of these publication.
To see the data from this visualization as text,
click here.
Year | Major Topic | Minor Topic | Total |
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1995 | 0 | 3 | 3 |
1996 | 0 | 4 | 4 |
1997 | 0 | 1 | 1 |
1998 | 0 | 4 | 4 |
1999 | 0 | 3 | 3 |
2000 | 0 | 2 | 2 |
2001 | 0 | 2 | 2 |
2002 | 0 | 3 | 3 |
2003 | 0 | 2 | 2 |
2004 | 0 | 1 | 1 |
2005 | 0 | 2 | 2 |
2006 | 0 | 1 | 1 |
2008 | 0 | 1 | 1 |
2009 | 0 | 2 | 2 |
2010 | 1 | 1 | 2 |
2011 | 0 | 1 | 1 |
2012 | 0 | 1 | 1 |
2013 | 2 | 1 | 3 |
2014 | 1 | 0 | 1 |
2015 | 0 | 1 | 1 |
2016 | 1 | 3 | 4 |
2017 | 0 | 1 | 1 |
2019 | 3 | 1 | 4 |
2020 | 2 | 2 | 4 |
2021 | 2 | 0 | 2 |
2022 | 0 | 1 | 1 |
2023 | 0 | 1 | 1 |
Below are the most recent publications written about "G Protein-Coupled Inwardly-Rectifying Potassium Channels" by people in Profiles.
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Cardiovascular and metabolic characters of KCNJ5 somatic mutations in primary aldosteronism. Front Endocrinol (Lausanne). 2023; 14:1061704.
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Case Report: Primary Aldosteronism Due to Bilateral Aldosterone-Producing Micronodules With HISTALDO Classical and Contralateral Non-Classical Pathology. Front Endocrinol (Lausanne). 2022; 13:816754.
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Aldosterone-producing adenoma-harbouring KCNJ5 mutations is associated with lower prevalence of metabolic disorders and abdominal obesity. J Hypertens. 2021 12 01; 39(12):2353-2360.
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Characterization of a mutated KCNJ5 gene, G387R, in unilateral primary aldosteronism. J Mol Endocrinol. 2021 09 28; 67(4):203-215.
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KCNJ5 Somatic Mutations in Aldosterone-Producing Adenoma Are Associated With a Worse Baseline Status and Better Recovery of Left Ventricular Remodeling and Diastolic Function. Hypertension. 2021 01; 77(1):114-125.
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Presence of Subclinical Hypercortisolism in Clinical Aldosterone-Producing Adenomas Predicts Lower Clinical Success. Hypertension. 2020 11; 76(5):1537-1544.
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Response to Letter to the Editor: "Adrenalectomy Completely Cured Hypertension in Familial Hyperaldosteronism Type I Patients with Somatic KCNJ5 Mutation". J Clin Endocrinol Metab. 2020 05 01; 105(5).
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The small molecule GAT1508 activates brain-specific GIRK1/2 channel heteromers and facilitates conditioned fear extinction in rodents. J Biol Chem. 2020 03 13; 295(11):3614-3634.
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Adrenalectomy Completely Cured Hypertension in Patients With Familial Hyperaldosteronism Type I Who Had Somatic KCNJ5 Mutation. J Clin Endocrinol Metab. 2019 11 01; 104(11):5462-5466.
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On the mechanism of GIRK2 channel gating by phosphatidylinositol bisphosphate, sodium, and the Gß? dimer. J Biol Chem. 2019 12 06; 294(49):18934-18948.