Pub. Date : 2013 Nov
PMID : 24037882
4 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Mutations in the KCNJ5 gene, which encodes the inward rectifier K(+) channel 4 (G protein-activated inward rectifier K(+) channel 4, Kir3.4), cause familial hyperaldosteronism type III (FH-III) and are involved in the pathogenesis of sporadic aldosterone-producing adenomas. | Aldosterone | potassium inwardly rectifying channel subfamily J member 5 | Homo sapiens |
| 2 | Mutations in the KCNJ5 gene, which encodes the inward rectifier K(+) channel 4 (G protein-activated inward rectifier K(+) channel 4, Kir3.4), cause familial hyperaldosteronism type III (FH-III) and are involved in the pathogenesis of sporadic aldosterone-producing adenomas. | Aldosterone | potassium inwardly rectifying channel subfamily J member 5 | Homo sapiens |
| 3 | The tyrosine-to-cysteine substitution resulted in pathological Na(+) permeability, cell membrane depolarization, and disturbed intracellular Ca(2+) homeostasis, effects similar, albeit smaller, to the ones demonstrated for other KCNJ5 mutations. | Tyrosine | potassium inwardly rectifying channel subfamily J member 5 | Homo sapiens |
| 4 | The tyrosine-to-cysteine substitution resulted in pathological Na(+) permeability, cell membrane depolarization, and disturbed intracellular Ca(2+) homeostasis, effects similar, albeit smaller, to the ones demonstrated for other KCNJ5 mutations. | Cysteine | potassium inwardly rectifying channel subfamily J member 5 | Homo sapiens |