Name | Number of supported studies | Average coverage | |
---|---|---|---|
glutamatergic neuron | 11 studies | 65% ± 24% | |
GABAergic neuron | 9 studies | 61% ± 24% | |
interneuron | 6 studies | 56% ± 31% | |
retina horizontal cell | 6 studies | 53% ± 20% | |
oligodendrocyte precursor cell | 5 studies | 21% ± 6% | |
neuron | 4 studies | 33% ± 9% | |
granule cell | 4 studies | 64% ± 19% | |
astrocyte | 4 studies | 35% ± 15% | |
endothelial cell | 3 studies | 42% ± 10% | |
epithelial cell | 3 studies | 24% ± 5% | |
retinal ganglion cell | 3 studies | 33% ± 20% | |
GABAergic amacrine cell | 3 studies | 32% ± 16% | |
glycinergic amacrine cell | 3 studies | 37% ± 15% |
Tissue | GTEx Coverage | GTEx Average TPM | GTEx Number of samples | TCGA Coverage | TCGA Average TPM | TCGA Number of samples |
---|---|---|---|---|---|---|
kidney | 97% | 589.53 | 86 / 89 | 80% | 14.57 | 717 / 901 |
brain | 81% | 2528.07 | 2152 / 2642 | 66% | 7.46 | 465 / 705 |
blood vessel | 88% | 746.20 | 1175 / 1335 | 0% | 0 | 0 / 0 |
prostate | 54% | 356.03 | 133 / 245 | 32% | 2.79 | 163 / 502 |
pancreas | 23% | 56.20 | 74 / 328 | 34% | 3.28 | 61 / 178 |
liver | 23% | 69.65 | 52 / 226 | 32% | 2.35 | 130 / 406 |
heart | 55% | 1324.95 | 473 / 861 | 0% | 0 | 0 / 0 |
intestine | 18% | 92.06 | 170 / 966 | 35% | 2.54 | 186 / 527 |
esophagus | 26% | 92.35 | 377 / 1445 | 23% | 2.72 | 43 / 183 |
breast | 2% | 6.78 | 8 / 459 | 43% | 46.48 | 484 / 1118 |
adrenal gland | 6% | 21.24 | 16 / 258 | 32% | 2.86 | 73 / 230 |
stomach | 5% | 11.78 | 19 / 359 | 30% | 2.86 | 85 / 286 |
bladder | 19% | 77.81 | 4 / 21 | 11% | 0.62 | 54 / 504 |
spleen | 12% | 32.08 | 30 / 241 | 0% | 0 | 0 / 0 |
uterus | 6% | 37.43 | 11 / 170 | 6% | 0.34 | 26 / 459 |
lung | 1% | 3.63 | 3 / 578 | 8% | 0.83 | 94 / 1155 |
ovary | 4% | 11.03 | 7 / 180 | 1% | 0.02 | 3 / 430 |
lymph node | 0% | 0 | 0 / 0 | 3% | 0.18 | 1 / 29 |
thymus | 1% | 5.66 | 5 / 653 | 3% | 0.22 | 16 / 605 |
adipose | 1% | 3.74 | 18 / 1204 | 0% | 0 | 0 / 0 |
eye | 0% | 0 | 0 / 0 | 1% | 0.07 | 1 / 80 |
skin | 0% | 0.23 | 2 / 1809 | 1% | 0.04 | 5 / 472 |
muscle | 0% | 1.69 | 4 / 803 | 0% | 0 | 0 / 0 |
peripheral blood | 0% | 0.61 | 2 / 929 | 0% | 0 | 0 / 0 |
abdomen | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
bone marrow | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
diaphragm | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
gingiva | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
nasal cavity | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
nasopharynx | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
nose | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
placenta | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
spinal column | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
tonsil | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 45 |
ureter | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 1 |
GO_0006813 | Biological process | potassium ion transport |
GO_0098914 | Biological process | membrane repolarization during atrial cardiac muscle cell action potential |
GO_0051602 | Biological process | response to electrical stimulus |
GO_0098915 | Biological process | membrane repolarization during ventricular cardiac muscle cell action potential |
GO_0071805 | Biological process | potassium ion transmembrane transport |
GO_0099625 | Biological process | ventricular cardiac muscle cell membrane repolarization |
GO_0099505 | Biological process | regulation of presynaptic membrane potential |
GO_0034765 | Biological process | regulation of monoatomic ion transmembrane transport |
GO_0086091 | Biological process | regulation of heart rate by cardiac conduction |
GO_1990573 | Biological process | potassium ion import across plasma membrane |
GO_0009897 | Cellular component | external side of plasma membrane |
GO_0005886 | Cellular component | plasma membrane |
GO_0042734 | Cellular component | presynaptic membrane |
GO_0030315 | Cellular component | T-tubule |
GO_0098688 | Cellular component | parallel fiber to Purkinje cell synapse |
GO_1990566 | Cellular component | I(KACh) inward rectifier potassium channel complex |
GO_0008076 | Cellular component | voltage-gated potassium channel complex |
GO_1902282 | Molecular function | voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarization |
GO_0015467 | Molecular function | G-protein activated inward rectifier potassium channel activity |
GO_0086089 | Molecular function | voltage-gated potassium channel activity involved in atrial cardiac muscle cell action potential repolarization |
GO_0099508 | Molecular function | voltage-gated monoatomic ion channel activity involved in regulation of presynaptic membrane potential |
GO_0005242 | Molecular function | inward rectifier potassium channel activity |
GO_0005515 | Molecular function | protein binding |
Gene name | KCNJ3 |
Protein name | Potassium inwardly-rectifying channel subfamily J member 3 splice variant 1e G protein-activated inward rectifier potassium channel 1 (GIRK-1) (Inward rectifier K(+) channel Kir3.1) (Potassium channel, inwardly rectifying subfamily J member 3) G protein-activated inward rectifier potassium channel 1 (Inward rectifier K(+) channel Kir3.1) (Potassium channel, inwardly rectifying subfamily J member 3) |
Synonyms | GIRK1 |
Description | FUNCTION: 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. This receptor plays a crucial role in regulating the heartbeat. FUNCTION: 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. This receptor plays a crucial role in regulating the heartbeat. . FUNCTION: 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. This receptor plays a crucial role in regulating the heartbeat. . FUNCTION: 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. This receptor plays a crucial role in regulating the heartbeat. . |
Accessions | ENST00000651198.1 D2XBF0 P48549 D2X9V0 Q53R59 A0A494C0M7 ENST00000295101.3 [P48549-1] ENST00000544049.2 [P48549-2] |