+ |
CACNA1G | up-regulates
|
Action_potential |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-264033 |
|
|
Mus musculus |
|
pmid |
sentence |
33393208 |
Adult hippocampal neurogenesis plays an important role in neuronal plasticity and maintenance in mammals. Low-threshold voltage-gated T-type calcium channels produce calcium spikes that increase fast action potentials in newborn cells in the hippocampal dentate gyrus (DG) |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
CACNA1G | up-regulates quantity
relocalization
|
calcium(2+) |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-264324 |
|
|
Homo sapiens |
|
pmid |
sentence |
30849329 |
Voltage-gated calcium channels mediate the influx of calcium in response to membrane depolarization in excitable cells. In presynaptic nerve terminals, this calcium influx triggers transmitter release for synaptic transmission. Several neurological and cardiac disorders are caused by pathogenic variants in genes encoding α1-subunits of voltage-gated calcium channels, including CACNA1A (MIM: 601011) (familial hemiplegic migraine [MIM: 141500], episodic ataxia [MIM: 108500], and epilepsy [MIM: 617106]),3, 4, 5 CACNA1C (MIM: 114205) (Timothy syndrome [MIM: 601005]),6, 7 CACNA1D (MIM: 114206) (primary aldosteronism, neurodevelopmental disorders [MIM: 615474]),8, 9 and CACNA1G (MIM: 604065) (spinocerebellar ataxia [MIM: 616795]). |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-264032 |
|
|
Mus musculus |
|
pmid |
sentence |
33393208 |
Adult hippocampal neurogenesis plays an important role in neuronal plasticity and maintenance in mammals. Low-threshold voltage-gated T-type calcium channels produce calcium spikes that increase fast action potentials in newborn cells in the hippocampal dentate gyrus (DG) |
|
Publications: |
2 |
Organism: |
Homo Sapiens, Mus Musculus |
+ |
CACNA1G | up-regulates
|
Excitatory_synaptic_transmission |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-264329 |
|
|
Homo sapiens |
|
pmid |
sentence |
30849329 |
Voltage-gated calcium channels mediate the influx of calcium in response to membrane depolarization in excitable cells. In presynaptic nerve terminals, this calcium influx triggers transmitter release for synaptic transmission. Several neurological and cardiac disorders are caused by pathogenic variants in genes encoding α1-subunits of voltage-gated calcium channels, including CACNA1A (MIM: 601011) (familial hemiplegic migraine [MIM: 141500], episodic ataxia [MIM: 108500], and epilepsy [MIM: 617106]),3, 4, 5 CACNA1C (MIM: 114205) (Timothy syndrome [MIM: 601005]),6, 7 CACNA1D (MIM: 114206) (primary aldosteronism, neurodevelopmental disorders [MIM: 615474]),8, 9 and CACNA1G (MIM: 604065) (spinocerebellar ataxia [MIM: 616795]). |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Central Nervous System |
+ |
SP1 | up-regulates quantity by expression
transcriptional regulation
|
CACNA1G |
0.264 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-264034 |
|
|
Mus musculus |
|
pmid |
sentence |
23868804 |
Consistent with this, Sp1 over-expression enhanced promoter activity while siRNA-mediated Sp1 silencing significantly decreased the level of CaV 3.1 protein and reduced the amplitude of whole-cell T-type Ca(2+) currents expressed in the N1E-115 cells. These results provide new insights into the molecular mechanisms that control CaV 3.1 channel expression. |
|
Publications: |
1 |
Organism: |
Mus Musculus |