| + |
EPAS1 | up-regulates quantity by expression 
transcriptional regulation
|
CACNA1A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264332 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15833863 |
A second hypoxia-responsive factor, HIF-2, can activate many of the same genes as HIF-1. Ten genes were preferentially activated by HIF-2alpha, including two (CACNA1A and PTPRZ1) implicated in neurologic diseases. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CACNA1A | up-regulates quantity 
relocalization
|
calcium(2+) |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264323 |
|
|
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-266708 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20655485 |
The main G b/g-dependent effectors of presynaptic GABAB receptors are P/Q-and N-type voltage-dependent Ca2+ channels. GABAB receptors inhibit these Ca2+ channels at excitatory and inhibitory terminals, thereby restricting neurotransmitter release. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Axon guidance, Neurotransmitters release |
| + |
CACNA1A | up-regulates
|
Excitatory_synaptic_transmission |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264328 |
|
|
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 |
| + |
ANK2 | up-regulates quantity
binding
|
CACNA1A |
0.267 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266706 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 24394417 |
Here, we demonstrate that ankyrin-B associates with Cav2.1 and Cav2.2 in cortex, cerebellum, and brain stem. Additionally, using in vitro and in vivo techniques, we demonstrate that ankyrin-B, via its membrane-binding domain, associates with a highly conserved motif in the DII/III loop domain of Cav2.1 and Cav2.2. Collectively, our findings identify an interaction between ankyrin-B and both Cav2.1 and Cav2.2 at the amino acid level that is necessary for proper Cav2.1 and Cav2.2 targeting in vivo. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
DCC | up-regulates activity
|
CACNA1A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268293 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12827203 |
DCC activation by a netrin-1 gradient creates a high-level [Ca2+]i gradient by triggering LCC activity and by stimulating the cAMP–PKA pathway, which further activates LCC in the plasma membrane (PM) and Ca2+ channels in the ER. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Axon guidance |
3.0
CACNA1A
- 
- 