| + |
NME2 | up-regulates 
phosphorylation
|
KCNN4 |
0.43 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-151130 |
His358 |
FRQVRLKhRKLREQV |
Homo sapiens |
|
| pmid |
sentence |
| 17157250 |
Ndpk-b directly binds and activates kca3.1 by phosphorylating histidine 358 in the carboxyl terminus of kca3.1 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-181083 |
His358 |
FRQVRLKhRKLREQV |
Homo sapiens |
|
| pmid |
sentence |
| 18796614 |
We previously showed that nucleoside diphosphate kinase beta (ndpk-b), a mammalian histidine kinase, is required for kca3.1 channel activation in human cd4 t lymphocytes. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
PHPT1 | down-regulates activity 
dephosphorylation
|
KCNN4 |
0.565 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277071 |
His358 |
FRQVRLKhRKLREQV |
Homo sapiens |
|
| pmid |
sentence |
| 18796614 |
We now show that the mammalian protein histidine phosphatase (PHPT-1) directly binds and inhibits KCa3.1 by dephosphorylating histidine 358 on KCa3.1.|Overexpression of wild-type, but not a phosphatase dead, PHPT-1 inhibited KCa3.1 channel activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PRKACA | down-regulates activity
phosphorylation
|
KCNN4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276855 |
Ser334 |
KHTRRKEsHAARRHQ |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 25274816 |
Mutating the single PKA site (S334A) in human KCa3.1 abolished the PKA-dependent regulation. CaM-affinity chromatography showed that CaM binding to KCa3.1 was decreased by PKA-dependent phosphorylation of S334, and this regulation was absent in the S334A mutant.The results above indicate that PKA activation led to a phosphorylation event that inhibited KCa3.1 channel activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TRAM-34 | up-regulates
chemical activation
|
KCNN4 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-207426 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Riluzole | up-regulates activity
chemical activation
|
KCNN4 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258022 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18955585 |
Here, we used the neuroprotectant riluzole as a template for the design of KCa2/3 channel activators that are potent enough for in vivo studies. Of a library of 41 benzothiazoles, we identified 2 compounds, anthra[2,1-d]thiazol-2-ylamine (SKA-20) and naphtho[1,2-d]thiazol-2-ylamine (SKA-31), which are 10 to 20 times more potent than riluzole and activate KCa2.1 with EC50 values of 430 nM and 2.9 μM, KCa2.2 with an EC50 value of 1.9 μM, KCa2.3 with EC50 values of 1.2 and 2.9 μM, and KCa3.1 with EC50 values of 115 and 260 nM. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KCNN4 | up-regulates quantity
relocalization
|
calcium(2+) |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276856 |
|
|
Rattus norvegicus |
Microglia |
| pmid |
sentence |
| 25274816 |
KCa3.1 activation is expected to maintain a negative membrane potential, which will increase Ca2+ influx through nonvoltage gated Ca2+-release-activated Ca2+ (CRAC) channels that are prevalent in rat microglia |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
clotrimazole | down-regulates activity
chemical inhibition
|
KCNN4 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258832 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 9730970 |
IK was blocked by the classical inhibitors of the Gardos channel charybdotoxin (IC50 28 nM) and clotrimazole (IC50 153 nM) as well as by nitrendipine (IC50 27 nM), Stichodactyla toxin (IC50 291 nM), margatoxin (IC50 459 nM), miconazole (IC50 785 nM), econazole (IC50 2.4 microM), and cetiedil (IC50 79 microM). Finally, 1-ethyl-2-benzimidazolinone, an opener of the T84 cell IK channel, activated hIK with an EC50 of 74 microM. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
nitrendipine | down-regulates activity
chemical inhibition
|
KCNN4 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258831 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9730970 |
IK was blocked by the classical inhibitors of the Gardos channel charybdotoxin (IC50 28 nM) and clotrimazole (IC50 153 nM) as well as by nitrendipine (IC50 27 nM), Stichodactyla toxin (IC50 291 nM), margatoxin (IC50 459 nM), miconazole (IC50 785 nM), econazole (IC50 2.4 microM), and cetiedil (IC50 79 microM). Finally, 1-ethyl-2-benzimidazolinone, an opener of the T84 cell IK channel, activated hIK with an EC50 of 74 microM. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Naphtho[1,2-d]thiazol-2-amine | up-regulates activity
chemical activation
|
KCNN4 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258025 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 18955585 |
Here, we used the neuroprotectant riluzole as a template for the design of KCa2/3 channel activators that are potent enough for in vivo studies. Of a library of 41 benzothiazoles, we identified 2 compounds, anthra[2,1-d]thiazol-2-ylamine (SKA-20) and naphtho[1,2-d]thiazol-2-ylamine (SKA-31), which are 10 to 20 times more potent than riluzole and activate KCa2.1 with EC50 values of 430 nM and 2.9 μM, KCa2.2 with an EC50 value of 1.9 μM, KCa2.3 with EC50 values of 1.2 and 2.9 μM, and KCa3.1 with EC50 values of 115 and 260 nM. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
KCNN4
- 
- 