Protein Variants | Comment | Organism |
---|---|---|
E226Q | catalytic site mutants which show no detectable creatine kinase activity demonstrate that enzymatic activity is not required for the regulation of NCX1 activity | Homo sapiens |
E227L | catalytic site mutants which show no detectable creatine kinase activity demonstrate that enzymatic activity is not required for the regulation of NCX1 activity | Homo sapiens |
E231Q | catalytic site mutants which show no detectable creatine kinase activity demonstrate that enzymatic activity is not required for the regulation of NCX1 activity | Homo sapiens |
E232L | catalytic site mutants which show no detectable creatine kinase activity demonstrate that enzymatic activity is not required for the regulation of NCX1 activity | Homo sapiens |
additional information | using chimeric mutants it is shown that C terminus of mitochondrial creatine kinase (sMiCK) and muscle creatine kinase (CKM) is required for the regulation of NCX1 activity | Homo sapiens |
S123A | mutation analysis show that a putative PKC phosphorylation site on sMiCK and CKM is required for the regulation of NCX1 activity: S123A mutant fails to produce a recovery in the decreased NCX1 activity under energy-compromised conditions | Homo sapiens |
S128A | mutation analysis show that a putative PKC phosphorylation site on sMiCK and CKM is required for the regulation of NCX1 activity: S123A mutant fails to produce a recovery in the decreased NCX1 activity under energy-compromised conditions | Homo sapiens |
T277V | autophosphorylation site mutant shows that autophosphorylation is not required for the regulation of NCX1 activity | Homo sapiens |
T282V | autophosphorylation site mutant shows that autophosphorylation is not required for the regulation of NCX1 activity | Homo sapiens |
T284V | autophosphorylation site mutant shows that autophosphorylation is not required for the regulation of NCX1 activity | Homo sapiens |
T289V | autophosphorylation site mutant shows that autophosphorylation is not required for the regulation of NCX1 activity | Homo sapiens |
T322V | autophosphorylation site mutant shows that autophosphorylation is not required for the regulation of NCX1 activity | Homo sapiens |
T327V | autophosphorylation site mutant shows that autophosphorylation is not required for the regulation of NCX1 activity | Homo sapiens |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
cytoplasm | - |
Homo sapiens | 5737 | - |
mitochondrion | - |
Homo sapiens | 5739 | - |
plasma membrane | under energy-compromised conditions, CKM is recruited to the plasma membrane and co-localizes with NCX1 | Homo sapiens | 5886 | - |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
additional information | Homo sapiens | using a yeast two-hybrid screening to search for molecules that interact with NCX1 (sodium-calcium exchanger) it is shown that sarcomeric mitochondrial creatine kinase (sMiCK) interacts with NCX1IL. In addition to sMiCK, cytoplasmic muscle-type CK (CKM) is also able to interact with NCX1 in mammalian cells | ? | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
heart | human heart cDNA library is used | Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
additional information | using a yeast two-hybrid screening to search for molecules that interact with NCX1 (sodium-calcium exchanger) it is shown that sarcomeric mitochondrial creatine kinase (sMiCK) interacts with NCX1IL. In addition to sMiCK, cytoplasmic muscle-type CK (CKM) is also able to interact with NCX1 in mammalian cells | Homo sapiens | ? | - |
? |
Synonyms | Comment | Organism |
---|---|---|
CKM | - |
Homo sapiens |
mitochondrial creatine kinase | - |
Homo sapiens |
muscle-type creatine kinase | - |
Homo sapiens |
sMiCK | - |
Homo sapiens |
General Information | Comment | Organism |
---|---|---|
physiological function | sarcomeric mitochondrial creatine kinase (sMiCK) interacts with NCX1IL (sodium-calcium exchanger). In addition to sMiCK, cytoplasmic muscle-type creatine kinase (CKM) is also able to interact with NCX1 in mammalian cells. Sarcomeric mitochondrial creatine kinase (sMiCK) and cytoplasmic muscle-type CK (CKM) are able to produce a recovery in the decreased NCX1 activity that is lost under energy-compromised conditions | Homo sapiens |