Cloned (Comment) | Organism |
---|---|
genotyping and association with type 2 diabetes mellitus , detailed overview | Homo sapiens |
Protein Variants | Comment | Organism |
---|---|---|
additional information | CAPN10 polymorphisms occur in the development of type 2 diabetes mellitus, ariation in the CAPN10 gene (SNP-43 G/G, InDel-19 3/2 and SNP-63 C/T) known as haplotype 121/112 | Homo sapiens |
Metals/Ions | Comment | Organism | Structure |
---|---|---|---|
Ca2+ | dependent on, enzyme activity on SNAP-25 protein in response to calcium influx, resulting in the release of insulin | Homo sapiens |
Molecular Weight [Da] | Molecular Weight Maximum [Da] | Comment | Organism |
---|---|---|---|
54000 | - |
x * 54000, SDS-PAGE | Homo sapiens |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
SNAP-25 + H2O | Homo sapiens | the 54 kDa isoform of calpain-10 proteolyzes SNAP-25, a member of SNARE family of proteins involved in vesicle fusion | ? | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q9HC96 | gene CAPN10 | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
adipocyte | - |
Homo sapiens | - |
skeletal muscle | - |
Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
SNAP-25 + H2O | the 54 kDa isoform of calpain-10 proteolyzes SNAP-25, a member of SNARE family of proteins involved in vesicle fusion | Homo sapiens | ? | - |
? |
Subunits | Comment | Organism |
---|---|---|
? | x * 54000, SDS-PAGE | Homo sapiens |
Synonyms | Comment | Organism |
---|---|---|
calpain-10 | - |
Homo sapiens |
CAPN10 | - |
Homo sapiens |
Organism | Comment | Expression |
---|---|---|
Homo sapiens | calpain-10 is overexpressed and activated through the inhibition of ryanodine receptor 2 under hypoglycemic and high fatty acid conditions, causing caspase-3-independent beta-cell death | up |
General Information | Comment | Organism |
---|---|---|
malfunction | enzyme knockdown in human primary muscle cells results in decreased insulin-stimulated glucose uptake and GLUT4 translocation to the plasma membrane through actin filament reorganization, with no changes in expression and activation of molecules involved in the insulin transduction pathway such as IRb, IRS1, IRS2 and Akt, or in glycogen synthesis. Calpain-10 is overexpressed and activated through the inhibition of ryanodine receptor 2 under hypoglycemic and high fatty acid conditions, causing caspase-3-independent beta-cell death | Homo sapiens |
metabolism | associations of the CAPN10 gene with metabolic phenotypes, overview. Key participation of the enzyme in glucose metabolism, role of calpain-10 in the development of type 2 diabetes mellitus and diabetes-related diseases, detailed overview. Calpains might function as sensors of glucose-induced calcium currents, which culminate with insulin secretion | Homo sapiens |
additional information | enzyme polymorphisms are associated with the risk of developing type 2 diabetes mellitus in Mexican-American populations with a high populationattributable risk | Homo sapiens |
physiological function | calpain-10 is required to maintain proper mitochondrial function by proteolysis of complex I subunits and the beta subunit of ATP synthase. Calpain-10 is involved in insulin-dependent GLUT4 externalization in adipocytes and muscle cells. Calpain-10 participates in insulin-stimulated glucose uptake. Calpain-10 is implicated in the development of type 2 diabetes, and polymorphisms in the CAPN10 gene are associated with an increased risk of developing this disease | Homo sapiens |