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Literature summary for 3.4.22.B30 extracted from

  • Panico, P.; Salazar, A.M.; Burns, A.L.; Ostrosky-Wegman, P.
    Role of calpain-10 in the development of diabetes mellitus and its complications (2014), Arch. Med. Res., 45, 103-115.
    View publication on PubMed

Cloned(Commentary)

Cloned (Comment) Organism
genotyping and association with type 2 diabetes mellitus , detailed overview Homo sapiens

Protein Variants

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

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 [Da] Molecular Weight Maximum [Da] Comment Organism
54000
-
x * 54000, SDS-PAGE Homo sapiens

Natural Substrates/ Products (Substrates)

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

Organism UniProt Comment Textmining
Homo sapiens Q9HC96 gene CAPN10
-

Source Tissue

Source Tissue Comment Organism Textmining
adipocyte
-
Homo sapiens
-
skeletal muscle
-
Homo sapiens
-

Substrates and Products (Substrate)

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

Subunits Comment Organism
? x * 54000, SDS-PAGE Homo sapiens

Synonyms

Synonyms Comment Organism
calpain-10
-
Homo sapiens
CAPN10
-
Homo sapiens

Expression

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

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