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Literature summary for 3.1.6.13 extracted from

  • Piquer, S.; Casas, S.; Quesada, I.; Nadal, A.; Julia, M.; Novials, A.; Gomis, R.
    Role of iduronate-2-sulfatase in glucose-stimulated insulin secretion by activation of exocytosis (2009), Am. J. Physiol. Endocrinol. Metab., 297, E793-E801.
    View publication on PubMed
Search for more literature for 3.1.6.13

Cloned(Commentary)

Cloned (Comment) Organism
hIDS c-myc subcloned into pcDNA 3.1/Hygro(-). INS1E cells transiently transfected with the IDS construct Homo sapiens

Metals/Ions

Metals/Ions Comment Organism Structure
additional information effect of IDS on insulin secretion does not result from increased intracellular Ca2+ signaling Homo sapiens

Molecular Weight [Da]

Molecular Weight [Da] Molecular Weight Maximum [Da] Comment Organism
45000
-
 Western blot analysis Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
pancreatic islet
-
 Homo sapiens
-

Synonyms

Synonyms Comment Organism
IDS
-
 Homo sapiens
iduronate-2-sulfatase
-
 Homo sapiens

Expression

Organism Comment Expression
Homo sapiens IDS expression restrictedly observed in human pancreatic islet up

General Information

General Information Comment Organism
physiological function overexpression of IDS enhances glucose-induced insulin secretion in INS1E cells by activation of the exocytotic process. IDS overexpression is associated with a gain of function detected by a reduction in heparan sulfate content. IDS potentiates the glucose-stimulated insulin secretory response compared with controls (61%) with no changes in insulin mRNA levels or insulin peptide content. Increase in the number of granules in the immediate vicinity of the plasma membrane in IDS-transfected cells and a decrease in total vesicles per square micrometer. IDS overexpression induces phosphorylation of protein kinase C alpha and its newly myristoylated alanine-rich C kinase substrate, MARCKS Homo sapiens