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Literature summary for 3.4.23.45 extracted from

  • Casas, S.; Casini, P.; Piquer, S.; Altirriba, J.; Soty, M.; Cadavez, L.; Gomis, R.; Novials, A.
    BACE2 plays a role in the insulin receptor trafficking in pancreatic beta-cells (2010), Am. J. Physiol. Endocrinol. Metab., 299, E1087-E1095.
    View publication on PubMed

Organism

Organism UniProt Comment Textmining
Homo sapiens
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Source Tissue

Source Tissue Comment Organism Textmining
pancreas in normal human pancreas, BACE2 expression is restricted to beta-cells. BACE2 colocalizes with clathrin-coated vesicles of the plasma membrane in MIN6 cells. Pharmacological inhibition of BACE2 results in increased BACE2 content in clathrin-coated vesicles, reduced insulin internalization rate, decreased in insulin receptor beta-subunit at the plasma membrane and increase in the Golgi apparatus, and a significant reduction in insulin gene expression. Similar results are obtained after specific BACE2 silencing in MIN6 cells. Data point to a role for BACE2 in the insulin receptor-beta subunit trafficking and insulin signaling Homo sapiens
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General Information

General Information Comment Organism
physiological function BACE2 colocalizes with clathrin-coated vesicles of the plasma membrane in MIN6 cells. Pharmacological inhibition of BACE2 results in increased BACE2 content in clathrin-coated vesicles, reduced insulin internalization rate, decreased in insulin receptor beta-subunit at the plasma membrane and increase in the Golgi apparatus, and a significant reduction in insulin gene expression. Similar results are obtained after specific BACE2 silencing in MIN6 cells. Data point to a role for BACE2 in the insulin receptor-beta subunit trafficking and insulin signaling Homo sapiens