Overexpression of sigma-1 receptor inhibits ADAM10 and ADAM17 mediated shedding in vitro
Protein & Cell
; (12): 153-159, 2012.
Article
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| ID: wpr-757300
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ABSTRACT
The sigma-1 receptor is a molecular chaperone protein highly enriched in the brain. Recent studies linked it to many diseases, such as drug addition, Alzheimer's disease, stroke, depression, and even cancer. Sigma-1 receptor is enriched in lipid rafts, which are membrane microdomains essential in signaling processes. One of those signaling processes is ADAM17- and ADAM10-dependent ectodomain shedding. By using an alkaline phosphatase tagged substrate reporter system, we have shown that ADAM10-dependent BTC shedding was very sensitive to both membrane lipid component change and sigma-1 receptor agonist DHEAS treatment while ADAM17-dependent HB-EGF shedding was not; and overexpression of sigma-1 receptor diminished ADAM17- and ADAM10-dependent shedding. Our results indicate that sigma-1 receptor plays an important role in modifying the function of transmembrane proteases.
Texte intégral:
1
Indice:
WPRIM
Sujet Principal:
Expression des gènes
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Chlorocebus aethiops
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Récepteur sigma
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Cellules COS
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Microdomaines membranaires
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Protéines et peptides de signalisation intercellulaire
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Protéines ADAM
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Amyloid precursor protein secretases
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Cellules HEK293
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Bêtacelluline
Limites du sujet:
Animals
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Humans
langue:
En
Texte intégral:
Protein & Cell
Année:
2012
Type:
Article