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Recombinant Human 14-3-3 tau/14-3-3 theta/YWHAQ Protein (GST Tag) (PKSH031392)

All Size Price Qty
100μg $ 680.00
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For research use only.

Synonyms 1C5, 41701, HS1
Species Human
Expression Host E.coli
Sequence Met 1-Asn 245
Accession P27348
Calculated Molecular Weight 54.6 kDa
Observed Molecular Weight 53 kDa
Tag N-GST
Bio-activity Not validated for activity
Purity > 88 % as determined by reducing SDS-PAGE.
Endotoxin Please contact us for more information.
Storage Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months.
Shipping This product is provided as lyophilized powder which is shipped with ice packs.
Formulation Lyophilized from sterile 20mM Tris, 0.15m NaCl, 20mM GSH, pH 7.5
Normally 5% - 8% trehalose, mannitol and 0.01% Tween 80 are added as protectants before lyophilization.
Please refer to the specific buffer information in the printed manual.
Reconstitution Please refer to the printed manual for detailed information.
Background G protein-coupled receptor kinase 5, also known as G protein-coupled receptor kinase GRK5 and GRK5, is a member of the protein kinase superfamily, AGC Ser/Thr protein kinase family and GPRK subfamily. GRKs specifically phosphorylate agonist-occupied G protein-coupled receptors at the inner surface of the plasma membrane (PM), leading to receptor desensitization. GRKs utilize a variety of mechanisms to bind tightly, and sometimes reversibly, to cellular membranes. GRKs play an important role in mediating agonist-specific desensitization of numerous G protein-coupled receptors. GRK5 contains oneAGC-kinase C-terminal domain, oneprotein kinase domain and oneRGS domain. GRK5 specifically phosphorylates the activated forms of G protein-coupled receptors. Phospholipid-stimulated autophosphorylation may represent a novel mechanism for membrane association and regulation of GRK5 activity. GRK5 deficiency significantly exaggerates microgliosis and astrogliosis in the presence of an inflammatory initiator, such as the excess fibrillar Abeta and the subsequent active inflammatory reactions. GRK5 deficiency has been linked to early Alzheimer's disease in humans and mouse models of the disease.
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