|Other Names||Arrestin domain-containing protein 3, TBP-2-like inducible membrane protein, TLIMP, ARRDC3, KIAA1376|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Adapter protein that plays a role in regulating cell- surface expression of adrenergic receptors and probably also other G protein-coupled receptors (PubMed:20559325, PubMed:21982743, PubMed:23208550). Plays a role in NEDD4-mediated ubiquitination and endocytosis af activated ADRB2 and subsequent ADRB2 degradation (PubMed:20559325, PubMed:23208550). May recruit NEDD4 to ADRB2 (PubMed:20559325). Alternatively, may function as adapter protein that does not play a major role in recruiting NEDD4 to ADRB2, but rather plays a role in a targeting ADRB2 to endosomes (PubMed:23208550).|
|Cellular Location||Cytoplasm. Cell membrane; Peripheral membrane protein; Cytoplasmic side. Lysosome Endosome. Early endosome Note=Associated with plasma membrane, as well as with endosomes and lysosomes during endocytosis (PubMed:16269462, PubMed:23208550, PubMed:20559325).|
|Tissue Location||Highly expressed in skeletal muscle, placenta, kidney, lung, liver, blood, adrenal gland, lymph node, mammary gland, thyroid, and trachea (PubMed:16269462, PubMed:21982743) Very low levels in colon, thymus, spleen, small intestine, bladder and bone marrow (PubMed:16269462). Strong expression in differentiated adipocytes compared to preadipocytes (PubMed:16269462). Detected in omental fat and subcutaneous fat tissue (PubMed:21982743).|
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Provided below are standard protocols that you may find useful for product applications.
The arrestins are a family of proteins that are important for regulating signal transduction within cells. Arrestins are part of a conserved two step mechanism for regulating the activity of G-protein coupled receptors (GPCRs). In response to a stimulus, GPCRs activate a heterotrimeric G protein. In order to turn off this response, or adapt to a constant stimulus, activated receptors need to be silenced. The first step is phosphorylation by a class of serine/threonine kinases called G protein coupled receptor kinases (GRKs). This phosphorylation specifically marks the activated receptor for arrestin binding. Once arrestin is bound to the receptor it is unable to signal further. Recent research continues to expand the known actions of arrestins, which can bind to other classes of receptors and can directly activate signaling pathways on their own.Different arrestins (visual arrestin (or Arrestin 1), beta-arrestin 1 (or Arrestin 2) and beta-arrestin 2 (or Arrestin 3) can reduce the activity of their target GPCRs in several different ways.
Davis, O.S., et al. Behav. Genet. 40(6):759-767(2010)Draheim, K.M., et al. Oncogene 29(36):5032-5047(2010)Nabhan, J.F., et al. EMBO Rep. 11(8):605-611(2010)Patwari, P., et al. J. Biol. Chem. 284(37):24996-25003(2009)Lamesch, P., et al. Genomics 89(3):307-315(2007)
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