Enables several functions, including AP-2 adaptor complex binding activity; G protein-coupled receptor binding activity; and arrestin family protein binding activity. Involved in several processes, including follicle-stimulating hormone signaling pathway; regulation of ERK1 and ERK2 cascade; and regulation of primary metabolic process. Located in several cellular components, including basolateral plasma membrane; dendritic spine; and postsynaptic membrane. Is active in glutamatergic synapse and postsynaptic density. Used to study congestive heart failure. Biomarker of colitis. Orthologous to human ARRB1 (arrestin beta 1); PARTICIPATES IN calcium signaling pathway via the calcium-sensing receptor; angiotensin II signaling pathway via AT1 receptor; corticotropin-releasing hormone signaling pathway; INTERACTS WITH 2,3,7,8-tetrachlorodibenzodioxine; 2,3,7,8-Tetrachlorodibenzofuran; 2,4,6-trinitrobenzenesulfonic acid.
ARRB1 protein affects the reaction [Nicotine promotes the reaction [RB1 protein binds to RAF1 protein]] and ARRB1 protein affects the reaction [Nicotine results in increased phosphorylation of and results in increased activity of SRC protein]
[Ibuprofen co-treated with hydroxyibuprofen co-treated with Diclofenac co-treated with Ethinyl Estradiol] results in increased expression of ARRB1 mRNA
Trinitrobenzenesulfonic Acid results in increased expression of ARRB1 mRNA and Trinitrobenzenesulfonic Acid results in increased expression of ARRB1 protein
[6-isopropoxy-9-oxoxanthene-2-carboxylic acid co-treated with AH 23848] inhibits the reaction [[ARRB1 protein modified form binds to SRC protein] which binds to IL1R1 protein] more ...
[NOG protein co-treated with belinostat co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of ARRB1 mRNA
[Chelating Agents binds to Copper] which results in decreased expression of ARRB1 mRNA and [NSC 689534 binds to Copper] which results in decreased expression of ARRB1 mRNA
[Chelating Agents binds to Copper] which results in decreased expression of ARRB1 mRNA and [NSC 689534 binds to Copper] which results in decreased expression of ARRB1 mRNA
[Ibuprofen co-treated with hydroxyibuprofen co-treated with Diclofenac co-treated with Ethinyl Estradiol] results in increased expression of ARRB1 mRNA
ARRB1 protein promotes the reaction [Dobutamine promotes the reaction [[ADRB1 protein co-treated with EGFR protein] results in increased phosphorylation of MAPK1 protein]] and ARRB1 protein promotes the reaction [Dobutamine promotes the reaction [[ADRB1 protein co-treated with EGFR protein] results in increased phosphorylation of MAPK3 protein]]
Dopamine promotes the reaction [DRD2 protein affects the localization of ARRB1 protein] and GRK2 protein promotes the reaction [Dopamine promotes the reaction [DRD2 protein affects the localization of ARRB1 protein]]
[NOG protein co-treated with entinostat co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of ARRB1 mRNA
[Ibuprofen co-treated with hydroxyibuprofen co-treated with Diclofenac co-treated with Ethinyl Estradiol] results in increased expression of ARRB1 mRNA
[NOG protein co-treated with mercuric bromide co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of ARRB1 mRNA
Mesalamine inhibits the reaction [Trinitrobenzenesulfonic Acid results in increased expression of ARRB1 mRNA] and Mesalamine inhibits the reaction [Trinitrobenzenesulfonic Acid results in increased expression of ARRB1 protein]
ARRB1 protein affects the reaction [Nicotine promotes the reaction [RB1 protein binds to RAF1 protein]] and ARRB1 protein affects the reaction [Nicotine results in increased phosphorylation of and results in increased activity of SRC protein]
[NOG protein co-treated with Panobinostat co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of ARRB1 mRNA
[NOG protein co-treated with Phenylmercuric Acetate co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of ARRB1 mRNA
[NOG protein co-treated with trichostatin A co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of ARRB1 mRNA
[NOG protein co-treated with Valproic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of ARRB1 mRNA
Insulin induces heterologous desensitization of G-protein-coupled receptor and insulin-like growth factor I signaling by downregulating beta-arrestin-1.
Role of G protein-coupled receptor kinase 4 and beta-arrestin 1 in agonist-stimulated metabotropic glutamate receptor 1 internalization and activation of mitogen-activated protein kinases.
Independent beta-arrestin2 and Gq/protein kinase Czeta pathways for ERK stimulated by angiotensin type 1A receptors in vascular smooth muscle cells converge on transactivation of the epidermal growth factor receptor.
Adrenal beta-arrestin 1 inhibition in vivo attenuates post-myocardial infarction progression to heart failure and adverse remodeling via reduction of circulating aldosterone levels.
The active conformation of beta-arrestin1: direct evidence for the phosphate sensor in the N-domain and conformational differences in the active states of beta-arrestins1 and -2.
Different internalization properties of the alpha1a- and alpha1b-adrenergic receptor subtypes: the potential role of receptor interaction with beta-arrestins and AP50.
The expression change of beta-arrestins in fibroblast-like synoviocytes from rats with collagen-induced arthritis and the effect of total glucosides of paeony.
PAR-1 activation rescues astrocytes through the PI3K/Akt signaling pathway from chemically induced apoptosis that is exacerbated by gene silencing of ß-arrestin 1.
