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Arrb1 reduced the chemotherapy-induced Lgr5 (show LGR5 ELISA Kits) stem cell apoptosis by inhibiting endoplasmic reticulum stress-mediated mitochondrial apoptotic signaling.
findings suggest that knockdown of beta-arrestin 1 can suppress glioblastoma multiforme cell proliferation, invasion and glycolysis by inhibiting Src (show SRC ELISA Kits) signaling
Results revealed that beta-arrestin-1 regulates lactate metabolism to contribute to beta2-adrenergic receptor (show ADRB2 ELISA Kits) functions in improved memory formation.
Study reports an X-ray free electron laser crystal structure of the rhodopsin (show RHO ELISA Kits)-arrestin (show SAG ELISA Kits) complex, in which the phosphorylated C terminus of rhodopsin (show RHO ELISA Kits) forms an extended intermolecular beta sheet with the N-terminal beta strands of arrestin (show SAG ELISA Kits). Phosphorylation was detected at rhodopsin (show RHO ELISA Kits) C-terminal tail residues T336 and S338.
Beta-arrestin-1 with beta-arrestin-2 shared common mechanisms to suppress podocyte autophagy by negative regulation of ATG12-ATG5 conjugation.
data suggest that beta-arr1 mediated nuclear signaling regulates the production of excretive factors derived from niche astrocytes and expansion of neural precursors in DG, thus maintaining homeostasis of adult hippocampal neurogenesis
beta-arr1 (show SAG ELISA Kits) has a critical role in modulating ERK (show EPHB2 ELISA Kits), JNK (show MAPK8 ELISA Kits) and p38 MAPK (show MAPK14 ELISA Kits) pathways mediated by TNF-alpha (show TNF ELISA Kits) in intestinal epithelial cells.
COX-2-derived PGE2 inhibits IL-10 expression in brain microglia through a novel EP2- and beta-arrestin-dependent signaling pathway.
A specific hyaluronan-blocking peptide (Pep-1 (show CNDP2 ELISA Kits)) has confirmed the inflammatory role of degraded hyaluronan as a mediator of the IL-1beta (show IL1B ELISA Kits)-induced activation of beta-arrestin-1.
Data suggest that ARRB1 enhances hepatocellular carcinogenesis by inflammation-mediated Akt (show AKT1 ELISA Kits) signaling.
This work demonstrates that the expression of FSHR (show FSHR ELISA Kits) and LHCGR (show LHCGR ELISA Kits) can be induced in hGL5 cells but that the FSHR (show FSHR ELISA Kits)-dependent cAMP/PKA pathway is constitutively silenced, possibly to protect cells from FSHR (show FSHR ELISA Kits)-cAMP-PKA-induced apoptosis.
This study reveals contrasting abilities of IGF-1R (show IGF1R ELISA Kits) to interact with each b-arrestin (show SAG ELISA Kits) isoform, depending on the presence of the ligand and demonstrates the antagonism between the two b-arrestin (show SAG ELISA Kits) isoforms in controlling IGF-1R (show IGF1R ELISA Kits) expression and function, which could be developed into a practical anti-IGF-1R (show IGF1R ELISA Kits) strategy for cancer therapy.
Lowering the level of cellular FLNA caused an elevation in RalA activity and resulted in selective interference with the normal intracellular trafficking and signaling of D3R through beta-arrestins.
the depleted beta-Arrestin1 reduced the interaction of P300 (show EP300 ELISA Kits) with Sp1 (show PSG1 ELISA Kits), thus to reduce Sp1 (show PSG1 ELISA Kits) binding to hTERT promoter, downregulate hTERT transcription, decrease telomerase activity, shorten telomere length, and promote Reh (show CES1 ELISA Kits) cell senescence.
Data show that endothelin A receptor (show EDNRA ELISA Kits) drives invadopodia function by direct interaction of beta-arrestin-1 (beta-arr1) with Rho guanine nucleotide exchange factor (GEF) 11 (show ARHGEF11 ELISA Kits) protein (PDZ-RhoGEF (show ARHGEF11 ELISA Kits)).
The small GTPase (show RACGAP1 ELISA Kits) Ras-related protein (show RASD1 ELISA Kits) 2 (Rap2 (show RAP2A ELISA Kits)) was found to bind ArrB1 under resting conditions but dissociated upon formyl-Met-Leu-Phe stimulation.
These results were consistent with those seen for beta2-AR. Thus, both beta-arrs negatively control AM1 receptor internalization, which depends on the C-tail of CLR (show DCLK3 ELISA Kits).
Results indicate a mechanism of beta-arrestin1 in modulating epithelial-mesenchymal transition (EMT (show ITK ELISA Kits)) and glycogen synthase kinase 3 beta (GSK-3beta (show GSK3b ELISA Kits))/beta-catenin (show CTNNB1 ELISA Kits) signaling in prostate cancer, and suggest that assessment of beta-arrestin1 may provide a potential therapeutic target for prostate cancer.
Using in vivo time-lapse imaging and three-dimensional morphology analysis of microglia in intact zebrafish larvae, study found that beta-arrestin1, a multifunctional protein involved in various signal transductions, cell-autonomously regulated the microglial morphology.
Study demonstrated that beta-arrestin1 is critically involved in zebrafish primitive hematopoiesis, where beta-arrestin1 binds to and sequesters the PcG recruiter YY1 (show YY1 ELISA Kits), thus relieving PcG-mediated repression of cdx4-hox (show MSH2 ELISA Kits) pathway.
The identified receptor-phospho-selective mechanism for arrestin (show SAG ELISA Kits) conformation and the spacing of the multiple phosphate-binding sites in the arrestin (show SAG ELISA Kits) enable arrestin (show SAG ELISA Kits) to recognize plethora phosphorylation states of numerous GPCRs.
The presented functional map quantitatively connects critical interactions in the polar core and along the C tail of arrestin (show SAG ELISA Kits).
Reduced binding of arrestin-1 (show SAG ELISA Kits) to the phospho-opsin (show RHO ELISA Kits) form of G90D mutant likely contributes to night blindness caused by this mutation.
3.0 A crystal structure of the bovine arrestin-1 splice variant p44, in which the activation step is mimicked by C-tail truncation
Conformational dynamics of helix 8 in the GPCR (show GPRC6A ELISA Kits) rhodopsin (show RHO ELISA Kits) controls arrestin (show SAG ELISA Kits) activation in the desensitization process
similar to transducin (show GNAT1 ELISA Kits) activation, rhodopsin (show RHO ELISA Kits) phosphorylation by GRK1 (show GRK1 ELISA Kits) and high affinity arrestin-1 (show SAG ELISA Kits) binding only requires a rhodopsin (show RHO ELISA Kits) monomer
Members of arrestin/beta-arrestin protein family are thought to participate in agonist-mediated desensitization of G-protein-coupled receptors and cause specific dampening of cellular responses to stimuli such as hormones, neurotransmitters, or sensory signals. Arrestin beta 1 is a cytosolic protein and acts as a cofactor in the beta-adrenergic receptor kinase (BARK) mediated desensitization of beta-adrenergic receptors. Besides the central nervous system, it is expressed at high levels in peripheral blood leukocytes, and thus the BARK/beta-arrestin system is believed to play a major role in regulating receptor-mediated immune functions. Alternatively spliced transcripts encoding different isoforms of arrestin beta 1 have been described.
arrestin, beta 1
, arrestin 1
, beta-arrestin 1
, arrestin beta 1
, arrestin beta-1
, arrestin 2