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Validated All-in-One™ qPCR Primer for ARRB1(NM_004041.4) Search again
Product ID:
HQP010962
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ARB1, ARR1
Gene Description:
arrestin beta 1
Target Gene Accession:
NM_004041.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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, however, their exact functions are not known. [provided by RefSeq].
Gene References into function
- Determinants in the receptor's core (Asn-289 and Lys-382) appear to regulate internalization of the receptor/beta-arrestin complex toward early endocytic endosomes during the initial step of endocytosis.
- findings suggest that beta-arrestin 1 acts as an effector for a novel function of PTHrP in cytoplasm
- role of beta-arrestin, dynamin, and clathrin-dependent pathway in internalization of the complement 5a anaphylatoxin receptor
- subcellular localization is determined by their intact N domain and the nuclear export signal at the C terminus
- examination of desensitization, internalization, and signaling functions demonstrated by RNA interference
- both beta-arrestin1 recruitment and the presence of Ser/Thr residues in the distal half of the C-terminal domain were necessary for maximal agonist-induced internalization
- results suggest that physiological levels of beta-arrestin1 may act as "dominant-negative" inhibitors of beta-arrestin2-mediated extracellular signal-regulated kinases 1 and 2 activation
- D6 is constitutively internalized via a ligand-independent, phosphorylation-independent association with beta-arrestin.
- protease-activated receptor-2-mediated migration of tumor cells requires both beta-arrestin-1 and -2
- c-Src has a role in regulating the dissociation of AP-2 from agonist-occupied AT1R and beta-arrestin during the clathrin-mediated internalization of receptors
- Mononuclear leukocytes of patients with depression showed significantly reduced immunoreactive quantities of beta-arrestin-1
- beta-Arrestin 1 and Galphaq/11 have roles in activating RhoA and stress fiber formation following receptor stimulation
- beta-Arrestins bind and decrease cell-surface abundance of the Na+/H+ exchanger NHE5 isoform.
- beta-arrestin has a role in ubiquitination and down-regulation of the insulin-like growth factor-1 receptor by acting as adaptor for the MDM2 E3 ligase
- Endogenous beta-arrestin1 functions exclusively in the phosphorylation-dependent receptor internalization, whereas endogenous beta-arrestin2, but not beta-arrestin1, is required for the phosphorylation-independent receptor internalization.
- the beta2 adrenergic receptor has a role in beta-arrestin-dependent, G protein-independent ERK1/2 activation
- results suggest that a GPCR conformation directed by the second intracellular loop, likely using the loop itself as a binding patch, may function as a switch for transitioning beta-arrestin from its inactive form to its active receptor-binding state.
- beta-arrestin 1 is a mediator of cellular migration and metastasis
- beta-arrestin and G proteins activate parathyroid hormone receptor-stimulated ERK1/2 pathways
- Our results show that PAR1-mediated activation of Src and ERK1/2 in HEK 293 cells was increased with overexpression of beta-arrestin1 or depletion of beta-arrestin2.
- ERK1/2 is activated by a chimeric neurokinin 1 receptor-beta-arrestin1 fusion protein
- Platelet-activating factor signaling requires beta-arrestin-1 recruitment of a p38 MAP kinase signalosome for transduction before neutrophil endosomal scission.
- analysis of the G protein-coupled receptor kinase and beta-arrestin-mediated desensitization of the angiotensin II type 1A receptor
- results demonstrate the ability of beta-arrestins to recruit diacylglycerol kinases to ligand-activated M1 muscarinic receptors
- Data show that 5-HT(4) receptor stimulation in primary neurons produced a potent but transient activation of the ERK pathway that is dependent on Src tyrosine kinase but totally independent of beta-arrestin.
- MS patients had a greater prevalence of positive T-cell proliferative responses to neuron-specific enolase [NSE], retinal arrestin, and beta-arrestin than healthy controls (p<0.0001).
- ARRB1 and ARRB2 play an important role in biological processes involved in the regulation of smoking urgency (that is time to smoke first cigarette).
- data suggest cells ruffle upon CaSR (calcium sensing receptor)stimulation via a mechanism that involves translocation of beta-arrestin 1 pre-assembled with the CaSR or ARNO (Arf nucleotide binding site opener)
- overexpression of beta-Arr1 promotes matrix metalloproteinase 9 activity and tumor angiogenesis by providing a suitable microenvironment for tumor progression
- the AIP4.arrestin-2 complex functions on endosomes to regulate sorting of CXCR4 into the degradative pathway
- beta-arrestins regulate protein synthesis
- beta-arrestins direct the localization of PIP5K Ialpha and PIP(2) production to agonist-activated 7TMRs, thereby regulating receptor internalization
- analysis of the protein kinase A-independent, beta-arrestin-1-dependent signaling pathway for p38 mitogen-activated protein kinase activation by beta2-adrenergic receptors
- Agonist-selective, receptor-specific interaction of human P2Y receptors with beta-arrestin-1 and -2.
- Results identify novel functions of beta-arrestin1 in binding to the beta1gamma2 subunits of heterotrimeric G-proteins and promoting G(betagamma)-mediated Akt signalling for NF-kappaB activation.
- These findings demonstrate that physical interaction of CaM with recombinant and native 5-HT(2C) receptors is critical for G protein-independent, arrestin-dependent receptor signaling.
- Results reveal that nuclear beta-arrestin1, acting as a scaffold for the dephosphorylation of STAT1, is an essential negative regulator of IFN-gamma signaling and participates in the IFN-gamma-induced cellular antiviral response.
- These results show that G(i2) protein is involved in D(2)R-mediated ERK activation but beta-arrestins 1 and 2 are either not involved or play minor role.