Recombinant Mouse Beta-Adrenergic Receptor Kinase 1 (GRK2) Protein (His-B2M)

Name: Recombinant Mouse Beta-Adrenergic Receptor Kinase 1 (GRK2) Protein (His-B2M)
Brand: Beta LifeScience
SKU: BLC-07760P
Availability: InStock

Greater than 85% as determined by SDS-PAGE.

Collections: All products, Fc receptors, High-quality recombinant proteins, Other recombinant proteins

Our products are highly customizable to meet your specific needs. You can choose options such as endotoxin removal, liquid or lyophilized forms, preferred tags, and the desired functional sequence range for proteins. Submitting a written inquiry expedites the quoting process.

Submit an inquiry today to inquire about all available size options and prices! Connect with us via the live chat in the bottom corner to receive immediate assistance.

Product Overview

Description	Recombinant Mouse Beta-Adrenergic Receptor Kinase 1 (GRK2) Protein (His-B2M) is produced by our E.coli expression system. This is a full length protein.
Purity	Greater than 85% as determined by SDS-PAGE.
Uniprotkb	Q99MK8
Target Symbol	GRK2
Synonyms	Beta-ARK-1;G-protein-coupled receptor kinase 2
Species	Mus musculus (Mouse)
Expression System	E.coli
Tag	N-6His-B2M
Target Protein Sequence	MADLEAVLADVSYLMAMEKSKATPAARASKKILLPEPSIRSVMQKYLEDRGEVTFEKIFSQKLGYLLFRDFCLNHLEEAKPLVEFYEEIKKYEKLETEEERVVRSREIFDSYIMKELLACSHPFSKNATEHVQGHLVKKQVPPDLFQPYIEEICQNLRGDVFQKFIESDKFTRFCQWKNVELNIHLTMNDFSVHRIIGRGGFGEVYGCRKADTGKMYAMKCLDKKRIKMKQGETLALNERIMLSLVSTGDCPFIVCMSYAFHTPDKLSFILDLMNGGDLHYHLSQHGVFSEADMRFYAAEIILGLEHMHNRFVVYRDLKPANILLDEHGHVRISDLGLACDFSKKRPHASVGTHGYMAPEVLQKGVAYDSSADWFSLGCMLFKLLRGHSPFRQHKTKDKHEIDRMTLTMAVELPDSFSPELRSLLEGLLQRDVNRRLGCLGRGAQEVKESPFFRSLDWQMVFLQKYPPPLIPPRGEVNAADAFDIGSFDEEDTKGIKLLDSDQELYRNFPLTISERWQQEVAETVFDTINAETDRLEARKKAKNKQLGHEEDYALGKDCIVHGYMSKMGNPFLTQWQRRYFYLFPNRLEWRGEGEAPQSLLTMEEIQSVEETQIKERKCLLLKIRGGKQFVLQCDSDPELVQWKKELRDAYREAQQLVQRVPKMKNKPRSPVVELSKVPLIQRGSANGL
Expression Range	1-689aa
Protein Length	Full Length
Mol. Weight	93.6 kDa
Research Area	Neuroscience
Form	Liquid or Lyophilized powder
Buffer	Liquid form: default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution	Briefly centrifuged the vial prior to opening to bring the contents to the bottom. Reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL. It is recommended to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. The default final concentration of glycerol is 50%.
Storage	1. Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. 2. Avoid repeated freeze-thaw cycles. 3. Store working aliquots at 4°C for up to one week. 4. In general, protein in liquid form is stable for up to 6 months at -20°C/-80°C. Protein in lyophilized powder form is stable for up to 12 months at -20°C/-80°C.
Notes	Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

Target Details

Target Function	Specifically phosphorylates the agonist-occupied form of the beta-adrenergic and closely related receptors, probably inducing a desensitization of them. Key regulator of LPAR1 signaling. Competes with RALA for binding to LPAR1 thus affecting the signaling properties of the receptor. Desensitizes LPAR1 and LPAR2 in a phosphorylation-independent manner. Positively regulates ciliary smoothened (SMO)-dependent Hedgehog (Hh) signaling pathway by facilitating the trafficking of SMO into the cilium and the stimulation of SMO activity. Inhibits relaxation of airway smooth muscle in response to blue light.
Subcellular Location	Cytoplasm. Cell membrane.
Protein Families	Protein kinase superfamily, AGC Ser/Thr protein kinase family, GPRK subfamily
Database References	KEGG: mmu:110355 STRING: 10090.ENSMUSP00000025791 UniGene: PMID: 28759639 Grk2 rescuing activity requires the integrity of domains essential for its interaction with GPCRs, we speculate that Grk2 may regulate Hh pathway activity by downregulation of a GPCR. PMID: 27113758 The main novelty presented here is to show that septic shock induces cardiac hyporesponsiveness to isoproterenol by a mechanism dependent on nitric oxide and mediated by G protein-coupled receptor kinase isoform 2. Therefore, G protein-coupled receptor kinase isoform 2 inhibition may be a potential therapeutic target in sepsis-induced cardiac dysfunction. PMID: 28526706 Data, including data from studies in heterozygous knockout mice, suggest that Grk2 is involved in TNFalpha-induced wound healing in epithelial cells of the colon; Grk2 appears to inhibit TNFalpha-induced apoptosis; Grk2 inhibits TNFalpha-induced ERK activation by inhibiting generation of reactive oxygen species. Homozygous knockout of Grk2 is embryonically lethal in mice. PMID: 28572156 GRK2 upregulation causes kappa-opioid receptor desensitization in diabetic heart PMID: 27865836 study provides the first insights into the role of GRK2 in skeletal muscle physiology and points to a role for GRK2 as a modulator of contractile properties in skeletal muscle as well as beta2AR-induced hypertrophy. PMID: 27566547 GRK2 loss confers a protective advantage over control mice after myocardial ischemia/reperfusion injury. Fibroblast GRK2 knockout mice presented with decreased infarct size and preserved cardiac function 24 hours post ischemia/reperfusion. They had decreased fibrosis and fibrotic gene expression. These protective effects correlated with decreased infiltration of neutrophils to the ischemia site and decreased TNF-alpha. PMID: 27601479 this study shows that astragaloside IV alleviates E. coli-caused peritonitis through modulating GRK2-CXCR2 signal in neutrophils PMID: 27543854 GRK2 down-regulation is cardioprotective during diet-induced obesity, reinforcing the protective effect of maintaining low levels of GRK2 under nutritional stress, and showing a role for this kinase in obesity-induced cardiac remodeling and steatosis. PMID: 27832814 The betaARKrgs peptide, but not endogenous GRK2, interacted with Galpha(q) and interfered with signaling through this G protein. These data support the development of GRK2-based therapeutic approaches to prevent hypertrophy and heart failure. PMID: 27016525 GRK2 is localized in the mitochondria and its kinase activity negatively impacts the function of this organelle by increasing superoxide levels and altering substrate utilization for energy production. PMID: 26506135 Erythropoietin seems to reverse sepsis-induced vasoplegia to NE through the preservation of alpha1D adrenoceptor mRNA/protein expression, inhibition of GRK2-mediated desensitization, and attenuation of NO overproduction in the mouse aorta. PMID: 26025460 In vitro, GRK2 inhibits Epac1-to-Rap1 signaling by phosphorylation of Epac1 at Ser-108 in the Disheveled/Egl-10/pleckstrin domain. GRK2 inhibits Epac1-mediated sensitization of Piezo2 which contributes to inflammatory mechanical hyperalgesia. PMID: 26929333 GRK2 ablation increases circadian amplitude and decreases circadian period. GRK2 suppresses mPeriod1 transcription,PERIOD1/2 nuclear trafficking and promotes PERIOD2 phosphorylation. PMID: 26279567 These results suggest GRK2 contributes to melanopsin deactivation, but that other mechanisms account for most of modulation of melanopsin activity in ipRGCs. PMID: 26069965 data suggest that inhibiting GRK2 could reverse an established insulin-resistant and obese phenotype PMID: 26198359 Post-MI AdipoR1 phosphorylation positively correlated with the expression level of GRK2. AdipoR1 is phosphorylatively modified and desensitized by GRK2 in failing cardiomyocytes, contributing to post-MI remodeling and HF progression. PMID: 25696921 findings indicate that the balance between mechanisms regulating vascular tone are shifted to favor vasoconstriction in the absence of GRK2 expression and that this leads to the age-dependent development of hypertension PMID: 25561731 Data indicate that G protein-coupled receptor kinase 2 (GRK2) downregulation enhances insulin signaling in adult mouse hearts. PMID: 25239306 Findings reveal a cell-type-specific role for GRK2 in the regulation of normal motor behavior, sensitivity to psychostimulants, dopamine neurotransmission, and D2 autoreceptor function PMID: 24776686 Attenuation of GRK2 is associated with defective differentiation of somatic muscles. PMID: 24927997 These data demonstrate that GRK2 modulates FcinRI signaling in mast cells via at least two mechanisms.One involves GRK2-RH and modulates tyrosine phosphorylation of Syk, and the other is mediated via the phosphorylation of p38 and Akt. PMID: 24904059 Data indicate that ischemic injury coupled to G protein-coupled receptor beta1/2 adrenergic receptors activation required GRK2 (GPCR kinase 2) activation. PMID: 24170934 Our results describe an important role for GRK2 in systemic hypertension. PMID: 24191280 GRK2 blockade with betaARKct is essential for cardiac beta2-adrenergic receptor signaling towards increased contractility. PMID: 23984976 decreased endothelial Grk2 dosage accelerated tumor growth, along with reduced pericyte vessel coverage and enhanced macrophage infiltration, and this transformed environment promoted decreased GRK2 in endothelial cells PMID: 24135140 GRK2 removal compromises vascular phenotype and integrity by increasing endothelial reactive oxygen species production. PMID: 23950144 These findings underline the critical role of GRK2 regulation in astrocytes for dampening the extent of brain damage after ischemia. PMID: 23313319 TNFalpha-induced betaAR desensitization is mediated by GRK2 and is independent of Gbetagamma, uncovering a hitherto unknown cross-talk between TNFalpha and betaAR function, providing the underpinnings of inflammation-mediated cardiac dysfunction. PMID: 23785004 study identified a novel interaction between TLR4 and chemokine receptors that can control monocyte migration, an essential component of innate immune response; results support a model in which LPS-TLR4 signaling augments monocyte migration by modulating cell surface expression of chemokine receptors in a GRK2-dependent manner PMID: 23772028 GRK2 plays a key role in modulating the aortic vasodilator effect of clonidine by selectively affecting the Akt/eNOS pathway, especially in males. PMID: 22925038 GRK2 localizes to mitochondria, providing novel insight into GRK2-dependent pathophysiological signaling mechanisms in wild-type mice. PMID: 23467820 Inhibition of G-protein-coupled receptor kinase 2 (GRK2) triggers the growth-promoting mitogen-activated protein kinase (MAPK) pathway PMID: 23362259 even partial hematopoietic GRK2 deficiency prevents atherosclerotic lesion progression beyond the fatty streak stage, identifying hematopoietic GRK2 as a potential target for intervention in atherosclerosis PMID: 23047899 GRK2 knockdown increases chemokine CXCR1-mediated exocytosis but decreases receptor phosphorylation and internalization. PMID: 22869904 This study demonstrated that the elimination of GRK2 in cholinergic neurons reduces sensitivity to select muscarinic-mediated behaviors PMID: 22895728 hemizygous mice displayed better thermogenic capacity and exhibited more oxidative phenotype in both BAT and WAT than WT littermates. Overexpression of GRK2 in brown adipocytes corroborated the negative effect in BAT function and differentiation PMID: 22516294 G protein-coupled receptor kinase 2 inhibitor normalizes vascular endothelial function in type 2 diabetic mice by improving beta-arrestin 2 translocation and ameliorating Akt/eNOS signal dysfunction PMID: 22581458 After beta-adrenergic stimulation, GRK2KO myocytes increased in contractility & Ca(2+) transients, not mediated through cardiac L-type Ca(2+) channels but thru increased SR Ca(2+), a novel form of differential regulation. PMID: 22496128 The data show a novel sub-cellular localization of GRK2 in the mitochondria and an unexpected role in regulating mitochondrial biogenesis and ATP generation. PMID: 21983013 Angiotensin II causes endothelial dysfunction in diabetes via the Akt/eNOS pathway, and an increase in plasma Angiotensin II increases the vascular GRK2 level. PMID: 21571071 Mouse models of chronic pain are associated with reduced cellular levels of GRK2. GRK2 is a newly discovered major player in the regulation of chronic pain. Review. PMID: 21473908 GRK2 functions in downregulation of S1PR1 on blood-exposed lymphocytes; GRK2-dependent S1PR1 desensitization allows lymphocytes to escape circulatory fluids and migrate to lymphoid tissues PMID: 21960637 Report dysfunctional endothelium-dependent relaxation to insulin via PKC-mediated GRK2/Akt activation in aortas of type 2 diabetic mice. PMID: 21572010 GRK2 is pathological in the injured heart;it is a critical mechanistic link within neurohormonal crosstalk governing cardiac contractile signaling/function through beta-adrenergic receptors and metabolism through the insulin receptor PMID: 21518983 role in chondrocyte mechanotransduction PMID: 21520257 These studies reveal previously undescribed negative regulatory role for GRK2 in TLR4-induced p105-ERK pathway as well as in the consequent inflammatory cytokine/chemokine production and endotoxemia in mice. PMID: 20717897 The evidence provided points toward the possibility that the acceleration of GIRK current desensitization by GRK2 is due to competition for Gbetagamma dimers with the channel. PMID: 21111235 desensitization of the dopamine D1-D2 receptor heteromer-mediated signal can occur by agonist occupancy even without activation and is dually regulated by both the catalytic and RGS domains of GRK2. PMID: 20807772 In vivo, low nociceptor GRK2 leads to prolonged inflammatory hyperalgesia via biased cAMP signaling from PKA to Epac-Rap1, ERK/PKCepsilon pathways. PMID: 20861385

FAQs

Please fill out the Online Inquiry form located on the product page. Key product information has been pre-populated. You may also email your questions and inquiry requests to sales1@betalifesci.com. We will do our best to get back to you within 4 business hours.

Feel free to use the Chat function to initiate a live chat. Our customer representative can provide you with a quote immediately.

Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

To learn more about how to properly dissolve the lyophilized recombinant protein, please visit Lyophilization FAQs.