Recombinant Mouse GRO beta / CXCL2 Protein (His & SUMO Tag)

Name: Recombinant Mouse GRO beta / CXCL2 Protein (His & SUMO Tag)
Brand: Beta LifeScience
SKU: BLPSN-2334
Availability: InStock

Collections: Chemokines and receptors, Cytokines and growth factors, 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

Tag	His&SUMO
Host Species	Mouse
Accession	P10889
Synonym	CINC-2a, Gro2, GROb, Mgsa-b, MIP-2, MIP-2a, Mip2, Scyb, Scyb2
Background	Chemokine (C-X-C motif) ligand 2 (CXCL2), also called macrophage inflammatory protein 2 (MIP-2), Growth-regulated protein beta (Gro-beta) and Gro oncogene-2 (Gro-2), is a small cytokine belonging to the CXC chemokine family. CXCL2/MIP-2 is selectively up-regulated in tolerance-conferring APCs and serves to recruit NKT cells to the splenic marginal zone, where they form clusters with APCs and T cells. In the absence of the high-affinity receptor for CXCL2/MIP-2 or in the presence of a blocking Ab to CXCL2/MIP-2, peripheral tolerance is prevented, and Ag-specific T regulatory cells are not generated. CXCL2/MIP-2 is selectively up-regulated in tolerance-conferring APCs and serves to recruit NKT cells to the splenic marginal zone, where they form clusters with APCs and T cells. In the absence of the high-affinity receptor for MIP-2 (as in CXCR2-deficient mice) or in the presence of a blocking Ab to MIP-2, peripheral tolerance is prevented, and Ag-specific T regulatory cells are not generated. Understanding the regulation of lymphocyte traffic during tolerance induction may lead to novel therapies for autoimmunity, graft acceptance, and tumor rejection. Several studies have implicated the CXCL2 chemokine as a mediator in the development of sepsis. CXCL2/MIP-2 also plays a major role in mediating the neutrophilic inflammatory response of the rodent lung to particles such as quartz, crocidolite asbestos, as well as high doses of other relative innocuous dusts such as titanium dioxide.
Description	A DNA sequence encoding the mature form of mouse CXCL2 (P10889-1) (Ala 28-Asn 100) was fused with a N-terminal His-tagged SUMO tag at the N-terminus.
Source	E.coli
Predicted N Terminal	Met
AA Sequence	Ala 28-Asn 100
Molecular Weight	The recombinant mouse CXCL2 consisting of 189 a.a. and has a calculated molecular mass of 21.2 kDa. It migrates as a 30 kDa band in SDS-PAGE under reducing conditions.
Purity	>95% as determined by SDS-PAGE
Endotoxin	Please contact us for more information.
Bioactivity	Please contact us for detailed information
Formulation	Lyophilized from sterile 0.1% TFA, pH 2.9.
Stability	The recombinant proteins are stable for up to 1 year from date of receipt at -70°C.
Usage	For Research Use Only
Storage	Store the protein under sterile conditions at -20°C to -80°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

Target Details

Target Function	Chemotactic for human polymorphonuclear leukocytes but does not induce chemokinesis or an oxidative burst.
Subcellular Location	Secreted.
Protein Families	Intercrine alpha (chemokine CxC) family
Database References	KEGG: mmu:20310 STRING: 10090.ENSMUSP00000074885 UniGene: Mm.4979

Gene Functions References

The studies revealed that, although overall structural and oligomerization features of CXCL3 and CXCL2 are similar, prominent differences were observed in their surface characteristics, thus implicating a functional divergence. PMID: 28928065
TIARP independently down-regulated CXCL2 and IL-6 production by fibroblast-like synoviocytes, and the expression of chemokine receptors (CXCR1 and CXCR2) in neutrophils, with resultant reduction of neutrophil migration into arthritic joints. PMID: 27995997
a paracrine role for Hippo-mediated secretion of CXCL1 and CXCL2 in the production of anti-microbial peptides (beta-defensins), iNOS, NOX2 and pro-inflammatory molecules during mycobacterial infection of the host, is reported. PMID: 27883091
Taken together, the data of the present study demonstrated that TcpC can induce MIP2 production, which may contribute to the characteristic histological change associated with pyelonephritis. PMID: 28765918
mip-2 siRNA and the MIP-2 antibody can reduce the inflammatory effects induced by lipopolysaccharide in macrophage cells. PMID: 28662496
this study demonstrates that in vivo blocking of CXCL1 and CXCL2 can significantly reduce the Mycobacterium tuberculosis-induced bioactive IL-1beta production PMID: 28739876
These data identify suppression of CXCL2 and CXCL5 chemoattractant expression by 11beta-HSD1 as a novel mechanism with potential for regulation of neutrophil recruitment to the injured myocardium, and cardiac fibroblasts as a key site for intracellular glucocorticoid regeneration during acute inflammation following myocardial injury. PMID: 28522730
findings show that SRC-3 contributes to host defense against enteric bacteria, at least in part via upregulating CXCL2 expression to recruit neutrophils PMID: 28053238
p53-mediated induction of PAI-1 expression due to chronic CS exposure exacerbates lung inflammation through elaboration of CXCL1, CXCL2, and CXCR2. PMID: 26747783
Social defeat induced an exposure-dependent increase in mRNA levels of E-selectin, CXCL1, and CXCL2 that increased with additional days of social defeat. PMID: 25445193
MIP-2 directly impairs neonatal pulmonary endothelial cell migration in vitro. PMID: 26163511
SIRT2 regulates LPS induced proximal renal tubules CXCL2 protein expression. PMID: 25349202
miR26a/-26b-COX-2-MIP-2 loop regulates allergic inflammation and the feedback relationship between allergic inflammation and the enhanced tumorigenic and metastatic potential PMID: 25907560
huH1N1 virus PA and NA mediated increased MIP-2 expression early postinfection, resulting in substantial pulmonary neutrophilia with enhanced lung pathology and disease PMID: 25762737
Syndecan-1 is expressed in the parietal peritoneum microvasculature but does not regulate leukocyte recruitment and is not necessary for the presentation of the chemokine MIP-2 in this tissue. PMID: 25184228
Identified TLR2 and S100A8/S100A9 as key regulators of hepatic CXCL-2 expression and neutrophil recruitment. PMID: 24333183
Suggest anti-inflammatory action of daidzein in lung epithelial cells is mediated via a direct interaction with PARP-1, which inhibits RelA/p65 protein PARylation required for the transcriptional modulation of pro-inflammatory chemokines such as Cxcl2. PMID: 24632845
suppression of CXCL2 expression may contribute to the beneficial effect of Am80 as a therapeutic agent for intracerebral hemorrhage. PMID: 24659080
Neutrophil recruitment and the neutrophil cytokines, CXCL1/CXCL2, were suppressed in apo(a)transgenic mice in the abdominal aortic aneurysm model. PMID: 24650562
These data identify a cytokine circuit that involves IL-1beta-induced production of CXCL1 and CXCL2 and leads the recruitment of neutrophils to streptococcal infection sites. PMID: 25114117
Data indicate that levels of toll-like receptors TLR4/4-stimulated chemokines CXCL1 and CXCL2 were selectively enhanced in stressed macrophages via receptor-interacting protein kinase 1 (RIPK1). PMID: 24920846
Commensal bacteria-dependent select expression of CXCL2 contributes to periodontal tissue homeostasis. PMID: 23433011
these results strongly suggest that both lack of HOCl and accumulation of H2O2 due to MPO deficiency contribute to the up-regulation of MIP-2 production in mouse neutrophils stimulated with zymosan PMID: 23438680
Interferonalpha stimulates production of maladaptive proinflammatory CXCL2 by renal tubular cells. PMID: 23657854
the model that mast cells, optimally positioned in close proximity to the vasculature, initiate an early phase of neutrophil recruitment by releasing the chemoattractants CXCL1/CXCL2. PMID: 23645836
The results of this study suggested that MIP-2gamma mediates the pathogenesis of central nervous system disorders associated with neutrophil infiltration in the brain and decreased GLT-1 activity. PMID: 23234294
Systemic treatment with CXCL12 promotes a more stable atherosclerotic lesion phenotype and enhances the accumulation of smooth muscle progenitor cells in these lesions without promoting atherosclerosis. PMID: 23393393
these results suggest that increased production of reactive oxygen species by ATP-stimulated macrophages activates the signalling pathways that promote MIP-2 production which, in turn, induces neutrophil migration PMID: 22564028
TNF-alfa and CXCL-2 mRNAs is induced in mice infected with Leptospira. PMID: 22342618
results show that augmentation of the MIP-2/CXCR2 axis by hyperacetylation of histone H3 on the promoter region of MIP-2 and CXCR2 located in the injured peripheral nerve elicits chronic neuroinflammation through neutrophil accumulation PMID: 22135382
Lipopolysaccharide stimulates the induction of CXCL2 in bone marrow macrophages (BMMs), osteoclast precursors, at the transcription level. PMID: 21507677
MIP-2/CXCL2 induced by Chlamydia pneumoniae infection may initiate lymphocytic lung infiltration that can have long-term effects on tissue (ectopic lymphoid tissue formation) after clearance of active infection. PMID: 20840653
Rho-kinase signalling regulates TNF-alpha and CXC chemokine formation as well as lipid peroxidation in the reperfused colon. PMID: 20593289
The aim of this study was to determine whether acinar cells are a source of KC and MIP-2 and to understand their transcriptional regulation. PMID: 20671197
ATP increases chemokine CXCL2 production via both NFAT transcription factor and protein kinase C/MAP kinase signaling pathways by purinergic receptor P2X7 stimulation in microglia. PMID: 20477948
Receptor activator of NF-kappa B ligand-induced CXCL2 in osteoclast (OC) precursors plays a key role in the attachment, migration, differentiation, and function of OCs. PMID: 20357249
Data show that rotavirus-infected macrophages promote neutrophil chemotaxis in response to rhesus rotavirus type A. PMID: 20234283
The distribution of the functional IL-8 homologues CXCL1/KC, CXCL2/MIP-2, and CXCL5-6/LIX in resting and inflamed murine vessels, is examined. PMID: 20007247
Neutralization of inflammatory chemokine MIP-2 (CXCL2/GRO-beta) attenuates the inflammation, weight loss, and clinical presentation of heterologously infected mice without impacting bacterial burden. PMID: 20065113
These data give strong evidence that TRPC6 operates downstream to CXC-type Gq-protein-coupled chemokine receptors upon stimulation with MIP-2 and is crucial for the arrangement of filamentous actin in migrating neutrophils. PMID: 18983454
Migration of PMNs to the CNS coincided with increased expression of transcripts specific for the CXCR2 ELR-positive chemokine ligands CXCL1, CXCL2, and CXCL5 within the brain PMID: 19893623
Neutrophil-directed MIP-2 expression and protein secretion are low at the incisional site during the first 6 hrs after experimental surgical injury and are at a high level 24 hrs following injury. PMID: 11907123
in study of relevance of chemokine expression to selective migration of t-cells and the disease localization in murine graft-versus-host disease, Mip2 was found to be predominantly expressed in spleen, liver, and skin, and not heart. PMID: 12098066
Macrophage inflammatory protein-2 regulates corneal neovascularization induced by infection with Pseudomonas aeruginosa PMID: 12121220
NO generated after administration of E. coli serves as an important proinflammatory signal to up-regulate MIP-2 expression in vivo. PMID: 12165537
Plasma levelof thisprotein was decreased significantly by clodronic acid-encapsulating liposomes in sepsis induced by P.aeruginosa. PMID: 12604029
High tidal volume ventilation in absence of underlying injury induces intrapulmonary TNF-alpha and MIP-2 expression in mice. PMID: 12807894
These data show that macrophage inflammatory protein (MIP-2) is important for hepatocyte proliferation after partial hepatectomy and that pharmacological MIP-2 doses after hepatic injury accelerate hepatic regeneration. PMID: 12875976
induction of secretion in fibrosarcoma cells by NFkappaB and activation of lymphotoxin beta receptor PMID: 12957791
CXC chemokines play a fundamental role in colonic ischemia/reperfusion and that functional interference with CXC chemokines may protect against pathological inflammation in the colon PMID: 14583342

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.