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Key Documents

SRP4251

Sigma-Aldrich

MIP-2 from mouse

recombinant, expressed in E. coli, ≥98% (SDS-PAGE), ≥98% (HPLC)

Synonyme(s) :

CXCL2, Gro-β, Growth- regulated protein β, MIP2-α, Macrophage inflammatory protein 2-α, chemokine (C-X-C motif) ligand 2

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About This Item

Numéro MDL:
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.32

Source biologique

mouse

Produit recombinant

expressed in E. coli

Pureté

≥98% (HPLC)
≥98% (SDS-PAGE)

Forme

lyophilized

Poids mol.

~7.8 kDa

Conditionnement

pkg of 20 μg

Impuretés

endotoxin, tested

Numéro d'accès NCBI

Conditions d'expédition

wet ice

Température de stockage

−20°C

Informations sur le gène

mouse ... Cxcl2(20310)

Description générale

MIP-2 (microphage inflammatory protein-2), or Cxcl2 ((C-X-C motif) ligand 2), was initially recognized as a 6kDa protein released by an LPS (lipopolysaccharide)-stimulated mouse macrophage cell line. It belongs to the chemokine family which contains 6-14kDa, heparin-binding cytokines. It is a member of the a (CXC) chemokine family, where any amino acid separates both conserved cysteines.
Mouse MIP-2 is a 7.8kDa protein containing 73 amino acid residues including the ‘RLR′ motif common to the CXC chemokine family that bind to CXCR1 or CXCR2.

Actions biochimiques/physiologiques

MIP-2 (microphage inflammatory protein-2), or Cxcl2 ((C-X-C motif) ligand 2), is a functional homolog of human IL-8 (interleukin) in mice, and like human IL-8 it induces a potent neutrophil chemotactic activity. It might be critical in the recruitment and influx of immune cells in inflammation and infection. Murine encephalomyelitis virus of Theiler (TMEV) induces the expression of MIP-2 in genetically susceptible but not in resistant mouse strains. In mice, in acute and chronic liver injury, TLR2 (Toll-like receptor)/S100A9/MIP-2 signaling pathways is crucial for neutrophil recruitment, and this might have therapeutic implications in selectively manipulating neutrophils in liver disease while circumventing normal wound healing and regenerative responses.

Forme physique

Sterile filtered and then lyophilized without additives.

Reconstitution

Centrifuge the vial prior to opening. Avoid freeze-thaw cycles.
Reconstitute in water to a concentration of 0.1-1 mg/mL. The solution can be diluted into other aqueous buffers.

Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

Theiler's virus induces the MIP-2 chemokine (CXCL2) in astrocytes from genetically susceptible but not from resistant mouse strains.
Rubio N et al
Cellular Immunology, 239(1), 31-40 (2006)
A TLR2/S100A9/CXCL-2 signaling network is necessary for neutrophil recruitment in acute and chronic liver injury in the mouse.
Moles A et al
Journal of Hepatology, 60(4), 782-791 (2014)
Stéphanie Val et al.
JAMA otolaryngology-- head & neck surgery, 141(11), 997-1005 (2015-10-30)
Chronic otitis media with effusion is characterized by middle ear secretion of mucin glycoproteins, predominantly MUC5B; MUC5AC, the other secretory mucin studied frequently, has also been identified in the middle ear. Emerging evidence suggests a dichotomous role for these mucins
Hassan O J Morad et al.
Scientific reports, 12(1), 11078-11078 (2022-07-01)
Immune cell chemotaxis to the sites of pathogen invasion is critical for fighting infection, but in life-threatening conditions such as sepsis and Covid-19, excess activation of the innate immune system is thought to cause a damaging invasion of immune cells
Lingtao Luo et al.
American journal of physiology. Lung cellular and molecular physiology, 307(7), L586-L596 (2014-08-03)
Excessive neutrophil activation is a major component in septic lung injury. Neutrophil-derived DNA may form extracellular traps in response to bacterial invasions. The aim of the present study was to investigate the potential role of neutrophil extracellular traps (NETs) in

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