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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.


MIP-2, CXCL2, macrophage inflammatory protein-2
chemokine involved in the pulmonary inflammatory response [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: MIP, Interleukin-6, CAN, V1a, HAD
Papers on MIP-2
Epithelial Nuclear Factor-x03BA;B Activation in Inflammatory Bowel Diseases and Colitis-Associated Carcinogenesis.
Watanabe et al., In Digestion, Feb 2016
Pro-tumorigenic cytokines such as interleukin (IL)-1β, IL-6 and macrophage inflammatory protein-2 at the lamina propria were increased in the setting of colitis and further increased in tumor tissues with upregulated epithelial TNFR2 and MLCK expressions in an animal model of CAC.
Helicobacter pullorum induces in murine macrophages nitric oxide release that promotes phagocytosis and killing.
Saraiva et al., Almozara, Spain. In Microbiology, Feb 2016
Interaction between H. pullorum and macrophages stimulated secretion of pro-inflammatory cytokines such as TNF-α, IL-1β, IL-6 and MIP-2.
SN50, a Cell-Permeable-Inhibitor of Nuclear Factor-κB, Attenuates Ventilator-Induced Lung Injury in an Isolated and Perfused Rat Lung Model.
Tsai et al., Taipei, Taiwan. In Shock, Feb 2016
VILI was demonstrated by increased pulmonary vascular permeability and lung weight gain, as well as by increased levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, myeloperoxidase, hydrogen peroxide, and macrophage inflammatory protein-2 in the bronchoalveolar lavage fluid.
Rosiglitazone pretreatment protects against lipopolysaccharide-induced fetal demise through inhibiting placental inflammation.
Xu et al., Hefei, China. In Mol Cell Endocrinol, Feb 2016
Additional experiment showed that rosiglitazone pretreatment inhibited LPS-induced expressions of tumor necrosis factor (Tnf)-α, interleukin (Il)-1β, Il-6, macrophage inflammatory protein (Mip)-2 and keratinocyte-derived chemokine (Kc) in mouse placenta.
CD26/dipeptidylpeptidase IV-chemokine interactions: double-edged regulation of inflammation and tumor biology.
Struyf et al., Leuven, Belgium. In J Leukoc Biol, Feb 2016
A large number of human chemokines, including CXCL2, CXCL6, CXCL9, CXCL10, CXCL11, CXCL12, CCL3L1, CCL4, CCL5, CCL11, CCL14, and CCL22, are cleaved by CD26; however, the efficiency is clearly influenced by the amino acids surrounding the cleavage site and although not yet proven, potentially affected by the chemokine concentration and interactions with third molecules.
Role of chitinase-like proteins in cancer.
Mitrofanova et al., In Biol Chem, Feb 2016
YKL-40 supports tumor angiogenesis by interaction with syndecan-1 on endothelial cells and metastatic spread by stimulating production of pro-inflammatory and pro-invasive factors MMP9, CCL2 and CXCL2.
Effect of M3 muscarinic acetylcholine receptor deficiency on collagen antibody-induced arthritis.
Lips et al., Gießen, Germany. In Arthritis Res Ther, Dec 2015
In M3R(-/-) mice, levels of neutrophil chemoattractant chemokine C-X-C-motif ligand 2 (CXCL2) as well as the pro-inflammatory cytokine interleukin-6 were already strongly increased in mice with low arthritis score, whereas WT mice only showed prominent expression of these markers when reaching high arthritis scores.
The proprotein convertase PC1/3 regulates TLR9 trafficking and the associated signaling pathways.
Salzet et al., Lille, France. In Sci Rep, Dec 2015
As a result, macrophages from PC1/3 KO mice and rat PC1/3-KD NR8383 macrophages secreted more pro-inflammatory cytokines such as TNF-α, IL6, IL1α and CXCL2.
Cytokines induce effector T-helper cells during invasive aspergillosis; what we have learned about T-helper cells?
Shankar et al., Solan, India. In Front Microbiol, 2014
Chemokines (CXCL1, CXCL2, CCL1, and CCL20) and their receptors associated to these TH-cells have also been observed in invasive aspergillosis.
A panoramic spectrum of complex interplay between the immune system and IL-32 during pathogenesis of various systemic infections and inflammation.
Sheikh et al., Lahore, Pakistan. In Eur J Med Res, 2014
It was found to stimulate the induction of various chemokines, pro-inflammatory cytokines including IL-1β, IL-6, IL-8, TNF-α and macrophage inflammatory protein-2 (MIP-2).
Perivascular leukocyte clusters are essential for efficient activation of effector T cells in the skin.
Kabashima et al., Kyoto, Japan. In Nat Immunol, 2014
Treatment with interleukin 1α (IL-1α) induced production of the chemokine CXCL2 by dermal macrophages, and DC clustering was suppressed by blockade of either the receptor for IL-1 (IL-1R) or the receptor for CXCL2 (CXCR2).
Crosstalk between sentinel and helper macrophages permits neutrophil migration into infected uroepithelium.
Engel et al., Bonn, Germany. In Cell, 2014
Such Ly6C(+) macrophages played a previously undescribed helper role: once recruited to the site of infection, they produced the cytokine TNF, which caused Ly6C(-) macrophages to secrete CXCL2.
CXCL2 synthesized by oral squamous cell carcinoma is involved in cancer-associated bone destruction.
Yamaguchi et al., Tokyo, Japan. In Biochem Biophys Res Commun, 2012
This is the first report showing the role of CXCL2 in cancer-associated bone destruction.
Extracellular ATP-stimulated macrophages produce macrophage inflammatory protein-2 which is important for neutrophil migration.
Abo et al., Niigata, Japan. In Immunology, 2012
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
A CXCL1 paracrine network links cancer chemoresistance and metastasis.
Massagué et al., New York City, United States. In Cell, 2012
Study uncovered a paracrine network, with the chemokines CXCL1 and 2 at its core, that mediates lung metastasis and chemoresistance in breast cancer.
ERK2-dependent activation of c-Jun is required for nontypeable Haemophilus influenzae-induced CXCL2 upregulation in inner ear fibrocytes.
Moon et al., Los Angeles, United States. In J Immunol, 2012
The rat spiral ligament fibrocytes were found to release CXCL2 in response to nontypeable H. influenzae via activation of c-Jun, leading to the recruitment of polymorphonuclear cells to the cochlea.
Induction of TNF-alfa and CXCL-2 mRNAs in different organs of mice infected with pathogenic Leptospira.
Martins et al., São Paulo, Brazil. In Microb Pathog, 2012
TNF-alfa and CXCL-2 mRNAs is induced in mice infected with Leptospira.
CXCL5 regulates chemokine scavenging and pulmonary host defense to bacterial infection.
Worthen et al., Philadelphia, United States. In Immunity, 2010
CXCL5 increased the plasma concentrations of CXCL1 and CXCL2 in part through inhibiting chemokine scavenging, impairing chemokine gradients and desensitizing CXCR2, which led to decreased neutrophil influx to the lung, increased lung bacterial burden and mortality in an Escherichia coli pneumonia model.
Lymphotoxin beta receptor signaling in intestinal epithelial cells orchestrates innate immune responses against mucosal bacterial infection.
Tumanov et al., Chicago, United States. In Immunity, 2010
We further determined that LTbetaR signaling in intestinal epithelial cells was required for recruitment of neutrophils to the infection site early during infection via production of CXCL1 and CXCL2 chemokines.
T cells dampen innate immune responses through inhibition of NLRP1 and NLRP3 inflammasomes.
Tschopp et al., Lausanne, Switzerland. In Nature, 2009
Inflammasome inhibition is observed for all tested NLRP1 (commonly called NALP1) and NLRP3 (NALP3 or cryopyrin) activators, whereas NLRC4 (IPAF) inflammasome function and release of other inflammatory mediators such as CXCL2, interleukin 6 and tumour necrosis factor are not affected.
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