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Macrophage migration inhibitory factor

macrophage migration inhibitory factor, GIF
This gene encodes a lymphokine involved in cell-mediated immunity, immunoregulation, and inflammation. It plays a role in the regulation of macrophage function in host defense through the suppression of anti-inflammatory effects of glucocorticoids. This lymphokine and the JAB1 protein form a complex in the cytosol near the peripheral plasma membrane, which may indicate an additional role in integrin signaling pathways. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, HAD, Interleukin-6, V1a, AGE
Papers using macrophage migration inhibitory factor antibodies
Direct association of thioredoxin-1 (TRX) with macrophage migration inhibitory factor (MIF): regulatory role of TRX on MIF internalization and signaling
Hofer Stefan et al., In Mediators of Inflammation, 2008
... R&D Systems, Minneapolis, MN, USA), Human Thioredoxin-1 (Human TRX1, LabFrontier Co., Ltd, Seoul, Korea), and Macrophage Migration Inhibitory Factor (Human MIF, RayBiotech, Inc., Norcross, GA, USA) ...
Papers on macrophage migration inhibitory factor
Targeting MIF in Cancer: Therapeutic Strategies, Current Developments, and Future Opportunities.
Donnelly et al., Dublin, Ireland. In Med Res Rev, Feb 2016
The multifunctional pro-inflammatory protein macrophage migration inhibitory factor (MIF) occupies a central role in the inflammatory pathway and has been implicated in the tumorigenesis, angiogenesis, and metastasis of many cancer phenotypes.
MIF reflects tissue damage rather than inflammation in post-cardiac arrest syndrome in a real life cohort.
Luedike et al., Essen, Germany. In Resuscitation, Feb 2016
We here examined the role of the pro-inflammatory cytokine macrophage migration inhibitory factor (MIF) in post-cardiac arrest syndrome.
MicroRNA‑451 inhibits neuroblastoma proliferation, invasion and migration by targeting macrophage migration inhibitory factor.
Hao et al., Xi'an, China. In Mol Med Report, Feb 2016
Furthermore, the present study demonstrated that macrophage migration inhibitory factor (MIF) was regulated directly by miR‑451 and was a critical mediator of the biological effects of miR‑451 in NB.
Transcription factor ICBP90 regulates the MIF promoter and immune susceptibility locus.
Bucala et al., In J Clin Invest, Feb 2016
UNASSIGNED: The immunoregulatory cytokine macrophage migration inhibitory factor (MIF) is encoded in a functionally polymorphic locus that is linked to the susceptibility of autoimmune and infectious diseases.
Inflammatory bowel disease as a disorder of an imbalance between pro- and anti-inflammatory molecules and deficiency of resolution bioactive lipids.
Das, Federal Way, United States. In Lipids Health Dis, Dec 2015
The inflammatory process seen in inflammatory bowel disease (IBD) is due to excess production of pro-inflammatory cytokines interleukin-1 (IL-1), IL-6, tumor necrosis factor-α (TNF-α), interferons (IFNs), macrophage migration inhibitory factor (MIF), HMGB1 (high mobility group B1) and possibly, a reduction in anti-inflammatory cytokines IL-10, IL-4, and transforming growth factor-β (TGF-β).
[The relationship between mRNA level of glucocorticoid receptor α, heat shock protein 90, protein level of macrophage migration inhibitory factor and glucocorticoid resistance in systemic lupus erythematosus].
Zhang et al., Dalian, China. In Zhonghua Nei Ke Za Zhi, Nov 2015
OBJECTIVE: To investigate the mRNA level of glucocorticoid receptor α (GRα) and heat shock protein 90 (HSP90) in peripheral blood mononuclear cells (PBMCs) and the plasma protein level of macrophage migration inhibitory factor (MIF) in patients with systemic lupus erythematosus (SLE) and to analyze their association with glucocorticoid (GC) resistance.
Secreted and O-GlcNAcylated MIF binds to the human EGF receptor and inhibits its activation.
Lu et al., Houston, United States. In Nat Cell Biol, Oct 2015
We found that human macrophage migration inhibitory factor (MIF) is O-GlcNAcylated at Ser 112/Thr 113 at its carboxy terminus.
Role of chemokine receptors CXCR4 and CXCR7 for platelet function.
Gawaz et al., Tübingen, Germany. In Biochem Soc Trans, Sep 2015
This review summarizes the relative expression of CXC chemokine receptor 4 (CXCR4) and CXCR7 in platelets, their dynamic trafficking in presence of ligands like chemokine C-X-C-motif ligand 11 (CXCL11), CXCL12 and MIF (macrophage migration inhibitory factor); how these receptors differentially mediate the functional and survival response to the chemokines CXCL11, CXCL12 and MIF.
Pancreatic cancer exosomes initiate pre-metastatic niche formation in the liver.
Lyden et al., New York City, United States. In Nat Cell Biol, Jun 2015
We found that macrophage migration inhibitory factor (MIF) was highly expressed in PDAC-derived exosomes, and its blockade prevented liver pre-metastatic niche formation and metastasis.
25 Years On: A Retrospective on Migration Inhibitory Factor in Tumor Angiogenesis.
Mitchell et al., Louisville, United States. In Mol Med, 2014
Twenty-five years ago marked the publication of the first report describing a functional contribution by the cytokine, macrophage migration inhibitory factor (MIF), to tumor-associated angiogenesis and growth.
CD74 in Kidney Disease.
Sanchez-Niño et al., Madrid, Spain. In Front Immunol, 2014
CD74 (invariant MHC class II) regulates protein trafficking and is a receptor for macrophage migration inhibitory factor (MIF) and d-dopachrome tautomerase (d-DT/MIF-2).
Diversity and Inter-Connections in the CXCR4 Chemokine Receptor/Ligand Family: Molecular Perspectives.
Noels et al., Aachen, Germany. In Front Immunol, 2014
CXCL12 was long thought to be the sole CXCR4 ligand, but more recently the atypical chemokine macrophage migration inhibitory factor (MIF) was identified as an alternative, non-cognate ligand for CXCR4 and shown to mediate chemotaxis and arrest of CXCR4-expressing T-cells.
Cytokine patterns in patients with cancer: a systematic review.
Lippitz, Stockholm, Sweden. In Lancet Oncol, 2013
In this Review of published clinical studies of patients with cancer, expression and interplay of the following cytokines are examined: interleukin 2, interleukin 6, interleukin 8, interleukin 10, interleukin 12, interleukin 18, tumour necrosis factor α (TNFα), transforming growth factor β (TGFβ), interferon-γ, HLA-DR, macrophage migration inhibitory factor (MIF), and C-X-C motif chemokine receptor 4 (CXCR4).
A novel allosteric inhibitor of macrophage migration inhibitory factor (MIF).
Anthony et al., New Haven, United States. In J Biol Chem, 2012
p425 blocked the interaction of MIF with its receptor, CD74, and interfered with the pro-inflammatory activities of the cytokine.
Macrophage migration inhibitory factor covalently complexed with phenethyl isothiocyanate.
Wilbanks et al., Dunedin, New Zealand. In Acta Crystallogr Sect F Struct Biol Cryst Commun, 2012
structure of the modified MIF obtained from X-ray diffraction data to 1.64 A resolution is presented
Macrophage migration inhibitory factor is involved in a positive feedback loop increasing aromatase expression in endometriosis.
Akoum et al., Québec, Canada. In Am J Pathol, 2012
The present study revealed the existence of a local positive feedback loop by which estrogen acts directly on ectopic endometrial cells to upregulate the expression of MIF, which, in turn, displays the capability of inducing the expression of aromatase.
Macrophage migration inhibitory factor antagonist blocks the development of endometriosis in vivo.
Akoum et al., Québec, Canada. In Plos One, 2011
Specific inhibition of MIF alters endometriotic tissue growth and progression in vivo and may represent a promising potential therapeutic avenue for endometriosis.
Macrophage migration inhibitory factor is enhanced in acute coronary syndromes and is associated with the inflammatory response.
Geisler et al., Tübingen, Germany. In Plos One, 2011
Study demonstrated enhanced expression of macrophage migration inhibitory factor in acute coronary syndromes.
Dual nature of the adaptive immune system in lampreys.
Cooper et al., Atlanta, United States. In Nature, 2009
Conversely, VLRA lymphocytes respond preferentially to a classical T-cell mitogen and upregulate the expression of the pro-inflammatory cytokine genes interleukin-17 (IL-17) and macrophage migration inhibitory factor (MIF).
Glucocorticoid resistance in inflammatory diseases.
Adcock et al., London, United Kingdom. In Lancet, 2009
Several molecular mechanisms of glucocorticoid resistance have now been identified, including activation of mitogen-activated protein (MAP) kinase pathways by certain cytokines, excessive activation of the transcription factor activator protein 1, reduced histone deacetylase-2 (HDAC2) expression, raised macrophage migration inhibitory factor, and increased P-glycoprotein-mediated drug efflux.
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