macrophage migration inhibitory factor
Direct association of thioredoxin-1 (TRX) with macrophage migration inhibitory factor (MIF): regulatory role of TRX on MIF internalization and signaling
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) ...
macrophage migration inhibitory factor
Involvement of CD74 in head and neck squamous cell carcinomas.
Mons, Belgium. In J Cancer Res Clin Oncol, Jun 2014
PURPOSE: While macrophage migration inhibitory factor (MIF) has been extensively studied in the context of inflammation and inflammatory disorders, less work has been devoted to its involvement in cancer, notably in neoplastic progression.
Antral atrophy, intestinal metaplasia, and preneoplastic markers in Mexican children with Helicobacter pylori-positive and Helicobacter pylori-negative gastritis.
Milwaukee, United States. In Ann Diagn Pathol, Jun 2014
Antral biopsies from 82 Mexican children (mean age, 8.3 ± 4.8 years) with chronic gastritis (36 H pylori+, 46 H pylori-) were examined for gastritis activity, atrophy, intestinal metaplasia (IM), and immunohistochemical expression of gastric carcinogenesis biomarkers caudal type homeobox 2 (CDX2), ephrin type-B receptor 4 (EphB4), matrix metalloproteinase 3 (MMP3), macrophage migration inhibitory factor (MIF), p53, β-catenin, and E-cadherin.
Cytokine patterns in patients with cancer: a systematic review.
Stockholm, Sweden. In Lancet Oncol, May 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).
Corticosteroid resistance in patients with asthma and chronic obstructive pulmonary disease.
London, United Kingdom. In J Allergy Clin Immunol, Mar 2013
Other mechanisms proposed include increased expression of GRβ, which competes with and thus inhibits activated GRα; increased secretion of macrophage migration inhibitory factor; competition with the transcription factor activator protein 1; and reduced expression of histone deacetylase (HDAC) 2. HDAC2 appears to mediate the action of steroids to switch off activated inflammatory genes, but in patients with COPD, patients with severe asthma, and smokers with asthma, HDAC2 activity and expression are reduced by oxidative stress through activation of phosphoinositide 3-kinase δ.
Hepatocyte nuclear factor (HNF)-1β and its physiological importance in endometriosis.
Nara, Japan. In Biomed Rep, 2013
HNF-1β regulates tissue-specific gene expression in endometriosis, as well as the expression of several genes, including CD44v9, which binds several molecules, including hyaluronan, epidermal growth factor receptor (EGFR), leukemia-associated Rho-guanine nucleotide exchange factor (LARG), IQ motif containing GTPase activating protein 1 (IQGAP1), macrophage migration inhibitory factor (MIF), major histocompatibility complex, class II invariant chain (CD74), cystine transporter subunit (xCT), Fas and extracellular matrix (ECM) proteins.
Dual nature of the adaptive immune system in lampreys.
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.
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.