scholarly journals Insight into the biology of Macrophage Migration Inhibitory Factor (MIF) revealed by the cloning of its cell surface receptor

Cell Research ◽  
2006 ◽  
Vol 16 (2) ◽  
pp. 162-168 ◽  
Author(s):  
Lin Leng ◽  
Richard Bucala
Keyword(s):  
Cell Surface ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Cell Surface Receptor ◽  
Macrophage Migration ◽  
Surface Receptor ◽  
Insight Into

scholarly journals CD74 is a novel transcription regulator

2016 ◽  
Vol 114 (3) ◽  
pp. 562-567 ◽  
Author(s):  
Naama Gil-Yarom ◽  
Lihi Radomir ◽  
Lital Sever ◽  
Matthias P. Kramer ◽  
Hadas Lewinsky ◽  
...  
Keyword(s):  
Cell Survival ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Cell Surface Receptor ◽  
Macrophage Migration ◽  
Regulation Of Expression ◽  
Surface Receptor ◽  
Related Transcription Factor ◽  
A Cell

CD74 is a cell-surface receptor for the cytokine macrophage migration inhibitory factor. Macrophage migration inhibitory factor binding to CD74 induces its intramembrane cleavage and the release of its cytosolic intracellular domain (CD74–ICD), which regulates cell survival. In the present study, we characterized the transcriptional activity of CD74–ICD in chronic lymphocytic B cells. We show that following CD74 activation, CD74–ICD interacts with the transcription factors RUNX (Runt related transcription factor) and NF-κB and binds to proximal and distal regulatory sites enriched for genes involved in apoptosis, immune response, and cell migration. This process leads to regulation of expression of these genes. Our results suggest that identifying targets of CD74 will help in understanding of essential pathways regulating B-cell survival in health and disease.

scholarly journals Substance P Increases Cell-Surface Expression of CD74 (Receptor for Macrophage Migration Inhibitory Factor): In Vivo Biotinylation of Urothelial Cell-Surface Proteins

2009 ◽  
Vol 2009 ◽  
pp. 1-8 ◽  
Author(s):  
Katherine L. Meyer-Siegler ◽  
Shen-Ling Xia ◽  
Pedro L. Vera
Keyword(s):  
Substance P ◽  
Cell Surface ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Urothelial Cell ◽  
Inhibitory Factor ◽  
Cell Surface Expression ◽  
Macrophage Migration ◽  
Urothelial Cells

Macrophage migration inhibitory factor (MIF), an inflammatory cytokine, and its receptor CD74 are upregulated by bladder inflammation. MIF-mediated signal transduction involves binding to cell-surface CD74, this study documents, in vivo, MIF-CD74interactions at the urothelial cell surface. N-hydroxysulfosuccinimide biotin ester-labeled surface urothelial proteins in rats treated either with saline or substance P (SP, 40 μg/kg). The bladder was examined by histology and confocal microscopy. Biotinylated proteins were purified by avidin agarose, immunoprecipitated with anti-MIF or anti-CD74 antibodies, and detected with strepavidin-HRP. Only superficial urothelial cells were biotinylated. These cells contained a biotinylated MIF/CD74 cell-surface complex that was increased in SP-treated animals. SP treatment increased MIF and CD74 mRNA in urothelial cells. Our data indicate that intraluminal MIF, released from urothelial cells as a consequence of SP treatment, interacts with urothelial cell-surface CD74. These results document that our previously described MIF-CD74 interaction occurs at the urothelial cell surface.

scholarly journals A Tautomerase-Null Macrophage Migration-Inhibitory Factor (MIF) Gene Knock-In Mouse Model Reveals That Protein Interactions and Not Enzymatic Activity Mediate MIF-Dependent Growth Regulation

2009 ◽  
Vol 29 (7) ◽  
pp. 1922-1932 ◽  
Author(s):  
Günter Fingerle-Rowson ◽  
Dayananda Rao Kaleswarapu ◽  
Corinna Schlander ◽  
Nazanin Kabgani ◽  
Tania Brocks ◽  
...  
Keyword(s):  
Protein Interactions ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Growth Regulation ◽  
Enzymatic Reaction ◽  
Growth Control ◽  
Inhibitory Factor ◽  
Cell Surface Receptor ◽  
Macrophage Migration

ABSTRACT Macrophage migration-inhibitory factor (MIF) is an upstream regulator of innate immunity and a potential molecular link between inflammation and cancer. The unusual structural homology between MIF and certain tautomerases, which includes both a conserved substrate-binding pocket and a catalytic N-terminal proline (Pro1), has fueled speculation that an enzymatic reaction underlies MIF's biologic function. To address the functional role of the MIF tautomerase activity in vivo, we created a knock-in mouse in which the endogenous mif gene was replaced by one encoding a tautomerase-null, Pro1→Gly1 MIF protein (P1G-MIF). While P1G-MIF is completely inactive catalytically, it maintains significant, albeit reduced, binding to its cell surface receptor (CD74) and to the intracellular binding protein JAB1/CSN5. P1G-MIF knock-in mice (mif P1G/P1G ) and cells derived from these mice show a phenotype in assays of growth control and tumor induction that is intermediate between those of the wild type (mif +/+) and complete MIF deficiency (mif − / −). These data provide genetic evidence that MIF's intrinsic tautomerase activity is dispensable for this cytokine's growth-regulatory properties and support a role for the N-terminal region in protein-protein interactions.

scholarly journals Brain Miffed by Macrophage Migration Inhibitory Factor

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Nic E. Savaskan ◽  
Günter Fingerle-Rowson ◽  
Michael Buchfelder ◽  
Ilker Y. Eyüpoglu
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Redox Regulation ◽  
Redox Balance ◽  
Cellular Systems ◽  
Inhibitory Factor ◽  
Cell Surface Receptor ◽  
Brain Diseases ◽  
Macrophage Migration ◽  
Dopachrome Tautomerase

Macrophage migration inhibitory factor (MIF) is a cytokine which also exhibits enzymatic properties like oxidoreductase and tautomerase. MIF plays a pivotal role in innate and acquired immunity as well as in the neuroendocrine axis. Since it is involved in the pathogenesis of acute and chronic inflammation, neoangiogenesis, and cancer, MIF and its signaling components are considered suitable targets for therapeutic intervention in several fields of medicine. In neurodegenerative and neurooncological diseases, MIF is a highly relevant, but still a hardly investigated mediator. MIF operates via intracellular protein-protein interaction as well as in CD74/CXCR2/CXCR4 receptor-mediated pathways to regulate essential cellular systems such as redox balance, HIF-1, and p53-mediated senescence and apoptosis as well as multiple signaling pathways. Acting as an endogenous glucocorticoid antagonist, MIF thus represents a relevant resistance gene in brain tumor therapies. Alongside this dual action, a functional homolog-annotated D-dopachrome tautomerase/MIF-2 has been uncovered utilizing the same cell surface receptor signaling cascade as MIF. Here we review MIF actions with respect to redox regulation in apoptosis and in tumor growth as well as its extracellular function with a focus on its potential role in brain diseases. We consider the possibility of MIF targeting in neurodegenerative processes and brain tumors by novel MIF-neutralizing approaches.

287: Macrophage Migration Inhibitory Factor and its Receptor CD74 are Upregulated in the Urothelium of Interstitial Cystitis Patients

2006 ◽  
Vol 175 (4S) ◽  
pp. 95-96 ◽  
Author(s):  
Pedro L. Vera ◽  
Kenneth A. lczkowski ◽  
Robert M. Moldwin ◽  
Leslie Kushner ◽  
Katherine L. Meyer-Siegler
Keyword(s):  
Interstitial Cystitis ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration
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