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MIF was found to be essential for axis formation and neural development of Xenopus embryos.
After 30 hours, mcp1 becomes important for hair cell development in both maculae
Data show that the mif pathway is required for both sensory hair cell (HC) and sensory neuronal cell survival in the ear, for HC differentiation, semicircular canal formation, statoacoustic ganglion (SAG) development, and lateral line HC differentiation.
conclude that paracrine signals from endothelial cells via MIF decrease PC contraction and enhance pericyte-regulated neutrophil transmigration
MIF is involved in the pathogenic pathways activated by IL-23 and required to achieve full-blown psoriasiform dermatitis.
These data provide evidence of a renoprotective role of MIF.
Macrophage migration inhibitory factor mediates metabolic dysfunction induced by atypical antipsychotic therapy.
modification of MIF by haptens may have an immunomodulating role in contact allergy as well as in other immunotoxicity reactions
MIF has a dual role in kidney diseases, promoting (auto)immune glomerular diseases and limiting tubular cell injury in the setting of acute and chronic kidney diseases. These data suggest potential safety issues of systemic MIF targeted therapies, but also open new therapeutic options by targeting MIF or its analogues to tubular cells.
Similar to the MIF-knockout mice, treatment with RPS19, but not the mutant RPS19, suppressed cisplatin-induced acute kidney injury (AKI). Mechanistically, we found that both genetic knockout and pharmacological inhibition of MIF protected against AKI by inactivating the CD74-nuclear factor kappaB (NF-kappaB) signaling.
this study reports the effects of MIF genetic depletion and pharmacologic inhibition on murine experimental retinal detachment
Treatments with ISO-1 or compound 31 attenuates BLM-induced inflammation and fibrosis in lung, and prevents PH development in mice, suggesting that MIF is an important factor for idiopathic pulmonary fibrosis-Pulmonary hypertension development
Findings demonstrated a mechanistic division between Toxoplasma gondii (T. gondii)-induced intracellular reactive oxygen species generation and MIF activation, which may contribute to protective immunity against T. gondii infection in mouse.
A novel link between MIF and B cells.
MIF functions as a braking factor in curbing dopaminergic descending inhibition in peripheral nerve injury-induced hypersensitivity by mediating Th gene methylation through G9a/SUV39H1-associated H3K9 methylation.
MIF mediates LPS-induced cardiac dysfunction in murine cardiomyocytes, which was attenuated by MIF knockout.
MIF attenuates oxygen-glucose deprivation-induced cochlear cells injury. MIF enhances Nrf2 and inhibit oxidative stress in cochlear cells. Enhanced Akt-Nrf2-HO-1 pathway may mediate cochlear protection by MIF.
Data indicate function of macrophage migration inhibitory factor (MIF) as a regulator of the NLR family pyrin domain containing 3 (NLRP3) inflammasome complex in macrophages.
that macrophage migration inhibitory factor directly engages in dengue NS1-induced glycocalyx degradation and that targeting MIF may represent a possible therapeutic approach for preventing dengue-induced vascular leakage
our data suggests a model in which MIF expression in the primary tumor dampens the anti-tumor immune response, promoting tumor growth
MIF knockdown significantly accentuates hearing loss in young mice.
Mif mediates PAR4-induced bladder pain through urothelial HMGB1.
These results show although high systemic levels of MIF contribute to the development of type 2 diabetes mellitus pathology.
The present study demonstrated that elevated plasma levels of MIF at admission were associated with increased risk of post-stroke depression in the next three months and might be useful in identifying stroke at risk for post-stroke depression for early prevention strategies.
This study suggests that polymorphic alleles of MIF polymorphisms could act as sex-specific disease modifiers that increase the severity and progression of multiple sclerosis in male Mexican-Mestizo western population.
Alanine-scanning, functional competition by RLR-containing peptides, and molecular docking indicate that the RLR residues directly participate in contacts between MIF and CXCR4 and highlight the importance of charge-interactions at this interface. Identification of the RLR region adds important structural information to the MIF/CXCR4 binding-site that distinguishes this interface from CXCR4/CXCL12
Results indicate that the macrophage inhibitory factor (MIF)-173G/C (rs755622) polymorphism is a risk factor for childhood ALL development with respect to both homozygous and combined polymorphic genotypes.
The expression of MIF is increased in intervertebral disc tissue in patients with disc herniation.
Elevated MIF expression identifies high-risk patients within the cytogenetically normal pediatric acute lymphoblastic leukemia cases. It is associated with higher mortality rates, lower complete remission rates, lower overall survival and disease-free survival.
study suggested a strong association between MIF gene -173G > C polymorphism and osteoporosis in a Turkish population
The increased MIF secretion by the A549R and H460R cells could be suppressed by a multiple kinase inhibitor, dasatinib, which resulted in the decreased of oncogenic network of Src, CD155 and MIF expression
MIF levels in STEMI patients with or without diabetes can reflect acute cardiac function.
MIF -173 G > C (rs755622) Gene Polymorphism is associated with Tuberculosis Risk.
Patients with granulomatosis with polyangiitis have an increased frequency of high MIF expression CATT alleles. Higher Mif expression increases the incidence of mortality and pulmonary granulomas in Mif lung-Tg2.1 mice, while anti-MIF treatment protects these mice against death.
Results suggest that transcriptional regulation of macrophage migration inhibitory factor (MIF) and pursuing pituitary-specific positive transcription factor 1 (Pit-1) as a therapeutic target to treat MIF-mediated inflammatory disorders.
Results indicated that MIF-CD74 interaction directly regulated the expression of PD-L1 and helps melanoma tumor cells escape from antitumorigenic immune responses.
Overexpression of miR-451a can inhibit cell proliferation and colony formation by inhibiting MIF expression in HepG2 cells.
Our data suggest that MIF-173 polymorphisms may be associated with a higher incidence of prostate cancer compared to controls. We believe that MIF-173 GC+CC genotype can be used as a predictive factor for aggressive behavior of prostate cancer including pathological stage and Gleason scores as well as metastatic potential.
This study investigated a bypass mechanism of resistance to MEK inhibition in KRAS colorectal cancer (CRC). KRAS mutant colorectal cancer cells with refametinib, MEK inhibitor, induced MIF secretion and resulted in activation of STAT3 and MAPK.
In conclusion, the bovine ampulla and isthmus have higher MIF expression during the postovulatory phase.
plasma MIF concentrations may increase with age in months and parity, but do not change either before and after parturition or before and after postpartum first ovulation in Japanese black cows
Data suggest that, in obese cows, expression of MIF is suppressed in the ampulla and isthmus of Fallopian tubes as compared to normal-weight cows; however, MIF expression is also lower in Fallopian tubes of lean cows. The primary site of MIF expression in Fallopian tube ampulla/isthmus is the tunica mucosa. These studies were conducted in Japanese Black calves.
The objective of the present study was to determine if SNPs in 5' region of bovine MIF affects its promoter activity.
MIF plays a role in early embryo development, and further characterization of MIF expression and its regulation in the endometrium will add significantly to our understanding of early embryo-uterine interactions
The diverse actions of MIF within the immuno-neuroendocrine system may be a result of its occurrence in different isoforms and oligomerization states.
The purification of macrophage migration inhibitory factor (MIF) from bovine brain cytosol and its partial characterization are reported.
Transcription of MIF is induced by activation of PPARgamma2 and inhibited by excessive resistin.
The high activity of MIF in the maternal and fetal tissues throughout placentation and its expression in the nonpregnant uterus indicate a regulatory role for MIF during embryo receptivity and epitheliochorial placentation
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.
, L-dopachrome tautomerase
, Phenylpyruvate tautomerase
, macrophage migration inhibitory factor
, phenylpyruvate tautomerase
, Macrophage migration inhibitory factor
, delayed early response protein 6
, glycosylation-inhibiting factor
, glutathione-binding 13 kDa protein