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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.
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.
High MIF expression is associated with progressive multiple sclerosis.
The lack of MIF leads to disturbances of systemic and hippocampal insulin sensitivity, which are possibly responsible for memory deficits and anxiety, most likely through decreased PSA-NCAM-mediated neuroplasticity rather than through neurotrophic factors.
These data indicate the functional role of the MIF-COX-p53 axis in inflammation and cancer at the genomic and proteomic levels in COX-2-ablated cells.
Our results showed that MIF regulates MCP-1 expression in hepatocytes of injured liver via CD74, CD44, and p38 MAPK in an autocrine manner.
MIF is involved in the pathogenesis of AF, probably by down-regulating the protein and gene expression of Cx43 via ERK1/2 kinase activation
Endogenous MIF reduces the accumulation and toxicity of misfolded SOD1 in a mouse model of amyotrophic lateral sclerosis.
Gene expression of MIF was 30-fold higher in the heart, compared to skeletal muscle and protein expression of MIF was 3-fold higher in the heart compared to skeletal muscle.
renal tubular MIF is an endogenous renoprotective factor in progressive kidney diseases
The meta-analysis indicated the MIF-794 allele CATT7 and CATT8 may be a risk factor to increase the susceptibility of tuberculosis, which was confirmed by trial sequential analysis.
Study found that plasma MIF and CCL3 were significantly elevated in nasopharyngeal carcinoma (NPC) patients and identified plasma MIF and CCL3 as a promising and potential complementary biomarkers to EBV viral capsid antigen (VCA-IgA) for more effective detection of NPC. The combination of MIF, CCL3 with the traditional NPC tumor marker VCA-IgA may significantly improve the specificity of detection of NPC.
As the CD138+ multiple myeloma (MM) cell is chemosensitive, targeting MIF-1 and/or the pathways that it regulates could be a viable way to modulate stemness and chemosensitivity, which could in turn transform the treatment of MM.
MIF, through CD74, constitutively activates NF-kappaB to control mitochondrial dynamics and stability for promoting carcinogenesis via averting apoptosis
Youth carrying the MIF-173*C and CATT7 alleles displayed attenuated cortisol reactivity when compared with non-carriers. Children with the CATT7-173*C haplotype displayed lower cortisol reactivity to the stressor compared to those without this haplotype. Additionally, the CATT5-173*C and CATT6-173*C haplotypes were associated with lower self-reported anxiety ratings across the stressor.
Blocking of MIF and CD74 signaling in B cells triggered CXCR4 expression.
An inverse correlation between miR-451 and macrophage migration inhibitory protein (MIF) protein expression occurred in colon cancer cells.
Basement membrane protein ladinin-1 and the MIF-CD44-beta1 integrin signaling axis are implicated in laryngeal cancer metastasis
Study found that the expression of MIF in lepromatous leprosy (LL) patients is similar to healthy subjects both in serum and in skin. However, the expression of CD74 is significantly increased in the skin lesions of LL patients, although its participation in the physiopathology leprosy remains unclear.
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
our results strongly suggest that the MIF binding site is located in the sequence between the transmembrane and the membrane-distal trimerisation domain of CD74, and comprises at least amino acids 113-125 of CD74
Studied macrophage migration inhibitory factor (MIF) gene -173 G>C polymorphism SNP variant in a Turkish coronary artery disease (CAD) and type 2 diabetes (T2DM) cohort. Found the MIF gene variant may contribute to CAD risk through T2DM in Turkish population.
Study shows that acute myeloid leukemia (AML) in the bone marrow has increased levels of MIF compared to other tissues. Further data report that hypoxia acting through HIF1alpha is responsible for the up-regulation of MIF and subsequent proliferation and survival of AML in the tumor microenvironment.
Results suggest that MIF can induce a differential inflammatory response in physiological and pathological conditions with a predominance of a Th17 cytokine profile in PBMC from HS and an increase in TNF-alpha and IL-6 expression in PBMC from active SLE patients.
MIF plays a critical role in the initiation and progression of Guillain-Barre syndrome and experimental autoimmune neuritis
Modulation of oxidative stress by MIF inhibits the radiation-induced senescence.
These results highlight the importance of MIF overexpression in pancreatic ductal adenocarcinoma aggressiveness, and indicate that MIF may be a potential therapeutic target for pancreatic cancer
MIF serum levels are elevated in erythema nodosum leprosum patients as compared to controls.
Overall, the present work showed that MIF is a shear stress-sensitive cytokine and is transcriptionally regulated by KLF2, suggesting that laminar shear stress exerts its athero-protective effect in part by directly inhibiting pro-inflammatory MIF expression.
Hypoxia-induced angiogenesis is a complex process that involves distinct but also overlapping functions of HIF-1alpha and HIF- 2alpha in regard to angiogenesis, bioenergetic adaption and the redundant transcriptional induction of MIF.
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