HCSGD entry for MIF


1. General information

Official gene symbolMIF
Entrez ID4282
Gene full namemacrophage migration inhibitory factor (glycosylation-inhibiting factor)
Other gene symbolsGIF GLIF MMIF
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

color bar
This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0001516Prostaglandin biosynthetic processIDAbiological_process
GO:0002906Negative regulation of mature B cell apoptotic processIEAbiological_process
GO:0004167Dopachrome isomerase activityIDAmolecular_function
GO:0005102Receptor bindingIPImolecular_function
GO:0005125Cytokine activityIDAmolecular_function
GO:0005126Cytokine receptor bindingIPImolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005576Extracellular regionIDAcellular_component
GO:0005615Extracellular spaceIEAcellular_component
GO:0005737CytoplasmIEAcellular_component
GO:0006954Inflammatory responseIEAbiological_process
GO:0007166Cell surface receptor signaling pathwayIDAbiological_process
GO:0007569Cell agingIEAbiological_process
GO:0008283Cell proliferationIDAbiological_process
GO:0009986Cell surfaceIDAcellular_component
GO:0010629Negative regulation of gene expressionIDAbiological_process
GO:0010739Positive regulation of protein kinase A signalingIDAbiological_process
GO:0019752Carboxylic acid metabolic processIDAbiological_process
GO:0030330DNA damage response, signal transduction by p53 class mediatorIEAbiological_process
GO:0030890Positive regulation of B cell proliferationIDAbiological_process
GO:0031666Positive regulation of lipopolysaccharide-mediated signaling pathwayIEAbiological_process
GO:0032269Negative regulation of cellular protein metabolic processIEAbiological_process
GO:0033033Negative regulation of myeloid cell apoptotic processIEAbiological_process
GO:0033138Positive regulation of peptidyl-serine phosphorylationIDAbiological_process
GO:0042056Chemoattractant activityIDAmolecular_function
GO:0042327Positive regulation of phosphorylationIDAbiological_process
GO:0043030Regulation of macrophage activationNASbiological_process
GO:0043066Negative regulation of apoptotic processIDAbiological_process
GO:0043406Positive regulation of MAP kinase activityIEAbiological_process
GO:0043518Negative regulation of DNA damage response, signal transduction by p53 class mediatorIDAbiological_process
GO:0045087Innate immune responseIEAbiological_process
GO:0048146Positive regulation of fibroblast proliferationIDAbiological_process
GO:0050178Phenylpyruvate tautomerase activityIDAmolecular_function
GO:0050715Positive regulation of cytokine secretionIDAbiological_process
GO:0050731Positive regulation of peptidyl-tyrosine phosphorylationIDAbiological_process
GO:0050918Positive chemotaxisIDAbiological_process
GO:0061078Positive regulation of prostaglandin secretion involved in immune responseIEAbiological_process
GO:0061081Positive regulation of myeloid leukocyte cytokine production involved in immune responseIEAbiological_process
GO:0070207Protein homotrimerizationIPIbiological_process
GO:0070374Positive regulation of ERK1 and ERK2 cascadeIDAbiological_process
GO:0071157Negative regulation of cell cycle arrestIDAbiological_process
GO:0090238Positive regulation of arachidonic acid secretionIEAbiological_process
GO:0090344Negative regulation of cell agingIDAbiological_process
GO:1902166Negative regulation of intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorIDAbiological_process
GO:2000343Positive regulation of chemokine (C-X-C motif) ligand 2 productionIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.07845692030.50905040460.59086254651.0000000000

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Down-0.1030838830
GSE13712_SHEARUp0.2580197078
GSE13712_STATICDown-0.0059635268
GSE19018Up1.1833514235
GSE19899_A1Up0.1396810231
GSE19899_A2Up0.1792033169
PubMed_21979375_A1Up2.3873386607
PubMed_21979375_A2Up0.1790371589
GSE35957Down-0.7739471709
GSE36640Down-1.5277258159
GSE54402Up0.2871785089
GSE9593Up0.1484485845
GSE43922--
GSE24585--
GSE37065--
GSE28863_A1Down-0.5080169980
GSE28863_A2Up0.1722927926
GSE28863_A3Up0.2944852007
GSE28863_A4Down-0.0800713205
GSE48662Up0.1823283975

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Compound

Target

Confidence score

Uniprot

CHEMBL1253381CHEMBL20859P14174
CHEMBL1253382CHEMBL20859P14174
CHEMBL1253380CHEMBL20859P14174
CHEMBL524449CHEMBL20859P14174
CHEMBL1256332CHEMBL20859P14174
CHEMBL549389CHEMBL20859P14174
CHEMBL210755CHEMBL20859P14174
CHEMBL1706034CHEMBL20859P14174
CHEMBL358206CHEMBL20859P14174
CHEMBL554271CHEMBL20859P14174
CHEMBL377038CHEMBL20859P14174
CHEMBL523238CHEMBL20859P14174
CHEMBL1253546CHEMBL20859P14174
CHEMBL497598CHEMBL20859P14174
CHEMBL210858CHEMBL20859P14174
CHEMBL549864CHEMBL20859P14174
CHEMBL562483CHEMBL20859P14174
CHEMBL565030CHEMBL20859P14174
CHEMBL211882CHEMBL20859P14174
CHEMBL201593CHEMBL20859P14174
CHEMBL153064CHEMBL20859P14174
CHEMBL550268CHEMBL20859P14174
CHEMBL1256306CHEMBL20859P14174
CHEMBL1256155CHEMBL20859P14174
CHEMBL209776CHEMBL20859P14174
CHEMBL1289631CHEMBL20859P14174
CHEMBL554271CHEMBL20859P14174
CHEMBL1807868CHEMBL20859P14174
CHEMBL13486CHEMBL20859P14174
CHEMBL523238CHEMBL20859P14174
CHEMBL1255900CHEMBL20859P14174
CHEMBL1807940CHEMBL20859P14174
CHEMBL524449CHEMBL20859P14174
CHEMBL554783CHEMBL20859P14174
CHEMBL201091CHEMBL20859P14174
CHEMBL209588CHEMBL20859P14174
CHEMBL1254441CHEMBL20859P14174
CHEMBL153064CHEMBL20859P14174
CHEMBL558731CHEMBL20859P14174
CHEMBL209401CHEMBL20859P14174
CHEMBL496155CHEMBL20859P14174
CHEMBL556445CHEMBL20859P14174
CHEMBL1927069CHEMBL20859P14174
CHEMBL378265CHEMBL20859P14174
CHEMBL1807863CHEMBL20859P14174
CHEMBL556445CHEMBL20859P14174
CHEMBL1253383CHEMBL20859P14174
CHEMBL1253491CHEMBL20859P14174
CHEMBL1927060CHEMBL20859P14174
CHEMBL211769CHEMBL20859P14174
CHEMBL556512CHEMBL20859P14174
CHEMBL1807865CHEMBL20859P14174
CHEMBL558731CHEMBL20859P14174
CHEMBL377184CHEMBL20859P14174
CHEMBL1289845CHEMBL20859P14174
CHEMBL1701846CHEMBL20859P14174
CHEMBL556445CHEMBL20859P14174
CHEMBL554732CHEMBL20859P14174
CHEMBL1256370CHEMBL20859P14174
CHEMBL1253380CHEMBL20859P14174
CHEMBL1807937CHEMBL20859P14174
CHEMBL1807942CHEMBL20859P14174
CHEMBL210592CHEMBL20859P14174
CHEMBL208716CHEMBL20859P14174
CHEMBL550268CHEMBL20859P14174
CHEMBL1253382CHEMBL20859P14174
CHEMBL1807866CHEMBL20859P14174
CHEMBL1253544CHEMBL20859P14174
CHEMBL1927059CHEMBL20859P14174
CHEMBL1807933CHEMBL20859P14174
CHEMBL1927061CHEMBL20859P14174
CHEMBL549864CHEMBL20859P14174
CHEMBL1289632CHEMBL20859P14174
CHEMBL497802CHEMBL20859P14174
CHEMBL1807938CHEMBL20859P14174
CHEMBL559125CHEMBL20859P14174
CHEMBL1927066CHEMBL20859P14174
CHEMBL211822CHEMBL20859P14174
CHEMBL1807861CHEMBL20859P14174
CHEMBL1927058CHEMBL20859P14174
CHEMBL212313CHEMBL20859P14174
CHEMBL210858CHEMBL20859P14174
CHEMBL1807930CHEMBL20859P14174
CHEMBL210529CHEMBL20859P14174
CHEMBL1253185CHEMBL20859P14174
CHEMBL1253383CHEMBL20859P14174
CHEMBL1256233CHEMBL20859P14174
CHEMBL1927067CHEMBL20859P14174
CHEMBL199750CHEMBL20859P14174
CHEMBL153505CHEMBL20859P14174
CHEMBL210426CHEMBL20859P14174
CHEMBL208659CHEMBL20859P14174
CHEMBL78684CHEMBL20859P14174
CHEMBL497176CHEMBL20859P14174
CHEMBL559951CHEMBL20859P14174
CHEMBL538172CHEMBL20859P14174
CHEMBL1807862CHEMBL20859P14174
CHEMBL554271CHEMBL20859P14174
CHEMBL564237CHEMBL20859P14174
CHEMBL1807935CHEMBL20859P14174
CHEMBL1257587CHEMBL20859P14174
CHEMBL559555CHEMBL20859P14174
CHEMBL553881CHEMBL20859P14174
CHEMBL208658CHEMBL20859P14174
CHEMBL1807939CHEMBL20859P14174
CHEMBL211769CHEMBL20859P14174
CHEMBL1253492CHEMBL20859P14174
CHEMBL153425CHEMBL20859P14174
CHEMBL211823CHEMBL20859P14174
CHEMBL211991CHEMBL20859P14174
CHEMBL1255975CHEMBL20859P14174
CHEMBL1253492CHEMBL20859P14174
CHEMBL558731CHEMBL20859P14174
CHEMBL563301CHEMBL20859P14174
CHEMBL554732CHEMBL20859P14174
CHEMBL155103CHEMBL20859P14174
CHEMBL549389CHEMBL20859P14174
CHEMBL1807936CHEMBL20859P14174
CHEMBL209822CHEMBL20859P14174
CHEMBL210858CHEMBL20859P14174
CHEMBL559951CHEMBL20859P14174
CHEMBL1256235CHEMBL20859P14174
CHEMBL201289CHEMBL20859P14174
CHEMBL1927070CHEMBL20859P14174
CHEMBL1290060CHEMBL20859P14174
CHEMBL549864CHEMBL20859P14174
CHEMBL1807931CHEMBL20859P14174
CHEMBL199691CHEMBL20859P14174
CHEMBL1807934CHEMBL20859P14174
CHEMBL1253493CHEMBL20859P14174
CHEMBL553881CHEMBL20859P14174
CHEMBL1253491CHEMBL20859P14174
CHEMBL559555CHEMBL20859P14174
CHEMBL1807932CHEMBL20859P14174
CHEMBL1807941CHEMBL20859P14174
CHEMBL564237CHEMBL20859P14174
CHEMBL1289843CHEMBL20859P14174
CHEMBL1807864CHEMBL20859P14174
CHEMBL1807867CHEMBL20859P14174
CHEMBL554732CHEMBL20859P14174
CHEMBL559555CHEMBL20859P14174
CHEMBL1253381CHEMBL20859P14174
CHEMBL1253185CHEMBL20859P14174
CHEMBL1314602CHEMBL20859P14174
CHEMBL559125CHEMBL20859P14174
CHEMBL559258CHEMBL20859P14174
CHEMBL589351CHEMBL20859P14174
CHEMBL562483CHEMBL20859P14174
CHEMBL1927057CHEMBL20859P14174
CHEMBL1927064CHEMBL20859P14174
CHEMBL1255974CHEMBL20859P14174
CHEMBL1089054CHEMBL20858P14174
CHEMBL256315CHEMBL20858P14174
CHEMBL150302CHEMBL20858P14174
CHEMBL223198CHEMBL20858P14174
CHEMBL221727CHEMBL20858P14174
CHEMBL150254CHEMBL20858P14174
CHEMBL224032CHEMBL20858P14174
CHEMBL257350CHEMBL20858P14174
CHEMBL358640CHEMBL20858P14174
CHEMBL153406CHEMBL20858P14174
CHEMBL374968CHEMBL20858P14174
CHEMBL310854CHEMBL20858P14174
CHEMBL358206CHEMBL20858P14174
CHEMBL13486CHEMBL20858P14174
CHEMBL224086CHEMBL20858P14174
CHEMBL221832CHEMBL20858P14174
CHEMBL150485CHEMBL20858P14174
CHEMBL255892CHEMBL20858P14174
CHEMBL153064CHEMBL20858P14174
CHEMBL253951CHEMBL20858P14174
CHEMBL223319CHEMBL20858P14174
CHEMBL430433CHEMBL20858P14174
CHEMBL78684CHEMBL20858P14174
CHEMBL1161326CHEMBL20858P14174
CHEMBL256314CHEMBL20858P14174
CHEMBL223348CHEMBL20858P14174
CHEMBL223266CHEMBL20858P14174
CHEMBL153425CHEMBL20858P14174
CHEMBL78684CHEMBL20858P14174
CHEMBL384671CHEMBL20858P14174
CHEMBL222491CHEMBL20858P14174
CHEMBL253950CHEMBL20858P14174
CHEMBL153074CHEMBL20858P14174
CHEMBL79113CHEMBL20858P14174
CHEMBL402006CHEMBL20858P14174
CHEMBL431392CHEMBL20858P14174
CHEMBL153505CHEMBL20858P14174
CHEMBL153002CHEMBL20858P14174
CHEMBL256939CHEMBL20858P14174
CHEMBL155103CHEMBL20858P14174
CHEMBL257614CHEMBL20858P14174
CHEMBL311576CHEMBL20858P14174
CHEMBL255736CHEMBL20858P14174
CHEMBL358644CHEMBL20858P14174
CHEMBL221786CHEMBL20858P14174
CHEMBL496378CHEMBL20855P14174
CHEMBL497801CHEMBL20855P14174
CHEMBL498410CHEMBL20855P14174
CHEMBL1257465CHEMBL20855P14174
CHEMBL496373CHEMBL20855P14174
CHEMBL1256304CHEMBL20855P14174
CHEMBL1257355CHEMBL20855P14174
CHEMBL496155CHEMBL20855P14174
CHEMBL1288977CHEMBL20855P14174
CHEMBL1289632CHEMBL20855P14174
CHEMBL1289631CHEMBL20855P14174
CHEMBL1256370CHEMBL20855P14174
CHEMBL523238CHEMBL20855P14174
CHEMBL1256369CHEMBL20855P14174
CHEMBL498412CHEMBL20855P14174
CHEMBL1255976CHEMBL20855P14174
CHEMBL1289525CHEMBL20855P14174
CHEMBL523238CHEMBL20855P14174
CHEMBL1256332CHEMBL20855P14174
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  • Drugs

Name

Drug

Accession number

3,4-Dihydroxycinnamic AcidDB01880 EXPT01188
7-Hydroxy-2-Oxo-Chromene-3-Carboxylic Acid Ethyl EsterDB02728 EXPT03279
Citric AcidDB04272 EXPT00922
3-(4-HYDROXY-PHENYL)PYRUVIC ACIDDB07718 -
3-(4-HYDROXYPHENYL)-4,5-DIHYDRO-5-ISOXAZOLE-ACETIC ACID METHYL ESTERDB07888 -
4-HYDROXYBENZALDEHYDE O-(CYCLOHEXYLCARBONYL)OXIMEDB08333 -
3-FLUORO-4-HYDROXYBENZALDEHYDE O-(CYCLOHEXYLCARBONYL)OXIMEDB08334 -
4-HYDROXYBENZALDEHYDE O-(3,3-DIMETHYLBUTANOYL)OXIMEDB08335 -
6-HYDROXY-1,3-BENZOTHIAZOLE-2-SULFONAMIDEDB08765 -

  • MicroRNAs

    • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-451aMIMAT0001631MIRT000046ELISA//Luciferase reporter assay//Microarray//qRT-PCR//Western blotFunctional MTI19318487
hsa-miR-744-5pMIMAT0004945MIRT037678CLASHFunctional MTI (Weak)23622248
hsa-miR-769-5pMIMAT0003886MIRT039145CLASHFunctional MTI (Weak)23622248
hsa-miR-320aMIMAT0000510MIRT044670CLASHFunctional MTI (Weak)23622248
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    • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 6 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

26160351Recent reports that migration inhibitory factor (MIF) or periodic fasting rejuvenate old MSCs provide the opportunity to link intrinsic and extrinsic mechanisms of aging in novel and potentially medically important ways and may lead to anti-aging treatments that reorganize the epigenome to rejuvenate cells and tissues
24441872Macrophage migration inhibitory factor deficiency in chronic obstructive pulmonary disease
24441872MIF plasma concentrations were measured in a cohort of 224 human participants
24274936Macrophage migration inhibitory factor regulates AKT signaling in hypoxic culture to modulate senescence of human mesenchymal stem cells
24274936The hypoxic condition also delayed cellular senescence of hMSCs, increased activation of AKT signaling, and upregulated both intra- and extracellular levels of macrophage migration inhibitory factor (MIF) compared to the normoxic condition
24274936The hypoxic condition also delayed cellular senescence of hMSCs, increased activation of AKT signaling, and upregulated both intra- and extracellular levels of macrophage migration inhibitory factor (MIF) compared to the normoxic condition
24274936On the other hand, upregulated intra- and extracellular levels of MIF by stable MIF overexpression in normoxic culture increased the activation of AKT while decreasing mRNA expression of senescence-associated markers and increasing expression of potency-associated markers
24274936On the other hand, upregulated intra- and extracellular levels of MIF by stable MIF overexpression in normoxic culture increased the activation of AKT while decreasing mRNA expression of senescence-associated markers and increasing expression of potency-associated markers
24274936Taken together, our findings suggest that hMSCs in hypoxic culture produce endogenous MIF to activate AKT signaling to delay the progression of cellular senescence
20940041Control of p53 and NF-kappaB signaling by WIP1 and MIF: role in cellular senescence and organismal aging
20940041WIP1 (wildtype p53-induced phosphatase 1) and MIF (macrophage migration inhibitory factor) are signaling molecules which link together the p53 and NF-kappaB pathways via positive and negative feedback loops
20940041WIP1 (wildtype p53-induced phosphatase 1) and MIF (macrophage migration inhibitory factor) are signaling molecules which link together the p53 and NF-kappaB pathways via positive and negative feedback loops
20940041MIF is a pro-inflammatory cytokine which inhibits the function of p53 signaling whereas it is linked to NF-kappaB signaling via a positive feedback loop
20940041MIF knockout mice are healthier and live longer than their wild-type counterparts
20940041An increased level of MIF can support inflammatory responses via enhancing NF-kappaB signaling and repressing the function of p53
20940041We will review the findings linking WIP1 and MIF to specific signaling responses of p53 and NF-kappaB and discuss their role in the regulation of cellular senescence and organismal aging
17998063Macrophage migration inhibitory factor manipulation and evaluation in tumoral hypoxic adaptation
17998063Increasingly clear is an important regulatory role for hypoxia-inducible factor 1alpha (HIF-1alpha) in the expression of the cytokine/growth factor macrophage migration inhibitory factor (MIF)
17998063Increasingly clear is an important regulatory role for hypoxia-inducible factor 1alpha (HIF-1alpha) in the expression of the cytokine/growth factor macrophage migration inhibitory factor (MIF)
17998063The functional significance of hypoxia-induced MIF expression is revealed by findings demonstrating that HIF-1alpha-dependent MIF expression is necessary for hypoxia-induced evasion from cell senescence and that MIF is necessary for HIF-1alpha stabilization induced by hypoxia and prolyl hydroxylase (PHD) inhibitors
17998063The functional significance of hypoxia-induced MIF expression is revealed by findings demonstrating that HIF-1alpha-dependent MIF expression is necessary for hypoxia-induced evasion from cell senescence and that MIF is necessary for HIF-1alpha stabilization induced by hypoxia and prolyl hydroxylase (PHD) inhibitors
17998063The functional significance of hypoxia-induced MIF expression is revealed by findings demonstrating that HIF-1alpha-dependent MIF expression is necessary for hypoxia-induced evasion from cell senescence and that MIF is necessary for HIF-1alpha stabilization induced by hypoxia and prolyl hydroxylase (PHD) inhibitors
17998063As the importance of MIF in hypoxic adaptation of human tumors is now becoming fully realized, we review protocols designed to evaluate MIF expression, activity, and functional consequences in hypoxic environments
17998063As the importance of MIF in hypoxic adaptation of human tumors is now becoming fully realized, we review protocols designed to evaluate MIF expression, activity, and functional consequences in hypoxic environments
17142669HIF1alpha delays premature senescence through the activation of MIF
17142669Furthermore, we identify the macrophage migration inhibitory factor (MIF) as a crucial effector of HIF1alpha that delays senescence
17142669Furthermore, we identify the macrophage migration inhibitory factor (MIF) as a crucial effector of HIF1alpha that delays senescence
17142669Inhibition of MIF phenocopies loss of HIF1alpha
17142669Our findings highlight a novel role for HIF1alpha under aerobic conditions, and identify MIF as a target responsible for this function
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