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Literature summary for 5.3.3.12 extracted from

  • Merk, M.; Mitchell, R.A.; Endres, S.; Bucala, R.
    D-dopachrome tautomerase (D-DT or MIF-2): doubling the MIF cytokine family (2012), Cytokine, 59, 10-17.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 5.3.3.12

Protein Variants

Protein Variants Comment Organism
P1G inactive Homo sapiens

Localization

Localization Comment Organism GeneOntology No. Textmining
cytoplasm
-
 Homo sapiens 5737
-

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
L-dopachrome Homo sapiens
-
 5,6-dihydroxyindole-2-carboxylate
-
 ?

Organism

Organism UniProt Comment Textmining
Homo sapiens P14174
-
-

Source Tissue

Source Tissue Comment Organism Textmining
B cell
-
 Homo sapiens
-
dendritic cell
-
 Homo sapiens
-
eosinophil
-
 Homo sapiens
-
heart
-
 Homo sapiens
-
intestine
-
 Homo sapiens
-
kidney
-
 Homo sapiens
-
liver
-
 Homo sapiens
-
macrophage
-
 Homo sapiens
-
neutrophil
-
 Homo sapiens
-
serum
-
 Homo sapiens
-
skin
-
 Homo sapiens
-
spleen
-
 Homo sapiens
-
T cell
-
 Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
L-dopachrome
-
 Homo sapiens 5,6-dihydroxyindole-2-carboxylate
-
 ?

Synonyms

Synonyms Comment Organism
macrophage inhibitory factor
-
 Homo sapiens
MIF
-
 Homo sapiens

Expression

Organism Comment Expression
Homo sapiens the enzyme is induced by low levels of glucocorticoids in vitro and in vivo up

General Information

General Information Comment Organism
malfunction a tautomerase-null protein shows reduced binding affinity to the receptors CD74 and CXCR2, and an impaired ability to induce ERK1/2 MAP kinase activation. Cells expressing the tautomerase-null protein show reduced proliferative capacity, and enzyme-deficient mice show a reduced development in benzo[a]pyrene-induced skin tumors. Homo sapiens
physiological function the enzyme inhibits the migration of macrophages. The enzyme activates the MAP kinase cascade, modulates cell migration, and counter-acts the immunosuppressive effects of glucocorticoids. For many cell types, the enzyme also acts as an important survival or anti-apoptotic factor. the enzyme is essential for the production of pro-inflammatory mediators such as tissue necrosis factor alpha, interleukin-1beta, prostaglandin E2 and nitric oxide by macrophages. The enzyme is necessary for maximal c-jun-N-terminal kinase-dependent AP-1 transactivation and subsequent CXCL8 and VEGF transcription in human lung adenocarcinoma cells Homo sapiens