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D-dopachrome tautomerase converts D-dopachrome into 5,6-dihydroxyindole. Additionally we are shipping D-Dopachrome Tautomerase Antibodies (88) and D-Dopachrome Tautomerase Proteins (18) and many more products for this protein.
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cardiomyocyte secretion of DDT has important autocrine/paracrine effects during ischemia-reperfusion that protect the heart against injury
These data point to a potential involvement of D-dopachrome tautomerase activity in the mature mouse brain, and suggest some functional and evolutionary relationship between innate immunity and tautomerization of D-dopachrome in mammalian species
These data indicate that D-DT is a MIF-like cytokine.
D-dopachrome tautomerase transcription may be regulated in a cell-dependent manner, and was enhanced by AMPK activation in SGBS adipocytes through inhibiting the mTOR signaling
The knockdown of D-DT and MIF, individually and additively, inhibited the proliferation, migration, and invasion in HeLa and SiHa cells and restrained the growth of xenograft tumor.
These results have implications for the manner in which D-DT and MIF compete with each other for binding to the CD74 receptor and for the relative potency of DRa1-MOG-35-55 and RTL1000 for competitive inhibition of D-DT and MIF binding and activation through CD74.
Study demonstrated that DDT was over- expressed in pancreatic ductal adenocarcinoma (PDAC) tissues and cell lines in a pattern correlated with MIF, and knockdown of DDT and MIF in PANC- 1 cells cooperatively inhibited cell proliferation, invasion and tumor formation. The tautomerase activities of both MIF and DDT are required for their negative regulatory role in p53 and their tumor-promoting functions.
DDT was increased in burn patients.
Gene expression level of DDT is significantly higher in AD patients when compared to normal controls.
High MIF-2 levels are predictive of the development of organ dysfunction in myocardial ischemia reperfusion injury.
Both p53 wildtype and mutant human lung adenocarcinoma tumors rely on MIF family members for maximal cell growth and survival.
findings identify DDT as a functionally redundant but more potent cytokine to MIF in cancer and suggest that current attempts to inhibit MIF signaling may fail because of DDT compensation.
D-dopachrome tautomerase secreted from adipocytes acts on preadipocytes to promote IL-6 expression and to inhibit adipogenesis by suppressing the induction of genes encoding adipogenic regulators
DDT acts on adipocytes to regulate lipid metabolism through AMPK and/or PKA pathway(s) and improves glucose intolerance caused by obesity.
D-DT-dependent beta-catenin stabilization is regulated by COX-2 expression, suggesting the existence of an amplification loop between COX-2- and beta-catenin-mediated transcription in these cells
role of tautomerase active site of macrophage migration inhibitory factor as a potential target for discovery of novel anti-inflammatory agents
DDT is for the first time demonstrated in the skin and can be related to inflammation, and its covariation with MIF strengthens this observation.
D-dopachrome tautomerase (D-DT) and macrophage migration inhibitory factor, individually and additively, promote vascular endothelial growth factor and CXCL8 expression in human lung adenocarcinoma cell lines.
D-dopachrome tautomerase converts D-dopachrome into 5,6-dihydroxyindole. The DDT gene is related to the migration inhibitory factor (MIF) in terms of sequence, enzyme activity, and gene structure. DDT and MIF are closely linked on chromosome 22.
, D-dopachrome tautomerase-B
, D-dopachrome decarboxylase
, D-dopachrome tautomerase
, D-dopachrome decarboxylase-A
, D-dopachrome tautomerase-A
, phenylpyruvate tautomerase II
, dopachrome isomerase
, LOW QUALITY PROTEIN: D-dopachrome decarboxylase