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1 on of an early zebrafish melanoblast marker, dopachrome tautomerase.
2 melanocytes, Tyr, Tyr-related protein 1, and dopachrome tautomerase accumulated in enlarged granules
3 also has been described recently to exhibit dopachrome tautomerase activity and to be structurally h
4 yphenylalanine oxidation drop rapidly, while DOPAchrome tautomerase activity increases and dihydroxyi
6 methyl ester (ISO-1), an inhibitor of MIF d-dopachrome tautomerase activity, reveals that ISO-1 bind
7 nd of the melanogenic enzymes tyrosinase and dopachrome tautomerase, all major players in melanogenes
8 and functional similarity, the MIF homolog D-dopachrome tautomerase (also called MIF-2) has low seque
10 cy of an enhancer required for expression of dopachrome tautomerase, an enzyme that functions in mela
11 igens gp100 and tyrosinase-related protein 2/dopachrome tautomerase and increased protection from a l
13 as tyrosinase, tyrosinase-related protein-1, dopachrome tautomerase, and Pmel17, are known, the funct
14 rophthalmia-associated transcription factor, dopachrome tautomerase, and tyrosinase promoters, leadin
15 n inhibitory factor (MIF) and its paralog, D-dopachrome tautomerase, are multifunctional inflammatory
16 hage migration inhibitory factor (MIF) and d-dopachrome tautomerase (d-DT or MIF2) play key roles in
17 tic understanding of the MIF homolog MIF-2/d-dopachrome tautomerase (d-DT) and its clinical translati
19 ally functionally redundant family member, D-dopachrome tautomerase (D-DT), also remains to be furthe
20 ation inhibitory factor (MIF), its homolog D-dopachrome tautomerase (D-DT), and their common receptor
21 y factor (MIF) and its functional homolog, d-dopachrome tautomerase (d-DT), have protumorigenic funct
22 rine MIF and its only known family member, D-dopachrome tautomerase (D-DT), promote the expression of
24 ew inflammatory activity for extracellular d-dopachrome tautomerase (D-DT), the recruitment of neutro
26 droxyphenylpyruvate dioxygenase (HPPD) and D-dopachrome tautomerase (D-DT); two additional enzymes th
27 iption of a second MIF superfamily member, D-dopachrome tautomerase (D-DT/MIF-2), prompted closer inv
33 inase, tyrosinase-related protein-1 (Tyrp1), dopachrome tautomerase (Dct), and LAMP1 and 3 localizati
34 essing neural precursor cells (line Ntva) or dopachrome tautomerase (DCT)-expressing melanoblasts (li
35 yrosinase-related protein-1 (TYRP1/gp75) and dopachrome tautomerase (DCT/TYRP2) belong to a family of
36 pression of members of the MIF family MIF, D-Dopachrome Tautomerase (DDT) and DDT-like (DDTL) in a lu
39 of the role of MIF (and its family member D-dopachrome tautomerase (DDT)) in genitourinary cancers a
42 tion genes, tyrosinase-related protein 1 and Dopachrome-tautomerase have lower protein levels in NPC1
44 ge migration inhibitory factor-2 (MIF-2 or D-dopachrome tautomerase) is a recently characterized seco
47 racterized three MIF orthologs (termed MIF/d-dopachrome tautomerase-like proteins or MDLs) of the mod
49 osinase or on the mRNA levels of tyrosinase, dopachrome tautomerase, Pmel17, or MITF mRNA levels.
52 (HO)2IndCOOH from dopachrome is catalyzed by dopachrome tautomerase, that the melanogenic protein tyr
54 tyrosinase, tyrosinase-related protein-1 and dopachrome tautomerase/tyrosinase-related protein-2 and