Sequence analysis of mouse tyrosinase cDNA and the effect of melanotropin on its gene expression

Kwon, Byoung S.; Wakulchik, Mark; Haq, Asifa K.; Halaban, Ruth; Kestler, Daniel P.

doi:10.1016/s0006-291x(88)81370-6

Cited by 155 publications

(50 citation statements)

References 13 publications

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“…It is conceivable that PKG phosphorylates some proteins involved in melanogenesis. For instance, tyrosinase, which controls melanogenesis, contains several consensual phosphorylation sites for PKG (32,33) and was reported to be phosphorylated (16). Furthermore, PKG was thought to mediate the activation of the transcription factor activator protein 1 by NO and cGMP in rodent fibroblasts and epithelial cell lines (34).…”

Section: Discussionmentioning

confidence: 99%

Ultraviolet B Radiation Acts through the Nitric Oxide and cGMP Signal Transduction Pathway to Stimulate Melanogenesis in Human Melanocytes

Romero-Graillet

Aberdam

Biagoli

et al. 1996

Journal of Biological Chemistry

170

144

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Ultraviolet B (UVB) radiation is the main physiological stimulus for human skin pigmentation; however, the molecular mechanisms underlying this process are still unclear. Recently, nitric oxide (NO) and cGMP have been involved in mediation of skin erythema induced by UVB. Therefore, we investigated the role of NO and cGMP in UVB-induced melanogenesis. In this study, we demonstrated that UVB stimulation of melanogenesis was mimicked by exogenous NO donors. Additionally, we showed that NO stimulated cGMP synthesis and that cGMP was also a potent stimulator of melanogenesis. Furthermore, the inhibition of the melanogenic effect of NO by guanylate cyclase inhibitor demonstrated that NO mediated its effect through the activation of guanylyl cyclase. Interestingly, 1 min after UVB irradiation, we observed a significant increase in cGMP content in melanocytes. The effects of UVB on cGMP production and on melanogenesis were blocked by both guanylate cyclase and NO synthase inhibitors. Additionally, inhibition of cGMP-dependent kinase also prevented the stimulation of melanogenesis by UVB and NO. Therefore, we concluded that NO and cGMP production is required for UVB-induced melanogenesis and that cGMP mediated its melanogenic effects mainly through the activation of cGMP-dependent kinase.Epidermal melanin is responsible for skin darkening and is synthesized by melanocytes as the result of a cascade of enzymatic reactions. Tyrosinase, which converts tyrosine to dopaquinone, is the rate-limiting enzyme involved in melanin synthesis and represents the major regulatory step in melanogenesis. Numerous stimuli are able to alter melanogenesis of cultured pigmented cells; vitamin D metabolites (1), retinoids (2, 3), melanocyte-stimulating hormone (4 -6), forskolin, cholera toxin, isobutylmethylxanthine (7,8), diacylglycerol analogs (9, 10), and UV irradiation (11)(12)(13)(14). Until now the molecular mechanism involved in the induction of melanogenesis by these agents was not fully elucidated. A role for the cAMP pathway has been proposed on the basis that adenylate cyclase activators such as melanocyte-stimulating hormone, forskolin, and cholera toxin or phosphodiesterase inhibitors (e.g. isobutylmethylxanthine) can stimulate melanogenesis (6). Additionally, the protein kinase C (PKC) 1 pathway was thought to be involved in the regulation of melanogenesis. Indeed, 1-oleyl-2-acetyl-glycerol, a PKC activator, stimulates melanogenesis (9, 10, 15), and a direct correlation between the level of PKC activity in melanocytes and the activity of tyrosinase has been shown (16). However, induction of melanogenesis by UVB or by 1-oleyl-2-acetyl-glycerol is unaffected by RO 31-8220, a PKC inhibitor (17), leading to the conclusion that protein kinase C does not play a pivotal role in the control of melanogenesis. In humans, only UVB radiation represents an established physiological stimulus of melanogenesis, and despite many efforts to identify the molecular events triggered by UVB radiation, the mechanisms underlying UVB-induced melanogene...

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Section: Discussionmentioning

confidence: 99%

Ultraviolet B Radiation Acts through the Nitric Oxide and cGMP Signal Transduction Pathway to Stimulate Melanogenesis in Human Melanocytes

Romero-Graillet

Aberdam

Biagoli

et al. 1996

Journal of Biological Chemistry

170

144

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“…Analysis of carboxyl(C)-terminus of those purified protein should elucidate this problem. Kwon et al (1988) reported the construction of mouse tyrosinase minigene PMTY811C which consisted of the 0.65 kb mouse genomic sequence PTY-1H (HindIIl/ HincII fragment) at the 5' side conjugated with the 1.31 kb mouse cDNA fragment MTY811H(HincII/ EcoRI fragment) at the 3'-side. Kwon's amino acid residues at positions 103 and 346 deduced from PMTY811 C are different from those of our Tyrs-J cDNA.…”

Section: Discussionmentioning

confidence: 99%

Melanin production in cultured albino melanocytes transfected with mouse tyrosinase cDNA.

Yamamoto

Tanaka

Kudo

et al. 1989

The Japanese journal of genetics

112

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An attempt was made in the present study to express mouse tyrosinase cDNAs fused with the authentic genomic 5' non-coding flanking sequence in cultured albino melanocytes. One of the cDNA sequences, which expressed successfully and produced melanin pigments, was analyzed with respect to deduced amino acid sequence. Sequencing of the tyrosinase genomic gene revealed the existence of several sets of a characteristic structure which consists of a chain of two successive stem structures, CCAAT-homology and TATA box at its 5' non-coding region.It seems possible that this region represents the regulatory element of the tyrosinase gene. Unusually long GA cluster at 5' upstream region was also found.

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“…The protyrosinase from A. oryzae was assumed to contain 2 g-atoms of copper\mol of the subunits with a molecular mass of 67 kDa [7]. A coupled pair of three histidine residues [His-63, His-84 and His-93 for Cu(A) ; His-290, His-294 and His-333 for Cu(B)] of the proenzyme from A. oryzae was assumed [7] to correspond to the Cu(II) ligand in the similar tyrosinases from Streptomyces antibioticus [13], mouse [14,15] and H. sapiens [12].…”

Section: Introductionmentioning

confidence: 99%

Identification of copper ligands in Aspergillus oryzae tyrosinase by site-directed mutagenesis

et al. 2000

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Sequence analysis of mouse tyrosinase cDNA and the effect of melanotropin on its gene expression

Cited by 155 publications

References 13 publications

Ultraviolet B Radiation Acts through the Nitric Oxide and cGMP Signal Transduction Pathway to Stimulate Melanogenesis in Human Melanocytes

Ultraviolet B Radiation Acts through the Nitric Oxide and cGMP Signal Transduction Pathway to Stimulate Melanogenesis in Human Melanocytes

Melanin production in cultured albino melanocytes transfected with mouse tyrosinase cDNA.

Identification of copper ligands in Aspergillus oryzae tyrosinase by site-directed mutagenesis

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