Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.10.3.1 (tyrosinase)
 9,065 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to generate a model for the reaction of proteins with nascent quinones, catechol and 4-methylcatechol were oxidized with silver-I-oxide in glacial acetic acid or with mushroom tyrosinase (EC 1.10.3.1) in phosphate buffer, respectively. The structures identified indicate that not only the amine reacts with the quinone by the well known addition-oxidation-mechanism, but also that solvent molecules may participate in product formation. The main product of the oxidation of catechol in glacial acid is N-(2-carbomethoxyethyl)-phenoxaz-2,3-dione.
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PMID:[Reactions of nascent quinones with methyl beta-alanate in glacial acetic acid and in aqueous solution (author's transl)]. 15 28

Conley et al., in 1971, described a special type of melanoma characterized by a superficial melanic lesion at the onset; repeated local relapses as subcutaneous tumorations with an histological picture closely resembling an atypical fibroxantoma or fibrosarcoma. After a review of all the published material the autors presents a personal case with the clinical, histological and evolutive characteristics of this disease. The most interesting findings of the published case are the following: The special stains for the melanocytes (silver stain, Dopa, tyrosinase and cholinesterase) were all negative. There was an intense positivity for the lisosomal enzymes (non specific sterases, and acid phosphatases). The ultrastructural study of the tumoral tissues as well as the cells of cultures showed abundant cells with tumoral aspects, with prominent nucleoli somewhat dilated granular endoplasmic reticulum, myelin-like figures, lipidic vacuoles and abundant lisosomes. No melanosomes or premelanosomes were observed. Beside these tumoral cells abundant typical fibroblastic elements were found. There was a great amount of collagen fibers with periodicity superior to the normal. The conclusion is that the desmoplastic melanoma must be considered as a tumor of mesenchimatous origin intervening in its development multiple local and general factors.
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PMID:[Desmoplastic melanoma]. 34 19

We describe a syndrome identified in three consanguineous families who had two and probably four common ancestors five generations ago. The syndrome is characterized by profound dysfunction of the central nervous system, silver-leaden colored hair, abnormal melanosomes and melanocytes, and abnormal inclusion bodies in fibroblasts, bone marrow histiocytes and lymphocytes which appear to represent abnormal lysosomal bodies. Because of the biochemical relationships between melanin-melanosomes and neuromelanin, we think that all the manifestations of the condition are related to and represent pleiotropic effects of a newly identified gene in man in its homozygous state. Biochemical reactions of the cells of these patients indicate presence of tyrosinase in the melanosomes.and show that the substance accumulated in cultured fibroblasts and in the bone marrow histiocytes is a PAS and Oil-red-O positive material but is Oil-red-O negative after extraction; it has the typical reactions of melanin withe the Masson and Fontana stain, but cannot be considered typical melanin, since without stain it is colorless. The ultrastructural studies showed round granules with variable matrix, similar in fibroblast and bone marrow, and with variable intensity of reaction to osmium. This mutation principally affects the neuroectoderm, but also the mesoderm.
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PMID:Mutations affecting pigmentation in man: I. Neuroectodermal melanolysosomal disease. 47 20

Melanocytes preferentially express an mRNA species, Pmel 17, whose protein product cross-reacts with anti-tyrosinase antibodies and whose expression correlates with the melanin content. We have now analyzed the deduced protein structure and mapped its chromosomal location in mouse and human. The amino acid sequence deduced from the nucleotide sequence of the Pmel 17 cDNA showed that the protein is composed of 645 amino acids with a molecular weight of 68,600. The Pmel 17 protein contains a putative leader sequence and a potential membrane anchor segment, which indicates that this may be a membrane-associated protein in melanocytes. The deduced protein contains five potential N-glycosylation sites and relatively high levels of serine and threonine. Three repeats of a 26-amino acid motif appear in the middle of the molecule. The human Pmel 17 gene, designated D12S53E, maps to chromosome 12, region 12pter-q21; and the mouse homologue, designated D12S53Eh, maps to the distal region of mouse chromosome 10, a region also known to carry the coat color locus si (silver).
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PMID:A melanocyte-specific gene, Pmel 17, maps near the silver coat color locus on mouse chromosome 10 and is in a syntenic region on human chromosome 12. 192 86

A case of dysplastic nevus syndrome in a 41-year-old tyrosinase-positive oculocutaneous albino man is presented. Clinically the patient exhibited multiple amelanotic lesions; histologic examination provided the diagnosis of dysplastic nevus syndrome. Fontana-Masson silver staining revealed the presence of melanin in the nevus cells. Hair bulbs incubated in tyrosine buffer produced melanin. This is the second reported case of dysplastic nevus syndrome in an oculocutaneous albino and the first case of dysplastic nevus syndrome in a tyrosinase-positive albino of which we are aware.
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PMID:Sporadic dysplastic nevus syndrome in a tyrosinase-positive oculocutaneous albino. 313 49

4-S-cysteinylphenol (4-S-CP), the S-homologue of tyrosine, has been recently synthesized as a selective chemotherapeutic agent against malignant melanoma and has been shown to be a specific substrate for tyrosinase in vitro. In vivo incorporation of 4-S-CP into the B16 and Harding Passey (HP) melanomas and the systemic organs have been evaluated by the autoradiographic method. The distribution of the silver grains indicated that 4-S-CP was selectively incorporated into both the B16 and HP melanomas. 4-S-CP was excreted mainly from the kidneys and there was an accumulation of 4-S-CP in the reticulo-endothelial system. These results seemed to contribute to the utilization of 4-S-CP and other related compounds as chemotherapeutic agents against malignant melanoma.
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PMID:Histological localization of 4-S-cysteinylphenol in melanoma-bearing mice. 332 27

The mode of differentiation of epidermal melanocytes was studied by ultrastructural cytochemistry in the skin of newborn mice of strain C57BL/10J. From observations of epidermal melanoblasts and melanocytes, stage I melanosomes, including both unit membranes and inner matrices, appear to be formed from Golgi vacuoles or rough endoplasmic reticulum (RER). Stage I melanosomes were positive to ammoniacal silver-nitrate reaction in the melanoblasts of 1-day-old mice. All stages of melanosomes were similarly positive in the differentiating melanocytes of 2-day-old mice. However, Golgi apparatus, RER, and vesicles were negative. Therefore, it is conceivable that structural proteins, originated from Golgi vacuoles or RER, are developed into specialized proteins and are detected by this reaction in stage I melanosomes. Stage I melanosomes were dopa-negative in the melanoblasts. Stage I and II melanosomes were similarly negative in the differentiating melanocytes. Thus, the melanoblasts are thought to begin production of stage I melanosomes prior to the onset of tyrosinase activity. In the differentiating melanocytes, dopa-melanin depositions were observed in stage III and IV melanosomes, trans Golgi saccules, and small vesicles derived from these saccules, but not in RER. These vesicles were in contact with, or fused to, melanosomes. These findings suggest that tyrosinase may be transferred by Golgi vesicles into stage I and II melanosomes originating from Golgi vacuoles or RER.
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PMID:Origin of melanosome structures and cytochemical localizations of tyrosinase activity in differentiating epidermal melanocytes of newborn mouse skin. 681 22

The administration of silver nitrate to rats in their food (10 mg/rat/day) led to the rapid disappearance of serum polyphenol oxidase activity. After 60 days silver nitrate treatment produced a decrease of adenohypophyseal weight. If given over a period of 40--60 days it also partially inhibited the adenohypophyseal response to oestradiol (a weight decrease and raised thyroxine binding by adenohypophyseal proteins in vitro). The mechanism by which silver nitrate diminishes basal and oestrogen-increased adenohypophyseal weight remains unknown.
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PMID:Partial inhibition of oestrogen-induced adenohypophyseal growth by silver nitrate. 739 1

Chronic oestradiol treatment (1 mg oestradiol benzoate, as an aqueous microcrystal suspension, i.m. twice a week for 6 weeks) produces in rats increased thyroxine-binding capacity of the adenohypophyseal proteins in vitro, an increase in the ceruloplasmin (polyphenol oxidase) level in blood and a decrease in the hypothalamic ascorbic acid concentration. The simultaneous administration of silver nitrate (10mg/rat/day in food) inhibits all these reactions in oestradiol. Apart from inhibiting blood polyphenol oxidase activity, silver nitrate itself has no effect. The possibility of the interaction of polyphenol oxidase(ceruloplasmin), silver nitrate and hypothalamic ascorbic acid in the dopaminergic modulation of the adenohypophyseal reaction to oestradiol is discussed.
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PMID:Modulation oestradiol effects by silver nitrate: inhibition of the adenohypophyseal reaction, block of the ceruloplasmin increase and block of hypothalamic ascorbic acid depletion. 744 47

Cutaneous melanomas of Tyr-SV40E transgenic mice (mice whose transgene consists of the tyrosinase promoter fused to the coding regions of simian virus 40 early genes) strikingly resemble human melanomas in their development and progression. Unlike human melanomas, the mouse tumors all arise in genetically identical individuals, thereby better enabling expression of specific genes to be characterized in relation to advancing malignancy. The products of pigment genes are of particular interest because peptides derived from these proteins have been reported to function as autoantigens with immunotherapeutic potential in some melanoma patients. However, the diminished pigmentation characteristic of many advanced melanomas raises the possibility that some of the relevant products may no longer be expressed in the most malignant cells. We have therefore investigated the contributions of several pigment genes in melanotic vs. relatively amelanotic components of primary and metastatic mouse melanomas. The analyses reveal marked differences within and among tumors in levels of mRNAs and proteins encoded by the wild-type alleles at the albino, brown, slaty, and silver loci. Tyrosinase (the protein encoded by the albino locus) was most often either absent or undetectable as melanization declined. The protein encoded by the slaty locus (tyrosinase-related protein 2) was the only one of those tested that was clearly present in all the tumor samples. These results suggest that sole reliance on targeting tyrosinase-based antigens might selectively favor survival of more malignant cells, whereas targeting the ensemble of the antigens tested might contribute toward a more inclusive and effective antimelanoma strategy.
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PMID:Changes in expression of putative antigens encoded by pigment genes in mouse melanomas at different stages of malignant progression. 747 44


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