Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.10.3.1 (tyrosinase)
9,065 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We isolated a novel inhibitor of melanin biosynthesis from the flowers of Arnica montana L. (Compositae), and identified it as a traxastane-type triterpene (3beta,16beta-dihydroxy-21alpha-hydroperoxy-20(30)-taraxastene) [1] by means of 1D or 2D-NMR and liquid chromatography/high-resolution mass spectrometry (LC-HR-MS). Compound [1] at the concentration of 0.53 muM completely inhibited melanin accumulation in cultured B16 melanoma cells. It is one of the most potent among known plant inhibitors of melanin biosynthesis in cultured cells, being 50 times more potent than 4-methoxyphenol, which is used as an anti-pigmentation agent. Its mechanism of action is considered to involve inhibition of transcriptional factor MITF-M (melanocyte-type isoform of microphthalmia-associated transcription factor), which would lead to a decrease of tyrosinase and related genes. We confirmed that compound [1] decreased the protein levels of tyrosinase and its related proteins in B16 melanoma cells. Further study revealed that a similar hydroperoxy triterpene also suppressed the melanin pigment accumulation of B16 melanoma cells. These results indicate that the hydroperoxy group may play an important role in the suppression of the melanin accumulation by compound [1].
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PMID:A novel melanin inhibitor: hydroperoxy traxastane-type triterpene from flowers of Arnica montana. 1747 28

An increased level of melanin is characteristic of a large number of skin diseases, including acquired hyperpigmentation conditions such as melasma, post inflammatory melanoderma, and solar lentigo. Thus, there is an increasing need for the development of depigmenting agents. In order to evaluate the depigmenting capacity of diosgenin and elucidate its mechanism of action, several experiments were performed in B16 melanoma cells. Melanin content and Western blots for proteins that are involved in melanogenesis were assessed in this study. The melanin content was significantly inhibited by diosgenin. To clarify the mechanism of the depigmenting property of diosgenin, we examined the involvement of diosgenin in the phosphatidylinositol-3-kinase (PI3K) pathway. In this study, diosgenin inhibited the reduction of Akt and GSK 3beta phosphorylation induced by LY294,002, a PI3K inhibitor. In accordance with this result, production levels of MITF (microphthalmia-associated transcription factor) and tyrosinase were increased by diosgenin. These data suggest that diosgenin inhibits melanogenesis through the activation of the PI3K pathway. This suggestion was further confirmed by the fact that the increased production level of melanin by LY294,002 was reduced by diosgenin in B16 melanoma cells. Our study shows that diosgenin inhibits melanogenesis by activating the PI3K pathway, and also suggests that diosgenin may be an effective inhibitor of hyperpigmentation.
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PMID:Diosgenin inhibits melanogenesis through the activation of phosphatidylinositol-3-kinase pathway (PI3K) signaling. 1756 20

The authors used the human embryonal eye to conduct immunohistochemical studies employing the tissue-specific markers of the melanocytic series (HMB45, tyrosinase, melanin A, and MITF) and neuronal differentiation (S100), as well as the markers of intermediate and muscular filaments (vimentin, desmin, smooth muscle actin). The nature of antigen expression was analyzed in different structures and portions of the vascular tract of the eye. The findings unveil the possibility of differentiating the vascular tract tumors of various genesis and their sites, by applying a plate containing the above markers.
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PMID:[Study of the expression of embryonal choroidal tissue-specific markers]. 1807 57

Melanoma has a wide spectrum of histologic features which mimic epithelial, hematologic, mesenchymal, and neural tumors. Immunohistochemistry has been the primary tool to distinguish melanomas from these other tumors; it has also been studied for use as an adjunct to distinguish benign and malignant melanocytic tumors and to elucidate prognosis. Furthermore, there has been extensive effort to find a suitable marker to differentiate spindle cell and desmoplastic melanoma from other tumors. We have reviewed the literature investigating melanocytic differentiation markers, proliferation markers, immunomodulatory markers, signaling molecules, and nerve growth factors and receptors. Despite the proliferation of immunohistochemical markers, S-100 remains the most sensitive marker for melanocytic lesions, while markers such as HMB-45, MART-1/Melan-A, tyrosinase, and MITF demonstrate relatively good specificity but not as good sensitivity as S-100. No marker has proven useful in distinguishing spindle cell and desmoplastic melanomas from other tumors. Ki67 remains the most useful adjunct in distinguishing benign from malignant melanocytic tumors. None of the markers reviewed has been shown conclusively to have prognostic value for melanocytic neoplasms.
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PMID:Immunohistochemical characteristics of melanoma. 1839 7

Warrgenburg syndrome type 2 (WS2) is the most common autosomal dominantly-inherited syndrome with hearing loss. MITF (microphthalmia associated transcription factor)is a basic-helix-loop-helix-luecine zipper (bHLHZip) factor which regulates expression of tyrosinase, and is involved in melanocyte differentiation. Mutations in MITF associated with WS2 have been identified in some but not all affected families. Here, we report a three-generation Chinese family with a point mutation in the MITF gene causing WS2. The proband exhibits congenital severe sensorineural hearing loss, heterochromia iridis and facial freckles. One of family members manifests sensorineural deafness, and the other patients show premature greying or/and freckles. This mutation, heterozygous deletion c.639delA, creates a stop codon in exon 7 and is predicted to result in a truncated protein lacking normal interaction with its target DNA motif. This mutation is a novel mutation and the third case identified in exon 7 of MITF in WS2. Though there is only one base pair distance between this novel mutation and the other two documented cases and similar amino acids change, significant difference is seen in clinical phenotype, which suggests genetic background may play an important role.
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PMID:[Mutation screening of MITF gene in patients with Waardenburg syndrome type 2]. 1842 13

Cholesterol has been suggested to regulate cell differentiation. In this study, we have examined the effects of cholesterol modulation on pigmentation of skin using a treatment with methyl-beta-cyclodextrin (MbetaCD), a specific cholesterol-binding agent. Treatment with MbetaCD reduced pigmentation in human melanocyte and cultured skin. This decrease in pigmentation was related to the inhibition of the expression of tyrosinase and microphthalmia-associated transcription factor of melanocytes. Stimulation of melanocytes with MbetaCD led to the time-dependent phosphorylation of extracellular signal-regulated kinase (ERK). Furthermore, ERK functionally regulated the MbetaCD-induced melanin formation in melanocytes; a ERK inhibitor, PD98059, almost completely attenuated the MbetaCD-mediated inhibition of melanin synthesis and down-regulation of MITF and tyrosinase expression. These results suggest that cholesterol reduction by MbetaCD inhibit melanin synthesis via ERK activation and subsequent MITF downregulation.
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PMID:Methyl-beta-cyclodextrin, a specific cholesterol-binding agent, inhibits melanogenesis in human melanocytes through activation of ERK. 1847 39

Hair graying is one of the prototypical signs of human aging, but its mechanism is largely unknown. To elucidate the mechanism of hair graying, we investigated gene expression related to melanogenesis in human hair. The key molecules in melanogenesis, microphthalmia-associated transcription factor-M (MITF-M), Sox10, Pax3, tyrosine related protein-1 (TRP-1), and tyrosinase, were absent or greatly reduced in the bulbs of white hair compared to black hair. Melanocyte stem cells (MSCs) or melanocytes express markers for neural crest cells, Sox10, Pax3, and MITF-M. Taken together, our data suggest that hair graying is caused by defective migration of MSCs into the bulb area of hair.
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PMID:Changing expression of the genes related to human hair graying. 1857 11

Melagenine, extracted from human placenta, has been shown to be effective in treating patients with vitiligo, yet the mechanisms of melagenine in inducing the repigmentation of vitiligo patients have not been fully investigated. Recent studies have suggested that melagenine stimulates melanocyte proliferation and melanogenesis. In this study, we utilized the NCCmelb4M5 melanoblast cell line to investigate the effects of melagenine on proliferation and differentiation of immature melanocytes or melanoblasts. NCCmelb4M5 cells were treated with different concentrations of melagenine (50-400 microg/ml), and MTT assay was performed to evaluate the effects of melagenine on proliferation of melanoblasts. RT-PCR and Western blotting were used to determine the expression of c-KIT and tyrosinase (TYR). Our results show that melagenine stimulates proliferation of NCCmelb4M5 cells in a dose-dependent manner with an optimal concentration of 100 microg/ml. Multipolar and highly branched dendritic network, as well as cluster-like growing cell assembly were visible in melagenine-treated NCCmelb4M5 cells. Melagenine induced expression of c-KIT, TYR and MITF. Our results provide insights into the molecular mechanism of the beneficial effect of melagenine in the treatment of vitiligo.
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PMID:Melagenine modulates proliferation and differentiation of melanoblasts. 1863 73

There is a great variety of histological patterns of skin melanoma and, in particular, that of its metastatic patterns. Malignant melanocytes are capable of influencing tumor-associated antigen expression. As of now, several varieties of melanoma-associated antigens (MAA) have been identified: MART1/melan A, tyrosinase, MITF, gp100, members of MAGE family, S100, CD63 and CD146. Peptides isolated from such molecules can induce MHC-restricted response of cytotoxic T-lymphocytes. It has been shown that level and nature of specific antigen expression caused by melanocytes correlate with tumor stage and a relationship between survival and MAA expression on tumor cells identified. Morphological features, growth pattern and proliferation rate varied in melanoma cell cultures used in our study. Our experiments involved evaluation of changes in the properties of antigens HLA (class 1 and 2), tumor tissue samples and cells isolated from them, which were capable of stable proliferative activity during passages 5, 10, 15, 20, 25, 30 and 35, and assay for MAA content. Levels of the antigens were significantly lower following long-term culturing melanoma cell melanoma cells in vitro. At initial passages (1-5), antigen profile in most cultures was similar to that in tumor tissue samples. Later on each cell population showed greater antigen expression heterogeneity matched by increased number of cells going through mitotic cycle; their nuclei were stained with antibodies to Ki-67. No HLF A/B/C molecule expression took place during tumor cell culturing: stained cells--in 68.9% of cultures (passages 1-5) and 36.3% (passage 35). However, HLA DQ/DP/DR molecule identification showed an inverse relationship: 44.1% (passage 5) while virtually all the cell lines did synthesize those molecules after passage 35. Hence, MAA and MHC (class 1 and 2) antigens expression in tumor cell should be monitored when they are used for preparation of autologuos and allogenic vaccines. In case of allogenic vaccine production, cell lines capable of stable production of MAA should be selected.
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PMID:[An immunocytochemical investigation of antigen expression by skin melanoma cells cultured for vaccine production]. 1865 34

For the immunohistochemical analysis of melanoma, various serological reagents are available. Melanocyte differentiation markers are reactive with cells and tumors of melanocytic lineage. HMB45 to gp100 has been the most commonly used melanocyte differentiation marker. Recently it was complemented by reagents such as antibodies to Melan-A/MART-1 and tyrosinase. Other reagents, whose reactivity is not strictly confined to melanocyte differentiation antigens, are also commonly used. Among them, the most prominent is S100. Other reagents are D5 to MITF or PNL-2. The properties of these reagents are presented, and their usefulness as markers in the setting of metastatic melanoma in sentinel lymph nodes is discussed.
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PMID:Serological reagents for the immunohistochemical analysis of melanoma metastases in sentinel lymph nodes. 1869 16


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