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[PMID]: 23414214 [Au] Autor: Morais M; Oliveira BL; Correia JD; Oliveira MC; Jiménez MA; Santos I; Raposinho PD [Ad] Dirección: Unidade de Ciências Químicas e Radiofarmacêuticas, IST/ITN, Instituto Superior Técnico, Universidade Técnica de Lisboa, Estrada Nacional 10, 2686-953, Sacavém, Portugal. [Ti] Título: Influence of the bifunctional chelator on the pharmacokinetic properties of 99mTc(CO)3-labeled cyclic α-melanocyte stimulating hormone analog. [So] Fuente: J Med Chem;56(5):1961-73, 2013 Mar 14. [Is] ISSN: 1520-4804 [Cp] País de publicación: United States [La] Idioma: eng [Ab] Resumen: Aiming at the design of specific melanocortin-1 receptor (MC1R) targeted imaging probes, we report on the effect of different azolyl-ring substitution patterns (carboxylate at the 4-position and/or methyl groups at the 3,5 positions) of pyrazolyl-diamine bifunctional chelators (Pz(2)-Pz(4)) on the pharmacokinetic profile of the (99m)Tc(CO)3-labeled lactam bridge-cyclized α-melanocyte stimulating hormone derivative, ßAlaNleCycMSH(hex). Three pyrazolyl-diamine-containing chelators were conjugated to ßAlaNleCycMSHhex, with the resulting peptide conjugates displaying subnanomolar MC1R binding affinity. Biodistribution studies in B16F1 melanoma-bearing mice show that all radiopeptides present a good melanoma uptake. The introduction of a carboxylate group in the azolyl-ring leads to a remarkable reduction of the kidney (>89%) and liver (>91%) accumulation for (99m)Tc(CO)3-Pz(3)-ßAlaNleCycMSH(hex) and (99m)Tc(CO)3-Pz(4)-ßAlaNleCycMSH(hex) when compared to the radiopeptide (99m)Tc(CO)3-Pz(1)-ßAlaNleCycMSH(hex), where that group is absent. The good tumor uptake and favorable tumor-to-nontarget-organs ratios of (99m)Tc(CO)3-Pz(3)-ßAlaNleCycMSH(hex) and (99m)Tc(CO)3-Pz(4)-ßAlaNleCycMSH(hex) highlights the potential of both compounds as melanoma imaging agents. [Mh] Términos MeSH primario: Quelantes/química Radiofármacos/uso diagnóstico alfa-MSH/análogos & derivados alfa-MSH/uso diagnóstico [Mh] Términos MeSH secundario: Animales Estabilidad de Medicamentos Humanos Melanoma Experimental/diagnóstico Melanoma Experimental/metabolismo Ratones Péptidos Cíclicos/síntesis química Péptidos Cíclicos/uso diagnóstico Péptidos Cíclicos/farmacocinética Radiofármacos/síntesis química Radiofármacos/farmacocinética Receptor de Melanocortina Tipo 1/química Receptor de Melanocortina Tipo 1/metabolismo Tecnecio/uso diagnóstico Tecnecio/farmacocinética alfa-MSH/metabolismo alfa-MSH/farmacocinética [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nombre de substancia: 0 (Chelating Agents); 0 (Peptides, Cyclic); 0 (Radiopharmaceuticals); 0 (Receptor, Melanocortin, Type 1); 581-05-5 (alpha-MSH); 7440-26-8 (Technetium) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130315 [St] Status: MEDLINE [do] DOI: 10.1021/jm301647t

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[PMID]: 23046118 [Au] Autor: Held L; Metzler G; Eigentler TK; Leiter U; Messina J; Gogel J; Bauer J; Garbe C [Ad] Dirección: Center for Dermatooncology, Department of Dermatology, University Hospital Tuebingen, Tuebingen, Germany. [Ti] Título: Recurrent nodules in a periauricular plaque-type blue nevus with fatal outcome. [So] Fuente: J Cutan Pathol;39(12):1088-93, 2012 Dec. [Is] ISSN: 1600-0560 [Cp] País de publicación: United States [La] Idioma: eng [Ab] Resumen: Plaque-type blue nevus is a rare variant of blue nevus characterized by grouped nodules displaying histomorphological features of a cellular blue nevus. We report the clinical, histopathologic and immunohistologic features of a patient with recurrent nodules in a periauricular plaque-type blue nevus with malignant transformation and fatal outcome. The nevus was characterized clinically by childhood onset, with slow enlargement during adolescence. At age 16, the patient presented with nodules located retroauricularly. Several surgical excisions with the intent of complete removal of the nodules and the nevus were performed. Histopathological, dermal and subcutaneous proliferations of pigmented melanocytes with melanophages were detected. The nodules showed some cellular atypia and few mitotic figures, (Ki67 estimated <1%). At age 20, the patient developed new nodules retroauricular, with histopathology similar to previous lesions; however, the proliferation rate was higher. A comparative genomic hybridization (CGH) showed chromosomal changes indicative of melanoma. At age 25, the patient developed multiple liver metastases and died after 4 weeks. A sequencing of the tumor DNA revealed a GNAQ Q209P mutation, whereas mutations of GNA11, BRAF, NRAS and cKIT were not detected. This case shows that nodules in plaque-type blue nevus may have malignant potential which may be uncovered by CGH. [Mh] Términos MeSH primario: Neoplasias Hepáticas/secundario Melanoma/secundario Recurrencia Local de Neoplasia Neoplasias Primarias Secundarias Nevo Azul/patología Neoplasias Cutáneas/patología [Mh] Términos MeSH secundario: Adulto Aberraciones Cromosómicas Hibridación Genómica Comparativa Análisis Mutacional de ADN Oído Resultado Fatal Subunidades alfa de la Proteína de Unión al GTP/genética Humanos Masculino Melanocitos/patología Melanoma/genética Mutación Nevo Azul/metabolismo Nevo Azul/cirugía Neoplasias Cutáneas/metabolismo Neoplasias Cutáneas/cirugía [Pt] Tipo de publicación: CASE REPORTS; JOURNAL ARTICLE [Nm] Nombre de substancia: 0 (GNAQ protein, human); 0 (GTP-Binding Protein alpha Subunits) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 121127 [St] Status: MEDLINE [do] DOI: 10.1111/cup.12021

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[PMID]: 23134995 [Au] Autor: Chawla S; Kvalnes K; deLong MA; Wickett R; Manga P; Boissy RE [Ad] Dirección: Department of Dermatology, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0592, USA. [Ti] Título: DeoxyArbutin and its derivatives inhibit tyrosinase activity and melanin synthesis without inducing reactive oxygen species or apoptosis. [So] Fuente: J Drugs Dermatol;11(10):e28-34, 2012 Oct. [Is] ISSN: 1545-9616 [Cp] País de publicación: United States [La] Idioma: eng [Ab] Resumen: Safety is a major concern in developing commercial skin-lightening agents. Here, we report the modulating effects of deoxyArbutin (dA) and its second-generation derivatives - deoxyFuran (dF), 2-fluorodeoxyArbutin (fdA), and thiodeoxyArbutin (tdA) - on tyrosinase, and consequently, on melanization. Results demonstrate that dA and its derivatives inhibit tyrosine hydroxylase and dopa oxidase activity of tyrosinase. The inhibition is dose-dependent, thereby inhibiting melanin synthesis in intact melanocytes, when used at concentrations that retain 95% viability of the treated cells in culture. Herein we demonstrate that dA, and its second-generation derivatives dF, fdA, and tdA, exhibit dose-dependent reductions in melanocyte cell number, primarily due to inhibition of proliferation rather than initiation of apoptosis as exemplified by hydroquinone (HQ), ie, cytostatic as opposed to cytotoxic. Human and murine melanocytes with functional mutations in either tyrosinase or tyrosinase-related protein 1 (Tyrp1) are less sensitive to the cytostatic effects of dA and its derivatives. Minimal amounts of reactive oxygen species (ROS) were generated upon treatment with dA and its derivatives, in contrast to a dramatic amount of ROS induced by HQ. This increase in ROS subsequently induced the expression of the endogenous antioxidant catalase in treated melanocytes. Treatment with exogenous antioxidants provided protection for melanocytes treated with HQ, but not dA and its derivatives, suggesting that HQ exerts more oxidative stress. These studies demonstrate that dA and its derivatives are relatively safe tyrosinase inhibitors for skin lightening or for ameliorating hyperpigmented lesions. [Mh] Términos MeSH primario: Arbutina/análogos & derivados Melaninas/biosíntesis Melanocitos/efectos de drogas Melanocitos/enzimología Monofenol Monooxigenasa/antagonistas & inhibidores Especies de Oxígeno Reactivo/metabolismo [Mh] Términos MeSH secundario: Albinismo Oculocutáneo/enzimología Animales Antioxidantes/farmacología Apoptosis Arbutina/farmacología Catalasa/metabolismo Proliferación de la Célula/efectos de drogas Supervivencia Celular/efectos de drogas Células Cultivadas Relación Dosis-Respuesta a Droga Humanos Hidroquinonas/farmacología Melanocitos/metabolismo Ratones Monofenol Monooxigenasa/metabolismo Oxidorreductasas/metabolismo Superóxido Dismutasa/farmacología Tirosina 3-Monooxigenasa/antagonistas & inhibidores Vitamina E/farmacología [Pt] Tipo de publicación: JOURNAL ARTICLE [Nm] Nombre de substancia: 0 (Antioxidants); 0 (Hydroquinones); 0 (Melanins); 0 (Reactive Oxygen Species); 123-31-9 (hydroquinone); 1406-18-4 (Vitamin E); 497-76-7 (Arbutin); EC 1.- (Oxidoreductases); EC 1.11.1.6 (Catalase); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 1.14.18.- (tyrosinase-related protein-1); EC 1.14.18.1 (Monophenol Monooxygenase); EC 1.15.1.1 (Superoxide Dismutase); RG969BY5EN (deoxyarbutin) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 121108 [St] Status: MEDLINE

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[PMID]: 23194049 [Au] Autor: Magro CM; Yang SE; Zippin JH; Zembowicz A [Ad] Dirección: Department of Pathology, Weill Medical College of Cornell University, New York, New York, USA. [Ti] Título: Expression of soluble adenylyl cyclase in lentigo maligna: use of immunohistochemistry with anti-soluble adenylyl cyclase antibody (R21) in diagnosis of lentigo maligna and assessment of margins. [So] Fuente: Arch Pathol Lab Med;136(12):1558-64, 2012 Dec. [Is] ISSN: 1543-2165 [Cp] País de publicación: United States [La] Idioma: eng [Ab] Resumen: CONTEXT: Soluble adenylyl cyclase (sAC) is an enzyme that generates cyclic adenosine monophosphate, a signaling molecule involved in regulating melanocyte functions. R21, a mouse monoclonal antibody against sAC, shows a striking pan-nuclear staining in lentigo maligna, indicating possible utility for diagnosis and margin assessment. OBJECTIVE: To evaluate R21 in the diagnosis and evaluation of margins in lentigo maligna. DESIGN: Thirty one re-excision specimens for lentigo maligna were evaluated for R21 expression using previously published protocol. In addition, 153 cases including 41 lentigo malignas, 30 non-lentigo maligna-type melanomas, 38 lentigos, and 44 nevi were evaluated using a modified stringent protocol to eliminate all nonmelanocyte staining. RESULTS: The sensitivity of nuclear staining with R21 in lentigo maligna was 87.8%. Nuclear expression of sAC was observed in 40% of other melanomas and 2.3% of benign nevi. R21 did not stain nuclei of resting melanocytes but was observed in 28.9% of melanocytic hyperplasias. These cases were easily distinguished from lentigo maligna in routine sections. R21 staining facilitated extent of the lesion in resection margins. In cases examined under the less stringent conditions, interpretation was facilitated by comparing R21 and Mart1/Melan A staining. Greater than 9 pan-nuclear staining melanocytes within one high-power field along with a pan-nuclear sAC/Melan A ratio greater than 0.5 was consistent with a positive margin whereas 5 or less pan-nuclear staining melanocytes along with a sAC/Melan A ratio of less than 0.3 constituted a negative margin. CONCLUSION: R21 is a useful diagnostic adjunct in the diagnosis and evaluation of margins in re-excision specimens in lentigo maligna. [Mh] Términos MeSH primario: Adenilato Ciclasa/metabolismo Anticuerpos Monoclonales/metabolismo Peca Melanótica de Hutchinson/metabolismo Proteínas de Neoplasias/metabolismo Neoplasias Cutáneas/metabolismo Piel/enzimología Marcadores Biológicos de Tumor/metabolismo [Mh] Términos MeSH secundario: Adenilato Ciclasa/química Especificidad de Anticuerpos Núcleo Celular/enzimología Núcleo Celular/metabolismo Núcleo Celular/patología Diagnóstico Diferencial Regulación Neoplásica de la Expresión Génica Humanos Peca Melanótica de Hutchinson/diagnóstico Peca Melanótica de Hutchinson/patología Peca Melanótica de Hutchinson/cirugía Hiperplasia Inmunohistoquímica Antígeno MART-1/metabolismo Melanocitos/enzimología Melanocitos/metabolismo Melanocitos/patología Melanoma/diagnóstico Melanoma/metabolismo Melanoma/patología Melanoma/cirugía Proteínas de Neoplasias/química Nevo/diagnóstico Nevo/metabolismo Nevo/patología Nevo/cirugía Sensibilidad y Especificidad Piel/metabolismo Piel/patología Neoplasias Cutáneas/diagnóstico Neoplasias Cutáneas/patología Neoplasias Cutáneas/cirugía Solubilidad Marcadores Biológicos de Tumor/química [Pt] Tipo de publicación: JOURNAL ARTICLE; MULTICENTER STUDY; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; VALIDATION STUDIES [Nm] Nombre de substancia: 0 (Antibodies, Monoclonal); 0 (MART-1 Antigen); 0 (Neoplasm Proteins); 0 (R21 monoclonal antibody); 0 (Tumor Markers, Biological); EC 4.6.1.1 (Adenylate Cyclase) [Em] Mes de ingreso: 1301 [Cu] Fecha actualización por clase: 130509 [Lr] Fecha última revisión: 130509 [Sb] Subgrupo de revista: AIM; IM [Da] Fecha de ingreso para procesamiento: 121130 [St] Status: MEDLINE [do] DOI: 10.5858/arpa.2011-0617-OA

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[PMID]: 23174301 [Au] Autor: Marks MS [Ad] Dirección: Department of Pathology & Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. marksm@mail.med.upenn.edu [Ti] Título: Organelle biogenesis: en BLOC exchange for RAB32 and RAB38. [So] Fuente: Curr Biol;22(22):R963-5, 2012 Nov 20. [Is] ISSN: 1879-0445 [Cp] País de publicación: England [La] Idioma: eng [Ab] Resumen: Prominent subtypes of the genetic disorder Hermansky-Pudlak syndrome result from defects in a mysterious protein complex, BLOC-3. New work identifies BLOC-3 as a guanine nucleotide exchange factor for two RAB GTPases previously implicated in lysosome-related organelle biogenesis. [Mh] Términos MeSH primario: Orgánulos/fisiología Proteínas de Unión al GTP rab/metabolismo [Mh] Términos MeSH secundario: Animales Línea Celular Tumoral Regulación de la Expresión Génica Factores de Intercambio de Guanina Nucleótido/genética Factores de Intercambio de Guanina Nucleótido/metabolismo Síndrome de Hermanski-Pudlak/genética Síndrome de Hermanski-Pudlak/metabolismo Humanos Melanocitos/metabolismo Ratones Complejos Multiproteinas/genética Complejos Multiproteinas/metabolismo Transporte de Proteína Ratas Proteínas de Unión al GTP rab/genética [Pt] Tipo de publicación: JOURNAL ARTICLE [Nm] Nombre de substancia: 0 (Guanine Nucleotide Exchange Factors); 0 (Multiprotein Complexes); EC 3.6.1.- (rab GTP-Binding Proteins) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 121123 [St] Status: MEDLINE

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[PMID]: 23321476 [Au] Autor: Cyr NE; Toorie AM; Steger JS; Sochat MM; Hyner S; Perello M; Stuart R; Nillni EA [Ad] Dirección: Division of Endocrinology, Department of Medicine, The Warren Alpert Medical School of Brown University/Rhode Island Hospital, Providence, RI 02903, USA. [Ti] Título: Mechanisms by which the orexigen NPY regulates anorexigenic α-MSH and TRH. [So] Fuente: Am J Physiol Endocrinol Metab;304(6):E640-50, 2013 Mar 15. [Is] ISSN: 1522-1555 [Cp] País de publicación: United States [La] Idioma: eng [Ab] Resumen: Protein posttranslational processing is a cellular mechanism fundamental to the generation of bioactive peptides, including the anorectic α-melanocyte-stimulating hormone (α-MSH) and thyrotropin-releasing hormone (TRH) peptides produced in the hypothalamic arcuate (ARC) and paraventricular (PVN) nuclei, respectively. Neuropeptide Y (NPY) promotes positive energy balance in part by suppressing α-MSH and TRH. The mechanism by which NPY regulates α-MSH output, however, is not well understood. Our results reveal that NPY inhibited the posttranslational processing of α-MSH's inactive precursor proopiomelanocortin (POMC) by decreasing the prohormone convertase-2 (PC2). We also found that early growth response protein-1 (Egr-1) and NPY-Y1 receptors mediated the NPY-induced decrease in PC2. NPY given intra-PVN also decreased PC2 in PVN samples, suggesting a reduction in PC2-mediated pro-TRH processing. In addition, NPY attenuated the α-MSH-induced increase in TRH production by two mechanisms. First, NPY decreased α-MSH-induced CREB phosphorylation, which normally enhances TRH transcription. Second, NPY decreased the amount of α-MSH in the PVN. Collectively, these results underscore the significance of the interaction between NPY and α-MSH in the central regulation of energy balance and indicate that posttranslational processing is a mechanism that plays a specific role in this interaction. [Mh] Términos MeSH primario: Regulación del Apetito Núcleo Arqueado/metabolismo Neuronas/metabolismo Neuropéptido Y/metabolismo Núcleo Hipotalámico Paraventricular/metabolismo Hormona Liberadora de Tirotropina/metabolismo alfa-MSH/metabolismo [Mh] Términos MeSH secundario: Animales Proteína de Unión a Elemento de Respuesta al AMP Cíclico/metabolismo Proteína 1 de la Respuesta de Crecimiento Precoz/metabolismo Infusiones Intraventriculares Masculino Modelos Biológicos Neuropéptido Y/administración & dosificación Fosforilación Proopiomelanocortina/metabolismo Proproteína Convertasa 2/metabolismo Procesamiento Proteico-Postraduccional Ratas Ratas Sprague-Dawley Receptores de Neuropéptido Y/metabolismo [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL [Nm] Nombre de substancia: 0 (CREB1 protein, rat); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Early Growth Response Protein 1); 0 (Egr1 protein, rat); 0 (Neuropeptide Y); 0 (Receptors, Neuropeptide Y); 0 (neuropeptide Y-Y1 receptor); 24305-27-9 (Thyrotropin-Releasing Hormone); 581-05-5 (alpha-MSH); 66796-54-1 (Pro-Opiomelanocortin); EC 3.4.21.94 (Proprotein Convertase 2) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 130318 [St] Status: MEDLINE [do] DOI: 10.1152/ajpendo.00448.2012

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[PMID]: 23149255 [Au] Autor: Bae SJ; Ha YM; Park YJ; Park JY; Song YM; Ha TK; Chun P; Moon HR; Chung HY [Ad] Dirección: Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University, Kumjeong-Gu, Busan 609-735, Republic of Korea. [Ti] Título: Design, synthesis, and evaluation of (E)-N-substituted benzylidene-aniline derivatives as tyrosinase inhibitors. [So] Fuente: Eur J Med Chem;57:383-90, 2012 Nov. [Is] ISSN: 1768-3254 [Cp] País de publicación: France [La] Idioma: eng [Ab] Resumen: We attempted to design and synthesize (E)-N-substituted benzylidene-hydroxy or methoxy-aniline derivatives and to evaluate their inhibitory effect on tyrosinase activity and anti-melanogenesis activity in murine B16F10 melanoma cells. Derivatives with a 4-methoxy- or 4-hydroxy-anilino group exerted more potent inhibition against mushroom tyrosinase than those with a 2-hydroxyanilino group. (E)-4-((4-Hydroxyphenylimino)methyl)benzene-1,2-diol exhibited the most potent and non-competitive inhibition on mushroom tyrosinase showing an IC(50) of 17.22 ± 0.38 µM and being more effective than kojic acid (51.11 ± 1.42 µM). This compound decreased melanin production stimulated by the alpha-melanocyte-stimulating hormone and inhibited murine tyrosinase activity in a dose-dependent manner. Therefore, we propose (E)-4-((4-hydroxyphenylimino)methyl)benzene-1,2-diol as a new candidate of potent tyrosinase inhibitors that could be used as therapeutic agent with safe skin-whitening efficiency. [Mh] Términos MeSH primario: Compuestos de Anilina/química Antineoplásicos/síntesis química Compuestos de Bencilideno/síntesis química Catecoles/síntesis química Inhibidores Enzimáticos/síntesis química Proteínas Fúngicas/antagonistas & inhibidores Melaninas/antagonistas & inhibidores Monofenol Monooxigenasa/antagonistas & inhibidores Bases de Schiff/síntesis química [Mh] Términos MeSH secundario: Agaricales/química Animales Antineoplásicos/farmacología Compuestos de Bencilideno/farmacología Catecoles/farmacología Supervivencia Celular/efectos de drogas Relación Dosis-Respuesta a Droga Pruebas de Enzimas Inhibidores Enzimáticos/farmacología Proteínas Fúngicas/metabolismo Cinética Melaninas/biosíntesis Melanoma Experimental/quimioterapia Melanoma Experimental/enzimología Ratones Monofenol Monooxigenasa/metabolismo Pironas/farmacología Bases de Schiff/farmacología Neoplasias Cutáneas/quimioterapia Neoplasias Cutáneas/enzimología Células Tumorales Cultivadas alfa-MSH/farmacología [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nombre de substancia: 0 (4-((4-hydroxyphenylimino)methyl)benzene-1,2-diol); 0 (Aniline Compounds); 0 (Antineoplastic Agents); 0 (Benzylidene Compounds); 0 (Catechols); 0 (Enzyme Inhibitors); 0 (Fungal Proteins); 0 (Melanins); 0 (Pyrones); 0 (Schiff Bases); 581-05-5 (alpha-MSH); 6K23F1TT52 (kojic acid); EC 1.14.18.1 (Monophenol Monooxygenase); SIR7XX2F1K (aniline) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 121126 [St] Status: MEDLINE

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[PMID]: 23176485 [Au] Autor: Booth AE; Seabra MC; Hume AN [Ad] Dirección: Molecular Medicine, National Heart and Lung Institute, Imperial College London, London SW7 2AZ, UK. [Ti] Título: Rab27a and melanosomes: a model to investigate the membrane targeting of Rabs. [So] Fuente: Biochem Soc Trans;40(6):1383-8, 2012 Dec 1. [Is] ISSN: 1470-8752 [Cp] País de publicación: England [La] Idioma: eng [Ab] Resumen: Rab proteins constitute the largest family within the Ras superfamily of small GTPases (>60 in mammals) and are essential regulators of transport between intracellular organelles. Key to this activity is their targeting to specific compartments within the cell. However, although great strides have been made over the last 25 years in assigning functions to individual Rabs and identifying their downstream effectors, the mechanism(s) regulating their targeting to specific subcellular membranes remains less well understood. In the present paper, we review the evidence supporting the proposed mechanisms of Rab targeting and highlight insights into this process provided by studies of Rab27a. [Mh] Términos MeSH primario: Melanosomas/enzimología Proteínas de Unión al GTP rab/metabolismo [Mh] Términos MeSH secundario: Secuencias de Aminoácidos Animales Inhibidores de Disociación de Guanina Nucleótido/fisiología Factores de Intercambio de Guanina Nucleótido/fisiología Humanos Membranas Intracelulares/enzimología Melanocitos/enzimología Transporte de Proteína Proteínas de Unión al GTP rab/química Proteínas de Unión al GTP rab/fisiología [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nombre de substancia: 0 (Guanine Nucleotide Dissociation Inhibitors); 0 (Guanine Nucleotide Exchange Factors); EC 3.6.1.- (rab GTP-Binding Proteins); EC 3.6.1.-. (RAB27A protein, human) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 121126 [St] Status: MEDLINE [do] DOI: 10.1042/BST20120200

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[PMID]: 22871993 [Au] Autor: Yao L; Hu DN; Chen M; Li SS [Ad] Dirección: Department of Dermatology and Venereology, First Hospital of Jilin University, Changchun, Jilin Province, China. [Ti] Título: Subtoxic levels hydrogen peroxide-induced expression of interleukin-6 by epidermal melanocytes. [So] Fuente: Arch Dermatol Res;304(10):831-8, 2012 Dec. [Is] ISSN: 1432-069X [Cp] País de publicación: Germany [La] Idioma: eng [Ab] Resumen: Oxidative stress and autoimmune reaction are involved in the pathogenesis of vitiligo. Levels of hydrogen peroxide (H(2)O(2)) and interleukin-6 (IL-6), a proinflammation cytokine and a key factor in the pathogenesis of autoimmune diseases, have been reported to be elevated in vitiligo lesions. The objective of this study was to evaluate the effects of subtoxic levels of H(2)O(2) on the expression of IL-6 by cultured human epidermal melanocytes and to explore the relevant signal pathways. Cultured human melanocytes were stimulated with of H(2)O(2) at subtoxic levels. Levels of IL-6 protein in the medium and IL-6 mRNA in the cells were measured by IL-6 ELISA analysis and RT-PCR, respectively. NF-κB and phosphorylated p38 mitogen-activated protein kinase (MAPK), ERK and JNK in cells cultured with and without H(2)O(2) were measured by relevant ELISA kits. In cultured melanocytes, subtoxic levels of H(2)O(2) (30-300 µM) significantly increased the IL-6 mRNA and protein levels in a dose-dependent manner. NF-κB in nuclear extracts and phosphorylated p38 MAPK levels in cell lysates were significantly increased in H(2)O(2) treated cells. Pretreatment of cells with inhibitors of p38 MAPK (SB203580) and NF-κB (BAY11-7082), but not inhibitors of ERK (UO1026) and JNK (SP600125), abolished H(2)O(2)-induced expression of IL-6. H(2)O(2)-induced overexpression of IL-6 by melanocytes may be a molecular linkage for the oxidative stress and inflammatory/autoimmune reactions in vitiligo and may provide a novel target for the treatment of vitiligo. [Mh] Términos MeSH primario: Epidermis/efectos de drogas Peróxido de Hidrógeno/toxicidad Interleucina-6/metabolismo Melanocitos/efectos de drogas Estrés Oxidativo Vitíligo/etiología [Mh] Términos MeSH secundario: Antracenos/farmacología Células Cultivadas Epidermis/inmunología Quinasas MAP Reguladas por Señal Extracelular/antagonistas & inhibidores Quinasas MAP Reguladas por Señal Extracelular/genética Quinasas MAP Reguladas por Señal Extracelular/metabolismo Humanos Imidazoles/farmacología Interleucina-6/genética Melanocitos/inmunología FN-kappa B/genética FN-kappa B/metabolismo Nitrilos/farmacología Piridinas/farmacología Sulfonas/farmacología Regulación hacia Arriba Vitíligo/inducido químicamente Vitíligo/inmunología Proteinas Quinasas Activadas por Mitógeno p38/antagonistas & inhibidores Proteinas Quinasas Activadas por Mitógeno p38/genética Proteinas Quinasas Activadas por Mitógeno p38/metabolismo [Pt] Tipo de publicación: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nombre de substancia: 0 (3-(4-methylphenylsulfonyl)-2-propenenitrile); 0 (Anthracenes); 0 (Imidazoles); 0 (Interleukin-6); 0 (NF-kappa B); 0 (Nitriles); 0 (Pyridines); 0 (SB 203580); 0 (Sulfones); 0 (anthra(1,9-cd)pyrazol-6(2H)-one); 7722-84-1 (Hydrogen Peroxide); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 121126 [St] Status: MEDLINE [do] DOI: 10.1007/s00403-012-1277-6

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[PMID]: 22639095 [Au] Autor: Nakajima H; Fukazawa K; Wakabayashi Y; Wakamatsu K; Senda K; Imokawa G [Ad] Dirección: School of Bioscience and Biotechnology, Tokyo University of Technology, Hachioji, Japan. [Ti] Título: Abrogating effect of a xanthophyll carotenoid astaxanthin on the stem cell factor-induced stimulation of human epidermal pigmentation. [So] Fuente: Arch Dermatol Res;304(10):803-16, 2012 Dec. [Is] ISSN: 1432-069X [Cp] País de publicación: Germany [La] Idioma: eng [Ab] Resumen: We established a model for the stem cell factor (SCF)-associated stimulation of human epidermal equivalent (HEE) pigmentation. The addition of SCF (at 5 nM) gradually stimulated the visible pigmentation of HEEs over 14 days of treatment. A time course study using real-time RT-PCR and western blotting analysis demonstrated that the expression of all melanocyte-specific genes and proteins examined was gradually up-regulated over 7-10 days of treatment with SCF. The addition of astaxanthin (Ax) at concentrations of 1, 4, or 8 µM markedly abolished the SCF- but not the endothelin (EDN)1-elicited increase in visible pigmentation over 14 days in a dose-dependent manner, with almost complete inhibition at 8 µM. While no degeneration of the epidermal tissue was visible at day 14 by HE staining, melanin deposition throughout the epidermis was markedly reduced in the Ax-treated HEEs at day 14 compared to untreated controls. Ax significantly reduced the eumelanin content of HEEs to the non-SCF-stimulated level at concentrations of 4 or 8 µM compared with untreated controls. Real-time RT-PCR and western blotting of Ax-treated HEEs revealed that the SCF-stimulated expression of tyrosinase (TYR), TYR-related protein-1 (TYRP1), and Pmel17, as well as microphthalmia-associated transcription factor (MITF), is significantly suppressed by Ax at the transcriptional and translational levels. Studies using cultured normal human melanocytes revealed that pre-treatment with Ax interrupts the SCF- but not the EDN1-induced stimulation of TYR activity, and there was no direct inhibitory effect of Ax on TYR activity in vitro. These findings indicate that Ax attenuates SCF-stimulated pigmentation by directly interrupting SCF-associated intracellular signaling linkages through increased expression of MITF, which leads to the stimulated expression of melanogenic genes and proteins in a reactive oxygen species depletion-independent mechanism. [Mh] Términos MeSH primario: Epidermis/efectos de drogas Hiperpigmentación/metabolismo Melanocitos/metabolismo Pigmentación de la Piel/efectos de drogas Factor de Células Madre/antagonistas & inhibidores [Mh] Términos MeSH secundario: Células Cultivadas Endotelina-1/metabolismo Activación Enzimática/efectos de drogas Activación Enzimática/inmunología Regulación de la Expresión Génica/efectos de drogas Humanos Melanocitos/efectos de drogas Glicoproteínas de Membrana/genética Glicoproteínas de Membrana/metabolismo Factor de Transcripción Asociado a Microftalmía/genética Factor de Transcripción Asociado a Microftalmía/metabolismo Monofenol Monooxigenasa/genética Monofenol Monooxigenasa/metabolismo Oxidorreductasas/genética Oxidorreductasas/metabolismo Factor de Células Madre/farmacología Xantófilas/farmacología Antígeno gp100 del Melanoma/metabolismo [Pt] Tipo de publicación: JOURNAL ARTICLE [Nm] Nombre de substancia: 0 (Endothelin-1); 0 (Membrane Glycoproteins); 0 (Microphthalmia-Associated Transcription Factor); 0 (Stem Cell Factor); 0 (Xanthophylls); 0 (gp100 Melanoma Antigen); 8XPW32PR7I (astaxanthine); EC 1.- (Oxidoreductases); EC 1.14.18.- (TYRP1 protein, human); EC 1.14.18.1 (Monophenol Monooxygenase) [Em] Mes de ingreso: 1305 [Sb] Subgrupo de revista: IM [Da] Fecha de ingreso para procesamiento: 121126 [St] Status: MEDLINE [do] DOI: 10.1007/s00403-012-1248-y

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