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[PMID]: 28458339 [Au] Autor: Hijioka M; Inden M; Yanagisawa D; Kitamura Y [Ad] Endereço: Laboratory of Pharmacology and Neurobiology, College of Pharmaceutical Sciences, Ritsumeikan University. [Ti] Título: DJ-1/PARK7: A New Therapeutic Target for Neurodegenerative Disorders. [So] Source: Biol Pharm Bull;40(5):548-552, 2017. [Is] ISSN: 1347-5215 [Cp] País de publicação: Japan [La] Idioma: eng [Ab] Resumo: DJ-1, encoded in a causative gene of familial Parkinson's disease (PARK7), has multiple functions: it works as an antioxidant, in transcriptional regulation, as a molecular chaperone and in protein degradation. Three types of pathogenic mutants of DJ-1 (M26I, D149A and L166P) have been reported to disrupt proper structures and lead to a loss of function. DJ-1 receives oxidation at the cysteine residue, and the degree of oxidation at the C106 residue determines DJ-1 activity. In this decade, DJ-1 has been reported to suppress the progression of various neurodegenerative disorders in animal models. The administration of recombinant wild-type DJ-1 protein suppresses the neuronal loss associated with both Parkinson's disease and ischemic stroke in rats. Furthermore, in studies focused on DJ-1 as the therapeutic target, compounds that have the capacity of binding to DJ-1 at the C106 residue have been reported to exert therapeutic effects on various neurodegenerative disorders such as Parkinson's disease, Alzheimer's disease and ischemic stroke. DJ-1 and DJ-1-targeting molecules/compounds will be useful therapeutic targets for various neurodegenerative disorders due to their various functions such as antioxidant capacity, chaperone function and as a proteolytic pathway. [Mh] Termos MeSH primário: Doenças Neurodegenerativas/tratamento farmacológico Doenças Neurodegenerativas/genética Proteína Desglicase DJ-1/efeitos dos fármacos Proteína Desglicase DJ-1/genética [Mh] Termos MeSH secundário: Animais Antiparkinsonianos/uso terapêutico Seres Humanos Doença de Parkinson/tratamento farmacológico Doença de Parkinson/genética [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (Antiparkinson Agents); EC 3.1.2.- (PARK7 protein, human); EC 3.1.2.- (Protein Deglycase DJ-1) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180212 [Lr] Data última revisão: 180212 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170502 [St] Status: MEDLINE [do] DOI: 10.1248/bpb.b16-01006

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[PMID]: 29272304 [Au] Autor: Zhou W; Barkow JC; Freed CR [Ad] Endereço: Division of Clinical Pharmacology and Toxicology, Departments of Medicine, Pharmacology, Neurology, and Neurosurgery; University of Colorado Denver, School of Medicine, Aurora, CO, United States of America. [Ti] Título: Running wheel exercise reduces α-synuclein aggregation and improves motor and cognitive function in a transgenic mouse model of Parkinson's disease. [So] Source: PLoS One;12(12):e0190160, 2017. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Exercise has been recommended to improve motor function in Parkinson patients, but its value in altering progression of disease is unknown. In this study, we examined the neuroprotective effects of running wheel exercise in mice. In adult wild-type mice, one week of running wheel activity led to significantly increased DJ-1 protein concentrations in muscle and plasma. In DJ-1 knockout mice, running wheel performance was much slower and Rotarod performance was reduced, suggesting that DJ-1 protein is required for normal motor activity. To see if exercise can prevent abnormal protein deposition and behavioral decline in transgenic animals expressing a mutant human form of α-synuclein in all neurons, we set up running wheels in the cages of pre-symptomatic animals at 12 months old. Activity was monitored for a 3-month period. After 3 months, motor and cognitive performance on the Rotarod and Morris Water Maze were significantly better in running animals compared to control transgenic animals with locked running wheels. Biochemical analysis revealed that running mice had significantly higher DJ-1, Hsp70 and BDNF concentrations and had significantly less α-synuclein aggregation in brain compared to control mice. By contrast, plasma concentrations of α-synuclein were significantly higher in exercising mice compared to control mice. Our results suggest that exercise may slow the progression of Parkinson's disease by preventing abnormal protein aggregation in brain. [Mh] Termos MeSH primário: Cognição Modelos Animais de Doenças Atividade Motora Doença de Parkinson/fisiopatologia Doença de Parkinson/psicologia Condicionamento Físico Animal alfa-Sinucleína/metabolismo [Mh] Termos MeSH secundário: Animais Comportamento Animal Encéfalo Fator Neurotrófico Derivado do Encéfalo/sangue Fator Neurotrófico Derivado do Encéfalo/metabolismo Feminino Proteínas de Choque Térmico HSP70/sangue Proteínas de Choque Térmico HSP70/metabolismo Masculino Camundongos Camundongos Endogâmicos C57BL Camundongos Transgênicos Músculo Esquelético/metabolismo Proteína Desglicase DJ-1/sangue Proteína Desglicase DJ-1/genética Proteína Desglicase DJ-1/metabolismo alfa-Sinucleína/genética [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Brain-Derived Neurotrophic Factor); 0 (HSP70 Heat-Shock Proteins); 0 (alpha-Synuclein); EC 3.1.2.- (PARK7 protein, mouse); EC 3.1.2.- (Protein Deglycase DJ-1) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180116 [Lr] Data última revisão: 180116 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171223 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0190160

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[PMID]: 29175327 [Au] Autor: Lee MK; Lee MS; Bae DW; Lee DH; Cha SS; Chi SW [Ad] Endereço: Disease Target Structure Research Center, KRIBB, Daejeon 34141, Republic of Korea. [Ti] Título: Structural basis for the interaction between DJ-1 and Bcl-X . [So] Source: Biochem Biophys Res Commun;495(1):1067-1073, 2018 01 01. [Is] ISSN: 1090-2104 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: DJ-1 is a multifunctional protein associated with Parkinson's disease (PD) and tumorigenesis. In response to ultraviolet B (UVB) irradiation, DJ-1 is translocated into the mitochondria, and its interaction with the mitochondrial protein Bcl-X protects cells against death. In this study, we characterized the molecular interaction between DJ-1 and Bcl-X by NMR spectroscopy. The NMR chemical shift perturbation data demonstrated that the oxidized but not the reduced form of DJ-1 binds to the predominantly hydrophobic groove surrounded by the BH1-BH3 domains in Bcl-X . In addition, our results showed that the C-terminal α8-helix peptide (Cpep) of DJ-1 binds to the pro-apoptotic BH3 peptide-binding hydrophobic groove in Bcl-X and, thus, acts as a Bcl-X -binding motif. In combination with the NMR chemical shift perturbation data, a refined structural model of the Bcl-X /DJ-1 Cpep complex revealed that the binding mode is remarkably similar to that of other Bcl-X /pro-apoptotic BH3 peptide complexes. Taken together, our results provide a structural basis for the binding mechanism between DJ-1 and Bcl-X , which will contribute to molecular understanding of the role of mitochondrial DJ-1 in Bcl-X regulation in response to oxidative stress. [Mh] Termos MeSH primário: Simulação de Acoplamento Molecular/métodos Proteína Desglicase DJ-1/química Mapeamento de Interação de Proteínas/métodos Proteína bcl-X/química Proteína bcl-X/ultraestrutura [Mh] Termos MeSH secundário: Sítios de Ligação Interações Hidrofóbicas e Hidrofílicas Espectroscopia de Ressonância Magnética/métodos Modelos Químicos Ligação Proteica Conformação Proteica Domínios Proteicos Relação Estrutura-Atividade [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (bcl-X Protein); EC 3.1.2.- (Protein Deglycase DJ-1) [Em] Mês de entrada: 1712 [Cu] Atualização por classe: 180105 [Lr] Data última revisão: 180105 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171128 [St] Status: MEDLINE

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[PMID]: 28941803 [Au] Autor: Xue R; Jiang J; Dong B; Tan W; Sun Y; Zhao J; Chen Y; Dong Y; Liu C [Ad] Endereço: Department of Cardiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China; Key Laboratory on Assisted Circulation, Ministry of Health, Guangzhou, China. [Ti] Título: DJ-1 activates autophagy in the repression of cardiac hypertrophy. [So] Source: Arch Biochem Biophys;633:124-132, 2017 Nov 01. [Is] ISSN: 1096-0384 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Cardiac hypertrophy is the risk factor of heart failure when the heart is confronted with pressure overload or neurohumoral stimuli. Autophagy, a conserved degradative pathway, is one of the important mechanisms involved in the regulation of cardiac hypertrophy. DJ-1 is a traditional anti-oxidative protein and emerging evidence suggested that DJ-1 might modulate autophagy. However, the regulation of autophagy by DJ-1 in the process of cardiac hypertrophy remains unknown. In our study, we firstly discovered that the expression of DJ-1declined in the process of pressure overload cardiac hypertrophy, and its alteration was parallel with the impairment of autophagy. Furthermore, we proved that DJ-1 knockout mice exhibited a more hypertrophied phenotype than wildtype mice in cardiac hypertrophy which indicated that DJ-1 is responsible for the repression of cardiac hypertrophy. Furthermore, DJ-1 knockout significantly exacerbated pulmonary edema due to cardiac hypertrophy. In the process of cardiac hypertrophy, DJ-1 knockout significantly impaired autophagy activation and enhanced mTORC1 and mTORC2 phosphorylation were found. Similarly, our in vitro study proved that DJ-1 overexpression ameliorated phenylephrine (PE)-induced cardiac hypertrophy and promoted autophagy activation. Taken together, DJ-1 might repress both pressure overload and PE-induced cardiac hypertrophy via the activation of autophagy. [Mh] Termos MeSH primário: Autofagia/genética Cardiomegalia/genética Pulmão/metabolismo Miocárdio/metabolismo Proteína Desglicase DJ-1/genética Edema Pulmonar/genética [Mh] Termos MeSH secundário: Animais Autofagia/efeitos dos fármacos Cardiomegalia/induzido quimicamente Cardiomegalia/metabolismo Cardiomegalia/patologia Regulação da Expressão Gênica Pulmão/patologia Alvo Mecanístico do Complexo 1 de Rapamicina Alvo Mecanístico do Complexo 2 de Rapamicina Camundongos Camundongos Endogâmicos C57BL Camundongos Knockout Complexos Multiproteicos/genética Complexos Multiproteicos/metabolismo Miocárdio/patologia Miócitos Cardíacos/efeitos dos fármacos Miócitos Cardíacos/metabolismo Miócitos Cardíacos/patologia Fenilefrina/efeitos adversos Fosforilação Cultura Primária de Células Proteína Desglicase DJ-1/deficiência Edema Pulmonar/induzido quimicamente Edema Pulmonar/metabolismo Edema Pulmonar/patologia Ratos Sprague-Dawley Índice de Gravidade de Doença Serina-Treonina Quinases TOR/genética Serina-Treonina Quinases TOR/metabolismo Vasoconstritores/efeitos adversos [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Multiprotein Complexes); 0 (Vasoconstrictor Agents); 1WS297W6MV (Phenylephrine); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 2); EC 3.1.2.- (PARK7 protein, mouse); EC 3.1.2.- (Protein Deglycase DJ-1) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171116 [Lr] Data última revisão: 171116 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170925 [St] Status: MEDLINE

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[PMID]: 28873462 [Au] Autor: Huo Z; Luo X; Zhan X; Chu Q; Xu Q; Yao J; Pang H [Ad] Endereço: Department of Forensic Genetics and Biology, China Medical University, Shenyang North New Area, Shenyang, P.R., China. [Ti] Título: Genetic analysis of indel markers in three loci associated with Parkinson's disease. [So] Source: PLoS One;12(9):e0184269, 2017. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: The causal mutations and genetic polymorphisms associated with susceptibility to Parkinson's disease (PD) have been extensively described. To explore the potential contribution of insertion (I)/deletion (D) polymorphisms (indels) to the risk of PD in a Chinese population, we performed genetic analyses of indel loci in ACE, DJ-1, and GIGYF2 genes. Genomic DNA was extracted from venous blood of 348 PD patients and 325 age- and sex-matched controls without neurodegenerative disease. Genotyping of the indel loci was performed by fragment length analysis after PCR and DNA sequencing. Our results showed a statistically significant association for both allele X (alleles without 5) vs. 5 (odds ratio = 1.378, 95% confidence interval = 1.112-1.708, P = 0.003) and genotype 5/X+X/X vs. 5/5 (odds ratio = 1.681, 95% confidence interval = 1.174-2.407, P = 0.004) in the GIGYF2 locus; however, no significant differences were detected for the ACE and DJ-1 indels. After stratification by gender, no significant differences were observed in any indels. These results indicate that the GIGYF2 indel may be associated with increased risk of PD in northern China. [Mh] Termos MeSH primário: Proteínas de Transporte/genética Loci Gênicos Predisposição Genética para Doença Mutação INDEL/genética Doença de Parkinson/genética Peptidil Dipeptidase A/genética Proteína Desglicase DJ-1/genética [Mh] Termos MeSH secundário: Alelos Feminino Frequência do Gene/genética Estudos de Associação Genética Marcadores Genéticos Técnicas de Genotipagem Seres Humanos Masculino Meia-Idade Modelos Genéticos Reação em Cadeia da Polimerase Polimorfismo de Nucleotídeo Único/genética [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Carrier Proteins); 0 (GIGYF2 protein, human); 0 (Genetic Markers); EC 3.1.2.- (PARK7 protein, human); EC 3.1.2.- (Protein Deglycase DJ-1); EC 3.4.15.1 (ACE protein, human); EC 3.4.15.1 (Peptidyl-Dipeptidase A) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171016 [Lr] Data última revisão: 171016 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170906 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0184269

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[PMID]: 28653888 [Au] Autor: Han B; Wang J; Gao J; Feng S; Zhu Y; Li X; Xiao T; Qi J; Cui W [Ad] Endereço: 1 Department of Clinical Laboratory, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China. [Ti] Título: DJ-1 as a potential biomarker for the early diagnosis in lung cancer patients. [So] Source: Tumour Biol;39(6):1010428317714625, 2017 Jun. [Is] ISSN: 1423-0380 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: DJ-1 is a novel oncogene that can transform NIH3T3 cells in cooperation with the activated ras gene. DJ-1 appears to have its greatest effect on tumourigenesis, and it may have a greater impact on early-stage lung cancers. In this study, we proposed to investigate the clinical value of DJ-1 protein in the early diagnosis of lung cancer and compared its diagnostic value with other biomarkers. Preoperative serum DJ-1 levels were measured in 300 lung cancer patients and compared with benign pulmonary disease (n = 44) and healthy volunteers (n = 64). Using tissue microarrays and immunohistochemical analyses, we compared the DJ-1 expression between the primary squamous cell carcinoma tumours and matched metastatic tissues from a lymph node. The baseline preoperative serum DJ-1 of lung cancer patients was significantly higher than that of benign diseases and healthy controls (p < 0.001). In the early-stage subgroup, the median DJ-1 concentration (ng/mL) was significantly higher than that of the advanced stage (12.90 vs 7.75, p < 0.05). Using immunohistochemistry, we observed that the DJ-1 staining intensity was generally weaker and less common in the metastatic tissues compared with that in the primary tumour (McNemar-Bowker Test, p = 0.008). DJ-1 was highly expressed in the early stage of lung cancer, and its expression was significantly decreased after metastasis. Therefore, DJ-1 may be a potential biomarker for the early diagnosis and monitoring of lung cancer metastasis. [Mh] Termos MeSH primário: Biomarcadores Tumorais/genética Neoplasias Pulmonares/diagnóstico Neoplasias Pulmonares/genética Proteína Desglicase DJ-1/genética [Mh] Termos MeSH secundário: Adulto Idoso Biomarcadores Tumorais/biossíntese Carcinogênese/genética Detecção Precoce de Câncer Feminino Regulação Neoplásica da Expressão Gênica Seres Humanos Neoplasias Pulmonares/patologia Linfonodos/patologia Masculino Meia-Idade Metástase Neoplásica Proteína Desglicase DJ-1/biossíntese [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Biomarkers, Tumor); EC 3.1.2.- (PARK7 protein, human); EC 3.1.2.- (Protein Deglycase DJ-1) [Em] Mês de entrada: 1707 [Cu] Atualização por classe: 170713 [Lr] Data última revisão: 170713 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170628 [St] Status: MEDLINE [do] DOI: 10.1177/1010428317714625

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[PMID]: 28618925 [Au] Autor: Di Cello A; Di Sanzo M; Perrone FM; Santamaria G; Rania E; Angotti E; Venturella R; Mancuso S; Zullo F; Cuda G; Costanzo F [Ad] Endereço: 1 Unit of Obstetrics and Gynaecology, Department of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy. [Ti] Título: DJ-1 is a reliable serum biomarker for discriminating high-risk endometrial cancer. [So] Source: Tumour Biol;39(6):1010428317705746, 2017 Jun. [Is] ISSN: 1423-0380 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: New reliable approaches to stratify patients with endometrial cancer into risk categories are highly needed. We have recently demonstrated that DJ-1 is overexpressed in endometrial cancer, showing significantly higher levels both in serum and tissue of patients with high-risk endometrial cancer compared with low-risk endometrial cancer. In this experimental study, we further extended our observation, evaluating the role of DJ-1 as an accurate serum biomarker for high-risk endometrial cancer. A total of 101 endometrial cancer patients and 44 healthy subjects were prospectively recruited. DJ-1 serum levels were evaluated comparing cases and controls and, among endometrial cancer patients, between high- and low-risk patients. The results demonstrate that DJ-1 levels are significantly higher in cases versus controls and in high- versus low-risk patients. The receiver operating characteristic curve analysis shows that DJ-1 has a very good diagnostic accuracy in discriminating endometrial cancer patients versus controls and an excellent accuracy in distinguishing, among endometrial cancer patients, low- from high-risk cases. DJ-1 sensitivity and specificity are the highest when high- and low-risk patients are compared, reaching the value of 95% and 99%, respectively. Moreover, DJ-1 serum levels seem to be correlated with worsening of the endometrial cancer grade and histotype, making it a reliable tool in the preoperative decision-making process. [Mh] Termos MeSH primário: Biomarcadores Tumorais/sangue Neoplasias do Endométrio/sangue Prognóstico Proteína Desglicase DJ-1/sangue [Mh] Termos MeSH secundário: Adulto Idoso Neoplasias do Endométrio/patologia Feminino Seres Humanos Meia-Idade [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Biomarkers, Tumor); EC 3.1.2.- (PARK7 protein, human); EC 3.1.2.- (Protein Deglycase DJ-1) [Em] Mês de entrada: 1706 [Cu] Atualização por classe: 170622 [Lr] Data última revisão: 170622 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170617 [St] Status: MEDLINE [do] DOI: 10.1177/1010428317705746

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[PMID]: 28615325 [Au] Autor: Zhang X; Yuan D; Sun Q; Xu L; Lee E; Lewis AJ; Zuckerbraun BS; Rosengart MR [Ad] Endereço: Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. [Ti] Título: Calcium/calmodulin-dependent protein kinase regulates the PINK1/Parkin and DJ-1 pathways of mitophagy during sepsis. [So] Source: FASEB J;31(10):4382-4395, 2017 Oct. [Is] ISSN: 1530-6860 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: During sepsis and shock states, mitochondrial dysfunction occurs. Consequently, adaptive mechanisms, such as fission, fusion, and mitophagy, are induced to eliminate damaged portions or entire dysfunctional mitochondria. The regulatory PINK1/Parkin and DJ-1 pathways are strongly induced by mitochondrial depolarization, although a direct link between loss of mitochondrial membrane potential (Δ ) and mitophagy has not been identified. Mitochondria also buffer Ca , and their buffering capacity is dependent on Δ Here, we characterize a role for calcium/calmodulin-dependent protein kinase (CaMK) I in the regulation of these mechanisms. Loss of Δ with either pharmacologic depolarization or LPS leads to Ca -dependent mitochondrial recruitment and activation of CaMKI that precedes the colocalization of PINK1/Parkin and DJ-1. CaMKI is required and serves as both a PINK1 and Parkin kinase. The mechanisms operate in both immune and nonimmune cells and are induced in models of endotoxemia, sepsis, and hemorrhagic shock. These data support the idea that CaMKI links mitochondrial stress with the PINK1/Parkin and DJ-1 mechanisms of mitophagy.-Zhang, X., Yuan, D., Sun, Q., Xu, L., Lee, E., Lewis, A. J., Zuckerbraun, B. S., Rosengart, M. R. Calcium/calmodulin-dependent protein kinase regulates the PINK1/Parkin and DJ-1 pathways of mitophagy during sepsis. [Mh] Termos MeSH primário: Proteínas Quinases Dependentes de Cálcio-Calmodulina/metabolismo Mitocôndrias/metabolismo Proteína Desglicase DJ-1/metabolismo Proteínas Quinases/metabolismo Sepse/metabolismo [Mh] Termos MeSH secundário: Animais Modelos Animais de Doenças Lipopolissacarídeos/farmacologia Masculino Potencial da Membrana Mitocondrial/efeitos dos fármacos Camundongos Endogâmicos C57BL Degradação Mitocondrial/efeitos dos fármacos Transporte Proteico/efeitos dos fármacos Proteínas Serina-Treonina Quinases/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Lipopolysaccharides); EC 2.7.- (Protein Kinases); EC 2.7.11.1 (PTEN-induced putative kinase); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases); EC 3.1.2.- (Protein Deglycase DJ-1) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171115 [Lr] Data última revisão: 171115 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170616 [St] Status: MEDLINE [do] DOI: 10.1096/fj.201601096RRR

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[PMID]: 28580701 [Au] Autor: Gao H; Niu Y; Li M; Fang S; Guo L [Ad] Endereço: Department of Pathology, Zhujiang Hospital, Southern Medical University, Guangzhou, China. [Ti] Título: Identification of DJ-1 as a contributor to multidrug resistance in human small-cell lung cancer using proteomic analysis. [So] Source: Int J Exp Pathol;98(2):67-74, 2017 Apr. [Is] ISSN: 1365-2613 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Proteomic approaches have been proven to provide an important tool in identifying drug resistance-associated proteins. The aim of this study was to investigate the protein profiling of drug resistance-related proteins in small-cell lung cancer (SCLC) by proteomic analysis. The proteomic profiling was performed by two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) coupled with MALDI-TOF-TOF of SCLC in the multidrug-resistant cell line H69AR and its parental cell line H69. A total of 11 proteins were identified to be >2-fold up-or downregulated between the two cell lines. DJ-1, one of the differently expressed proteins identified by proteomics, was further examined by immunohistochemistry staining in 116 cases of SCLC tissues. Immunohistochemical results demonstrated that DJ-1 was expressed in 51.7% (60/116) of SCLC. DJ-1 expression was correlated significantly with survival time of SCLC patients (P < 0.05), but not with other clinical parameters such as gender, age and clinical stage (P > 0.05). Downregulation of DJ-1 using DJ-1-siRNA in H69AR cells sensitized cancer cells to chemotherapeutic drugs through increasing drug-induced cell apoptosis accompanied with G0-G1 phase arrest. These findings suggest DJ-1 may serve as a potential biomarker for chemoresistance and prognostic factor for patients with SCLC. [Mh] Termos MeSH primário: Antineoplásicos/farmacologia Resistência a Medicamentos Antineoplásicos Neoplasias Pulmonares/metabolismo Proteína Desglicase DJ-1/metabolismo Proteômica Carcinoma de Pequenas Células do Pulmão/tratamento farmacológico [Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos Linhagem Celular Tumoral Regulação para Baixo Resistência a Múltiplos Medicamentos Seres Humanos Neoplasias Pulmonares/tratamento farmacológico Neoplasias Pulmonares/patologia Proteína Desglicase DJ-1/genética RNA Interferente Pequeno Carcinoma de Pequenas Células do Pulmão/metabolismo Carcinoma de Pequenas Células do Pulmão/patologia Espectrometria de Massas por Ionização e Dessorção a Laser Assistida por Matriz Eletroforese em Gel Diferencial Bidimensional [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antineoplastic Agents); 0 (RNA, Small Interfering); EC 3.1.2.- (PARK7 protein, human); EC 3.1.2.- (Protein Deglycase DJ-1) [Em] Mês de entrada: 1708 [Cu] Atualização por classe: 170829 [Lr] Data última revisão: 170829 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170606 [St] Status: MEDLINE [do] DOI: 10.1111/iep.12221

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[PMID]: 28541025 [Au] Autor: Bandrés-Ciga S; Ruz C; Barrero FJ; Escamilla-Sevilla F; Pelegrina J; Vives F; Duran R [Ad] Endereço: Department of Physiology and Institute of Neurosciences Federico Olóriz, Biomedical Research Centre (BRC), University of Granada, Granada, Spain. [Ti] Título: Structural genomic variations and Parkinson's disease. [So] Source: Minerva Med;108(5):438-447, 2017 Oct. [Is] ISSN: 1827-1669 [Cp] País de publicação: Italy [La] Idioma: eng [Ab] Resumo: Parkinson's disease (PD) is the second most common neurodegenerative disease, whose prevalence is projected to be between 8.7 and 9.3 million by 2030. Until about 20 years ago, PD was considered to be the textbook example of a "non-genetic" disorder. Nowadays, PD is generally considered a multifactorial disorder that arises from the combination and complex interaction of genes and environmental factors. To date, a total of 7 genes including SNCA, LRRK2, PARK2, DJ-1, PINK 1, VPS35 and ATP13A2 have been seen to cause unequivocally Mendelian PD. Also, variants with incomplete penetrance in the genes LRRK2 and GBA are considered to be strong risk factors for PD worldwide. Although genetic studies have provided valuable insights into the pathogenic mechanisms underlying PD, the role of structural variation in PD has been understudied in comparison with other genomic variations. Structural genomic variations might substantially account for such genetic substrates yet to be discovered. The present review aims to provide an overview of the structural genomic variants implicated in the pathogenesis of PD. [Mh] Termos MeSH primário: Predisposição Genética para Doença Genômica Serina-Treonina Proteína Quinase-2 com Repetições Ricas em Leucina/genética Mutação/genética Doença de Parkinson/genética alfa-Sinucleína/genética [Mh] Termos MeSH secundário: Biomarcadores/sangue Éxons/genética Genótipo Seres Humanos Doença de Parkinson/diagnóstico Doença de Parkinson/epidemiologia Fenótipo Prevalência Proteína Desglicase DJ-1/genética Proteínas Quinases/genética ATPases Translocadoras de Prótons/genética Fatores de Risco Espanha/epidemiologia Ubiquitina-Proteína Ligases/genética Proteínas de Transporte Vesicular/genética [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (Biomarkers); 0 (SNCA protein, human); 0 (VPS35 protein, human); 0 (Vesicular Transport Proteins); 0 (alpha-Synuclein); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.3.2.27 (parkin protein); EC 2.7.- (Protein Kinases); EC 2.7.11.1 (LRRK2 protein, human); EC 2.7.11.1 (Leucine-Rich Repeat Serine-Threonine Protein Kinase-2); EC 2.7.11.1 (PTEN-induced putative kinase); EC 3.1.2.- (PARK7 protein, human); EC 3.1.2.- (Protein Deglycase DJ-1); EC 3.6.3.14 (ATP13A2 protein, human); EC 3.6.3.14 (Proton-Translocating ATPases) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170904 [Lr] Data última revisão: 170904 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170526 [St] Status: MEDLINE [do] DOI: 10.23736/S0026-4806.17.05246-6

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