Base de dados : MEDLINE
Pesquisa : D12.776.575 [Categoria DeCS]
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[PMID]:29031613
[Au] Autor:Majd H; King MS; Smith AC; Kunji ERS
[Ad] Endereço:Medical Research Council Mitochondrial Biology Unit, University of Cambridge, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
[Ti] Título:Pathogenic mutations of the human mitochondrial citrate carrier SLC25A1 lead to impaired citrate export required for lipid, dolichol, ubiquinone and sterol synthesis.
[So] Source:Biochim Biophys Acta;1859(1):1-7, 2018 01.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Missense mutations of the human mitochondrial citrate carrier, encoded by the SLC25A1 gene, lead to an autosomal recessive neurometabolic disorder characterised by neonatal-onset encephalopathy with severe muscular weakness, intractable seizures, respiratory distress, and lack of psychomotor development, often resulting in early death. Here, we have measured the effect of all twelve known pathogenic mutations on the transport activity. The results show that nine mutations abolish transport of citrate completely, whereas the other three reduce the transport rate by >70%, indicating that impaired citrate transport is the most likely primary cause of the disease. Some mutations may be detrimental to the structure of the carrier, whereas others may impair key functional elements, such as the substrate binding site and the salt bridge network on the matrix side of the carrier. To understand the consequences of impaired citrate transport on metabolism, the substrate specificity was also determined, showing that the human citrate carrier predominantly transports citrate, isocitrate, cis-aconitate, phosphoenolpyruvate and malate. Although D-2- and L-2 hydroxyglutaric aciduria is a metabolic hallmark of the disease, it is unlikely that the citrate carrier plays a significant role in the removal of hydroxyglutarate from the cytosol for oxidation to oxoglutarate in the mitochondrial matrix. In contrast, computer simulations of central metabolism predict that the export of citrate from the mitochondrion cannot be fully compensated by other pathways, restricting the cytosolic production of acetyl-CoA that is required for the synthesis of lipids, sterols, dolichols and ubiquinone, which in turn explains the severe disease phenotypes.
[Mh] Termos MeSH primário: Proteínas de Transporte de Ânions
Ácido Cítrico/metabolismo
Simulação por Computador
Dolicol
Proteínas Mitocondriais
Modelos Biológicos
Mutação de Sentido Incorreto
Esteróis
Ubiquinona
[Mh] Termos MeSH secundário: Proteínas de Transporte de Ânions/química
Proteínas de Transporte de Ânions/genética
Proteínas de Transporte de Ânions/metabolismo
Transporte Biológico Ativo/genética
Encefalopatias Metabólicas Congênitas/enzimologia
Encefalopatias Metabólicas Congênitas/genética
Domínio Catalítico
Dolicol/biossíntese
Dolicol/química
Dolicol/genética
Seres Humanos
Proteínas Mitocondriais/química
Proteínas Mitocondriais/genética
Proteínas Mitocondriais/metabolismo
Esteróis/biossíntese
Esteróis/química
Esteróis/metabolismo
Ubiquinona/biossíntese
Ubiquinona/química
Ubiquinona/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anion Transport Proteins); 0 (Mitochondrial Proteins); 0 (Slc25a1 protein, human); 0 (Sterols); 1339-63-5 (Ubiquinone); 2067-66-5 (Dolichol); 2968PHW8QP (Citric Acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171017
[St] Status:MEDLINE


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[PMID]:29182013
[Au] Autor:Dickerson T; Jauregui CE; Teng Y
[Ad] Endereço:College of Science & Mathematics, Augusta University, Augusta, GA 30912, USA.
[Ti] Título:Friend or foe? Mitochondria as a pharmacological target in cancer treatment.
[So] Source:Future Med Chem;9(18):2197-2210, 2017 12.
[Is] ISSN:1756-8927
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitochondria have acquired numerous functions over the course of evolution, such as those involved in controlling energy production, cellular metabolism, cell survival, apoptosis and autophagy within host cells. Tumor cells can develop defects in mitochondrial function, presenting a potential strategy for designing selective anticancer therapies. Therefore, cancer has been the main focus of recent research to uncover possible mitochondrial targets for therapeutic benefit. This comprehensive review covers not only the recent discoveries of the roles of mitochondria in cancer development, progression and therapeutic implications but also the findings regarding emerging mitochondrial therapeutic targets and mitochondria-targeted agents. Current challenges and future directions for developments and applications of mitochondrial-targeted therapeutics are also discussed.
[Mh] Termos MeSH primário: Mitocôndrias/metabolismo
Neoplasias/tratamento farmacológico
[Mh] Termos MeSH secundário: ATPases Associadas a Diversas Atividades Celulares/metabolismo
Trifosfato de Adenosina/metabolismo
Animais
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
DNA Mitocondrial/efeitos dos fármacos
DNA Mitocondrial/metabolismo
Metabolismo Energético/efeitos dos fármacos
Seres Humanos
Proteínas de Membrana/metabolismo
Mitocôndrias/genética
Proteínas Mitocondriais/metabolismo
Neoplasias/metabolismo
Neoplasias/patologia
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ATAD3A protein, human); 0 (Antineoplastic Agents); 0 (DNA, Mitochondrial); 0 (Membrane Proteins); 0 (Mitochondrial Proteins); 0 (Reactive Oxygen Species); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.4.- (ATPases Associated with Diverse Cellular Activities)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.4155/fmc-2017-0110


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[PMID]:29311576
[Au] Autor:Razew M; Warkocki Z; Taube M; Kolondra A; Czarnocki-Cieciura M; Nowak E; Labedzka-Dmoch K; Kawinska A; Piatkowski J; Golik P; Kozak M; Dziembowski A; Nowotny M
[Ad] Endereço:Laboratory of Protein Structure, International Institute of Molecular and Cell Biology, Trojdena 4, 02-109, Warsaw, Poland.
[Ti] Título:Structural analysis of mtEXO mitochondrial RNA degradosome reveals tight coupling of nuclease and helicase components.
[So] Source:Nat Commun;9(1):97, 2018 01 08.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nuclease and helicase activities play pivotal roles in various aspects of RNA processing and degradation. These two activities are often present in multi-subunit complexes from nucleic acid metabolism. In the mitochondrial exoribonuclease complex (mtEXO) both enzymatic activities are tightly coupled making it an excellent minimal system to study helicase-exoribonuclease coordination. mtEXO is composed of Dss1 3'-to-5' exoribonuclease and Suv3 helicase. It is the master regulator of mitochondrial gene expression in yeast. Here, we present the structure of mtEXO and a description of its mechanism of action. The crystal structure of Dss1 reveals domains that are responsible for interactions with Suv3. Importantly, these interactions are compatible with the conformational changes of Suv3 domains during the helicase cycle. We demonstrate that mtEXO is an intimate complex which forms an RNA-binding channel spanning its entire structure, with Suv3 helicase feeding the 3' end of the RNA toward the active site of Dss1.
[Mh] Termos MeSH primário: Endorribonucleases/metabolismo
Exorribonucleases/metabolismo
Proteínas Mitocondriais/metabolismo
Complexos Multienzimáticos/metabolismo
Polirribonucleotídeo Nucleotidiltransferase/metabolismo
RNA Helicases/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Sequência de Bases
Candida glabrata/enzimologia
Candida glabrata/genética
Candida glabrata/metabolismo
Cristalografia por Raios X
RNA Helicases DEAD-box/química
RNA Helicases DEAD-box/genética
RNA Helicases DEAD-box/metabolismo
Endorribonucleases/química
Endorribonucleases/genética
Exorribonucleases/química
Exorribonucleases/genética
Proteínas Mitocondriais/química
Proteínas Mitocondriais/genética
Complexos Multienzimáticos/química
Complexos Multienzimáticos/genética
Conformação de Ácido Nucleico
Polirribonucleotídeo Nucleotidiltransferase/química
Polirribonucleotídeo Nucleotidiltransferase/genética
Ligação Proteica
Conformação Proteica
RNA/química
RNA/genética
RNA/metabolismo
RNA Helicases/química
RNA Helicases/genética
Saccharomyces cerevisiae/enzimologia
Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/metabolismo
Proteínas de Saccharomyces cerevisiae/química
Proteínas de Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/metabolismo
Homologia de Sequência de Aminoácidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mitochondrial Proteins); 0 (Multienzyme Complexes); 0 (RNA, mitochondrial); 0 (Saccharomyces cerevisiae Proteins); 0 (degradosome); 63231-63-0 (RNA); EC 2.7.7.8 (Polyribonucleotide Nucleotidyltransferase); EC 3.1.- (Endoribonucleases); EC 3.1.- (Exoribonucleases); EC 3.1.13.1 (DSS1 protein, S cerevisiae); EC 3.6.1.- (SUV3 protein, S cerevisiae); EC 3.6.4.13 (DEAD-box RNA Helicases); EC 3.6.4.13 (RNA Helicases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02570-5


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[PMID]:29302033
[Au] Autor:Ignatenko O; Chilov D; Paetau I; de Miguel E; Jackson CB; Capin G; Paetau A; Terzioglu M; Euro L; Suomalainen A
[Ad] Endereço:Research Programs Unit, Molecular Neurology, Biomedicum Helsinki, Haartmaninkatu 8, University of Helsinki, Helsinki, 00014, Finland.
[Ti] Título:Loss of mtDNA activates astrocytes and leads to spongiotic encephalopathy.
[So] Source:Nat Commun;9(1):70, 2018 01 04.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitochondrial dysfunction manifests as different neurological diseases, but the mechanisms underlying the clinical variability remain poorly understood. To clarify whether different brain cells have differential sensitivity to mitochondrial dysfunction, we induced mitochondrial DNA (mtDNA) depletion in either neurons or astrocytes of mice, by inactivating Twinkle (TwKO), the replicative mtDNA helicase. Here we show that astrocytes, the most abundant cerebral cell type, are chronically activated upon mtDNA loss, leading to early-onset spongiotic degeneration of brain parenchyma, microgliosis and secondary neurodegeneration. Neuronal mtDNA loss does not, however, cause symptoms until 8 months of age. Findings in astrocyte-TwKO mimic neuropathology of Alpers syndrome, infantile-onset mitochondrial spongiotic encephalopathy caused by mtDNA maintenance defects. Our evidence indicates that (1) astrocytes are dependent on mtDNA integrity; (2) mitochondrial metabolism contributes to their activation; (3) chronic astrocyte activation has devastating consequences, underlying spongiotic encephalopathy; and that (4) astrocytes are a potential target for interventions.
[Mh] Termos MeSH primário: Astrócitos/metabolismo
Encefalopatias/genética
DNA Mitocondrial/genética
Doenças Mitocondriais/genética
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Encéfalo/ultraestrutura
DNA Helicases/genética
DNA Helicases/metabolismo
DNA Mitocondrial/metabolismo
Camundongos Knockout
Microscopia Eletrônica
Proteínas Mitocondriais/genética
Proteínas Mitocondriais/metabolismo
Mutação
Neurônios/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Mitochondrial); 0 (Mitochondrial Proteins); EC 3.6.1.- (Peo1 protein, mouse); EC 3.6.4.- (DNA Helicases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-01859-9


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[PMID]:29382326
[Au] Autor:Chen X; Wu RZ; Zhu YQ; Ren ZM; Tong YL; Yang F; Dai GH
[Ad] Endereço:Institute of Basic Medicine, Zhejiang Academy of Traditional Chinese Medicine, No. 132, Tianmushan Road, Xihu District, Hangzhou, Zhejiang, China.
[Ti] Título:Study on the inhibition of Mfn1 by plant-derived miR5338 mediating the treatment of BPH with rape bee pollen.
[So] Source:BMC Complement Altern Med;18(1):38, 2018 Jan 30.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Recent studies have found that plant derived microRNA can cross-kingdom regulate the expression of genes in humans and other mammals, thereby resisting diseases. Can exogenous miRNAs cross the blood-prostate barrier and entry prostate then participate in prostate disease treatment? METHODS: Using HiSeq sequencing and RT-qPCR technology, we detected plant miRNAs that enriched in the prostates of rats among the normal group, BPH model group and rape bee pollen group. To forecast the functions of these miRNAs, the psRobot software and TargetFinder software were used to predict their candidate target genes in rat genome. The qRT-PCR technology was used to validate the expression of candidate target genes. RESULTS: Plant miR5338 was enriched in the posterior lobes of prostate gland of rats fed with rape bee pollen, which was accompanied by the improvement of BPH. Among the predicted target genes of miR5338, Mfn1 was significantly lower in posterior lobes of prostates of rats in the rape bee pollen group than control groups. Further experiments suggested that Mfn1 was highly related to BPH. CONCLUSIONS: These results suggesting that plant-derived miR5338 may involve in treatment of rat BPH through inhibiting Mfn1 in prostate. These results will provide more evidence for plant miRNAs cross-kingdom regulation of animal gene, and will provide preliminary theoretical and experimental basis for development of rape bee pollen into innovative health care product or medicine for the treatment of BPH.
[Mh] Termos MeSH primário: Proteínas de Membrana/antagonistas & inibidores
MicroRNAs/farmacologia
Proteínas Mitocondriais/antagonistas & inibidores
Pólen
Próstata/efeitos dos fármacos
Hiperplasia Prostática/metabolismo
RNA de Plantas/farmacologia
[Mh] Termos MeSH secundário: Animais
Abelhas
Peso Corporal/efeitos dos fármacos
Masculino
Proteínas de Membrana/metabolismo
Proteínas Mitocondriais/metabolismo
Tamanho do Órgão/efeitos dos fármacos
RNA de Plantas/farmacocinética
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (MicroRNAs); 0 (Mitochondrial Proteins); 0 (RNA, Plant); 0 (mitofusin 1 protein, rat)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-018-2107-y


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[PMID]:28465355
[Au] Autor:Lan L; Guo M; Ai Y; Chen F; Zhang Y; Xia L; Huang D; Niu L; Zheng Y; Suzuki CK; Zhang Y; Liu Y; Lu B
[Ad] Endereço:Department of Biochemistry, Institute of Biophysics, Attardi Institute of Mitochondrial Biomedicine and Zhejiang Provincial Key Laboratory of Medical Genetics, School of Life Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.
[Ti] Título:Tetramethylpyrazine blocks TFAM degradation and up-regulates mitochondrial DNA copy number by interacting with TFAM.
[So] Source:Biosci Rep;37(3), 2017 Jun 30.
[Is] ISSN:1573-4935
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The natural small molecule compound: 2,3,5,6-tetramethylpyrazine (TMP), is a major component of the Chinese medicine , which has wide clinical applications in dilating blood vessels, inhibiting platelet aggregation and treating thrombosis. Recent work suggests that TMP is also an antitumour agent. Despite its chemotherapeutic potential, the mechanism(s) underlying TMP action are unknown. Herein, we demonstrate that TMP binds to mitochondrial transcription factor A (TFAM) and blocks its degradation by the mitochondrial Lon protease. TFAM is a key regulator of mtDNA replication, transcription and transmission. Our previous work showed that when TFAM is not bound to DNA, it is rapidly degraded by the ATP-dependent Lon protease, which is essential for mitochondrial proteostasis. In cultured cells, TMP specifically blocks Lon-mediated degradation of TFAM, leading to TFAM accumulation and subsequent up-regulation of mtDNA content in cells with substantially low levels of mtDNA. protease assays show that TMP does not directly inhibit mitochondrial Lon, rather interacts with TFAM and blocks degradation. Pull-down assays show that biotinylated TMP interacts with TFAM. These findings suggest a novel mechanism whereby TMP stabilizes TFAM and confers resistance to Lon-mediated degradation, thereby promoting mtDNA up-regulation in cells with low mtDNA content.
[Mh] Termos MeSH primário: DNA Mitocondrial/efeitos dos fármacos
Proteínas de Ligação a DNA/genética
Dosagem de Genes/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
Proteínas Mitocondriais/genética
Pirazinas/farmacologia
Fatores de Transcrição/genética
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Replicação do DNA/efeitos dos fármacos
Células HCT116
Células HeLa
Seres Humanos
Peptídeo Hidrolases/genética
Transcrição Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Mitochondrial); 0 (DNA-Binding Proteins); 0 (Mitochondrial Proteins); 0 (Pyrazines); 0 (TFAM protein, human); 0 (Transcription Factors); EC 3.4.- (Peptide Hydrolases); V80F4IA5XG (tetramethylpyrazine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:29413990
[Au] Autor:Kelly J; Murphy JE
[Ad] Endereço:Mitochondrial Biology & Radiation Research Centre, Dept. of Life Sciences, Institute of Technology Sligo, Ash Lane, Sligo, Ireland. Electronic address: janiskelly@mail.itsligo.ie.
[Ti] Título:Mitochondrial gene expression changes in cultured human skin cells following simulated sunlight irradiation.
[So] Source:J Photochem Photobiol B;179:167-174, 2018 Feb.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Exposure of skin to simulated sunlight irradiation (SSI) has being extensively researched and shown to be the main cause for changes in the skin including changes in cellular function and generation of reactive oxygen species (ROS). This oxidative stress can subsequently exert downstream effects and the subcellular compartments most affected by this oxidative stress are mitochondria. The importance of functional mitochondrial morphology is apparent as morphological defects are related to many human diseases including diabetes mellitus, liver disease, neurodegenerative diseases, aging and cancer. OBJECTIVE: The main objective of this study was to evaluate solar radiation-induced changes in mitochondrial gene expression in human skin cells using a Q-Sun solar simulator to deliver a close match to the intensity of summer sunlight. METHODS: Spontaneously immortalised human skin epidermal keratinocytes (HaCaT) and Human Dermal Fibroblasts (HDFn) were divided into two groups. Group A were irradiated once and Group B twice 7days apart; following irradiation, mitochondrial gene expression was evaluated 1, 4 and 7days post primary exposure for group A and 1, 4, 7 and 14days post-secondary exposure for group B. RESULTS: Both the epidermal and dermal cells displayed significant reduced expression of the genes analysed for mitochondrial morphology and function; however, epidermal cells displayed this reduction post SSI earlier then dermal cells at multiple time points. CONCLUSION: The data presented here reinforces the fact that epidermal cells, while displaying a heightened sensitivity to sunlight, are less prone to changes in gene expression, while dermal cells, which appear to be more resilient are possibly more prone to genomic instability and mitochondrial damage.
[Mh] Termos MeSH primário: Expressão Gênica/efeitos da radiação
Mitocôndrias/genética
Luz Solar
[Mh] Termos MeSH secundário: ATPases Associadas a Diversas Atividades Celulares/genética
ATPases Associadas a Diversas Atividades Celulares/metabolismo
Linhagem Celular
Derme/citologia
Epiderme/citologia
GTP Fosfo-Hidrolases/genética
GTP Fosfo-Hidrolases/metabolismo
Seres Humanos
Queratinócitos/citologia
Queratinócitos/metabolismo
Queratinócitos/efeitos da radiação
Metaloendopeptidases/genética
Metaloendopeptidases/metabolismo
Mitocôndrias/efeitos da radiação
Proteínas de Transporte da Membrana Mitocondrial/genética
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Proteínas Mitocondriais/genética
Proteínas Mitocondriais/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Superóxido Dismutase/genética
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mitochondrial Membrane Transport Proteins); 0 (Mitochondrial Proteins); 0 (Reactive Oxygen Species); EC 1.15.1.1 (Superoxide Dismutase); EC 1.15.1.1 (superoxide dismutase 2); EC 3.4.24.- (Metalloendopeptidases); EC 3.4.24.- (YME1L1 protein, human); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.1.- (MFN2 protein, human); EC 3.6.1.- (OPA1 protein, human); EC 3.6.4.- (ATPases Associated with Diverse Cellular Activities); EC 3.6.5.- (Mfn1 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE


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[PMID]:29391135
[Au] Autor:Qi R; Wang D; Xing L; Wu Z
[Ad] Endereço:Departrment of General Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China; Departrment of Thoracic Surgery, Inner Mongolia People's Hospital, Hohhot City, Inner Mongolia, 010017, China.
[Ti] Título:Cyclosporin A inhibits mitochondrial biogenesis in Hep G2 cells.
[So] Source:Biochem Biophys Res Commun;496(3):941-946, 2018 02 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dysregulation of mitochondrial biogenesis is associated with pathogenesis in many diseases, including liver diseases. Cyclosporine A (CsA), one of the most commonly used drug to treat many autoimmune diseases and to prevent allograft rejection after organ transplantation, has been reported to cause mitochondrial dysfunction. However, the cellular mechanisms underlying CsA on mitochondrial dysfunction remain at present not completely elucidated. In this study, we found that CsA reduced the expression of PGC-1α at both the mRNA and protein levels in HepG2 cells. Correspondingly, the expressions of its target genes NRF 1 and TFAM were reduced in response to CsA treatment. In addition, mtDNA/nDNA, mitochondria mass, ATP production, and cytochrome C oxidase activity were significantly reduced by treatment with CsA. Over-expression of PGC-1α was found to rescue the negative effect of CsA administration on mitochondrial biogenesis. Mechanistically, CREB was involved in the inhibitory effects of CsA in mitochondrial biogenesis.
[Mh] Termos MeSH primário: Ciclosporina/administração & dosagem
Mitocôndrias Hepáticas/efeitos dos fármacos
Mitocôndrias Hepáticas/metabolismo
Proteínas Mitocondriais/metabolismo
Biogênese de Organelas
[Mh] Termos MeSH secundário: Relação Dose-Resposta a Droga
Células Hep G2
Seres Humanos
Mitocôndrias Hepáticas/ultraestrutura
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mitochondrial Proteins); 83HN0GTJ6D (Cyclosporine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE


  9 / 16351 MEDLINE  
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[PMID]:29293638
[Au] Autor:Campos MD; Valadas V; Campos C; Morello L; Braglia L; Breviario D; Cardoso HG
[Ad] Endereço:ICAAM-Instituto de Ciências Agrárias e Ambientais Mediterrânicas, Universidade de Évora, Pólo da Mitra, Évora, Portugal.
[Ti] Título:A TaqMan real-time PCR method based on alternative oxidase genes for detection of plant species in animal feed samples.
[So] Source:PLoS One;13(1):e0190668, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Traceability of processed food and feed products has been gaining importance due to the impact that those products can have on human/animal health and to the associated economic and legal concerns, often related to adulterations and frauds as it can be the case for meat and milk. Despite mandatory traceability requirements for the analysis of feed composition, few reliable and accurate methods are presently available to enforce the legislative frame and allow the authentication of animal feeds. In this study, nine sensitive and species-specific real-time PCR TaqMan MGB assays are described for plant species detection in animal feed samples. The method is based on selective real-time qPCR (RT-qPCR) amplification of target genes belonging to the alternative oxidase (AOX) gene family. The plant species selected for detection in feed samples were wheat, maize, barley, soybean, rice and sunflower as common components of feeds, and cotton, flax and peanut as possible undesirable contaminants. The obtained results were compared with end-point PCR methodology. The applicability of the AOX TaqMan assays was evaluated through the screening of commercial feed samples, and by the analysis of plant mixtures with known composition. The RT-qPCR methodology allowed the detection of the most abundant species in feeds but also the identification of contaminant species present in lower amounts, down to 1% w/w. AOX-based methodology provides a suitable molecular marker approach to ascertain plant species composition of animal feed samples, thus supporting feed control and enforcement of the feed sector and animal production.
[Mh] Termos MeSH primário: Ração Animal/análise
Contaminação de Alimentos/análise
Proteínas Mitocondriais/genética
Oxirredutases/genética
Proteínas de Plantas/genética
Plantas
Reação em Cadeia da Polimerase em Tempo Real/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mitochondrial Proteins); 0 (Plant Proteins); EC 1.- (Oxidoreductases); EC 1.- (alternative oxidase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190668


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[PMID]:29241732
[Au] Autor:Park YS; Choi SE; Koh HC
[Ad] Endereço:Department of Pharmacology, College of Medicine, Hanyang University, Seoul, Republic of Korea; Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, Republic of Korea.
[Ti] Título:PGAM5 regulates PINK1/Parkin-mediated mitophagy via DRP1 in CCCP-induced mitochondrial dysfunction.
[So] Source:Toxicol Lett;284:120-128, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mitochondrial dynamics and mitophagy are critical processes for regulating mitochondrial homeostasis. Phosphoglycerate mutase family member 5 (PGAM5) is a mitochondrial protein that plays crucial roles in apoptosis and necroptosis, but the roles of PGAM5 in mitochondrial dynamics and mitophagy remain unclear. In this study, we investigated the role of PGAM5 in carbonyl cyanide m-chlorophenylhydrazone (CCCP)-induced mitochondrial damage and the correlation between mitochondrial dynamics and mitophagy using SH-SY5Y cells. We found that CCCP decreased mitochondrial membrane potential, resulting in mitochondrial dysfunction. CCCP increased PGAM5, dynamin-related protein 1 (DRP1), and optic atrophy 1 (OPA1) expression of the mitochondrial fraction in a time-dependent manner. Knockdown of PGAM5 inhibited DRP1 translocation without a change in OPA1 expression in CCCP-treated cells. Furthermore, knockdown of PGAM5 and DRP1 significantly blocked the increase of PTEN-induced putative protein kinase 1 (PINK1) and Parkin expression in the mitochondrial fraction of CCCP-treated cells. Interestingly, CCCP did not alter PINK1/Parkin expression in the mitochondrial fraction of OPA1 knockdown cells. Inhibiting mitophagy by PGAM5 knockdown accelerated CCCP-induced apoptosis. CCCP treatment also results in PINK1 stabilization on the mitochondrial membrane, which subsequently increases Parkin recruitment from the cytosol to abnormal mitochondria. In addition, we found that CCCP increased the level of mitochondrial LC3II, indicating that Parkin recruitment of PINK1 is a result of mitophagy. We propose that activation of PGAM5 is associated with DRP1 recruitment and PINK1 stabilization, which contribute to the modulation of mitophagy in CCCP-treated cells with mitochondrial dysfunction. In conclusion, we demonstrated that PGAM5 regulates PINK1-Parkin-mediated mitophagy, which can exert a neuroprotective effect against CCCP-induced apoptosis.
[Mh] Termos MeSH primário: Carbonil Cianeto m-Clorofenil Hidrazona/toxicidade
GTP Fosfo-Hidrolases/metabolismo
Proteínas Associadas aos Microtúbulos/metabolismo
Degradação Mitocondrial/efeitos dos fármacos
Proteínas Mitocondriais/metabolismo
Fosfoproteínas Fosfatases/metabolismo
Proteínas Quinases/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
GTP Fosfo-Hidrolases/genética
Técnicas de Silenciamento de Genes
Seres Humanos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Proteínas Associadas aos Microtúbulos/genética
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Mitocôndrias/patologia
Proteínas Mitocondriais/genética
Fosfoproteínas Fosfatases/genética
Proteínas Quinases/genética
Ubiquitina-Proteína Ligases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Microtubule-Associated Proteins); 0 (Mitochondrial Proteins); 555-60-2 (Carbonyl Cyanide m-Chlorophenyl Hydrazone); 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 (PTEN-induced putative kinase); EC 3.1.3.16 (PGAM5 protein, human); EC 3.1.3.16 (Phosphoprotein Phosphatases); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.5.5 (DNM1L protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE



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