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Pesquisa : D08.811.520.224.125.100.500 [Categoria DeCS]
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[PMID]:27869544
[Au] Autor:Tsukioka D; Izumi S; Adachi T
[Ad] Endereço:a Faculty of Science, Department of Biological Sciences , Kanagawa University , Hiratsuka , Japan.
[Ti] Título:Cloning and expression analysis of a novel tissue-specific dopa decarboxylase mRNA splicing variant in Bombyx mori.
[So] Source:Biosci Biotechnol Biochem;81(3):555-557, 2017 Mar.
[Is] ISSN:1347-6947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Dopa decarboxylase (DDC) protein is involved in the synthesis of dopamine and serotonin. Here, we show that in the silkworm Bombyx mori, a novel DDC splicing variant is selectively expressed in the brain and subesophageal ganglia. In Drosophila melanogaster, a neuron-specific isoform of DDC is known to be alternatively spliced in a similar manner.
[Mh] Termos MeSH primário: Bombyx/genética
Dopa Descarboxilase/genética
Proteínas de Insetos/genética
[Mh] Termos MeSH secundário: Regiões 5' não Traduzidas
Processamento Alternativo
Animais
Encéfalo/enzimologia
Clonagem Molecular
Dopa Descarboxilase/metabolismo
Gânglios dos Invertebrados/enzimologia
Regulação Enzimológica da Expressão Gênica
Proteínas de Insetos/metabolismo
Especificidade de Órgãos
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
RNA Mensageiro/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5' Untranslated Regions); 0 (Insect Proteins); 0 (Protein Isoforms); 0 (RNA, Messenger); EC 4.1.1.- (Dopa Decarboxylase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170306
[Lr] Data última revisão:
170306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161122
[St] Status:MEDLINE
[do] DOI:10.1080/09168451.2016.1258987


  2 / 1066 MEDLINE  
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[PMID]:28100850
[Au] Autor:Guenter J; Lenartowski R
[Ad] Endereço:Zaklad Genetyki, Uniwersytet Mikolaja Kopernika w Toruniu.
[Ti] Título:Molecular characteristic and physiological role of DOPA-decarboxylase.
[So] Source:Postepy Hig Med Dosw (Online);70(0):1424-1440, 2016 Dec 31.
[Is] ISSN:1732-2693
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:The enzyme DOPA decarboxylase (aromatic-L-amino-acid decarboxylase, DDC) plays an important role in the dopaminergic system and participates in the uptake and decarboxylation of amine precursors in the peripheral tissues. Apart from catecholamines, DDC catalyses the biosynthesis of serotonin and trace amines. It has been shown that the DDC amino acid sequence is highly evolutionarily conserved across many species. The activity of holoenzyme is regulated by stimulation/blockade of membrane receptors, phosphorylation of serine residues, and DDC interaction with regulatory proteins. A single gene codes for DDC both in neuronal and non-neuronal tissue, but synthesized isoforms of mRNA differ in the 5' UTR and in the presence of alternative exons. Tissue-specific expression of the DDC gene is controlled by two spatially distinct promoters - neuronal and non-neuronal. Several consensus sequences recognized by the HNF and POU family proteins have been mapped in the neuronal DDC promoter. Since DDC is located close to the imprinted gene cluster, its expression can be subjected to tightly controlled epigenetic regulation. Perturbations in DDC expression result in a range of neurodegenerative and psychiatric disorders and correlate with neoplasia. Apart from the above issues, the role of DDC in prostate cancer, bipolar affective disorder, Parkinson's disease and DDC deficiency is discussed in our review. Moreover, novel and prospective clinical treatments based on gene therapy and stem cells for the diseases mentioned above are described.
[Mh] Termos MeSH primário: Dopa Descarboxilase/metabolismo
[Mh] Termos MeSH secundário: Erros Inatos do Metabolismo dos Aminoácidos/metabolismo
Descarboxilases de Aminoácido-L-Aromático/deficiência
Descarboxilases de Aminoácido-L-Aromático/metabolismo
Catecolaminas/biossíntese
Dopa Descarboxilase/química
Dopa Descarboxilase/genética
Dopa Descarboxilase/fisiologia
Feminino
Regulação da Expressão Gênica
Seres Humanos
Masculino
Doença de Parkinson/metabolismo
Neoplasias da Próstata/metabolismo
Conformação Proteica
Isoformas de Proteínas/metabolismo
Serotonina/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Catecholamines); 0 (Protein Isoforms); 333DO1RDJY (Serotonin); EC 4.1.1.- (Dopa Decarboxylase); EC 4.1.1.28 (Aromatic-L-Amino-Acid Decarboxylases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE
[do] DOI:10.5604/17322693.1227773


  3 / 1066 MEDLINE  
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[PMID]:27813607
[Au] Autor:M'Angale PG; Staveley BE
[Ad] Endereço:Department of Biology, Memorial University of Newfoundland, St. John's, Newfoundland and Labrador, Canada.
[Ti] Título:Inhibition of Atg6 and Pi3K59F autophagy genes in neurons decreases lifespan and locomotor ability in Drosophila melanogaster.
[So] Source:Genet Mol Res;15(4), 2016 Oct 24.
[Is] ISSN:1676-5680
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Autophagy is a cellular mechanism implicated in the pathology of Parkinson's disease. The proteins Atg6 (Beclin 1) and Pi3K59F are involved in autophagosome formation, a key step in the initiation of autophagy. We first used the GMR-Gal4 driver to determine the effect of reducing the expression of the genes encoding these proteins on the developing Drosophila melanogaster eye. Subsequently, we inhibited their expression in D. melanogaster neurons under the direction of a Dopa decarboxylase (Ddc) transgene, and examined the effects on longevity and motor function. Decreased longevity coupled with an age-dependent loss of climbing ability was observed. In addition, we investigated the roles of these genes in the well-studied α-synuclein-induced Drosophila model of Parkinson's disease. In this context, lowered expression of Atg6 or Pi3K59F in Ddc-Gal4-expressing neurons results in decreased longevity and associated age-dependent loss of locomotor ability. Inhibition of Atg6 or Pi3K59F together with overexpression of the sole pro-survival Bcl-2 Drosophila homolog Buffy in Ddc-Gal4-expressing neurons resulted in further decrease in the survival and climbing ability of Atg6-RNAi flies, whereas these measures were ameliorated in Pi3K59F-RNAi flies.
[Mh] Termos MeSH primário: Autofagia/genética
Beclina-1/genética
Dopa Descarboxilase/genética
Proteínas de Drosophila/genética
Doença de Parkinson/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Beclina-1/biossíntese
Modelos Animais de Doenças
Dopa Descarboxilase/biossíntese
Proteínas de Drosophila/biossíntese
Drosophila melanogaster/genética
Olho/crescimento & desenvolvimento
Olho/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Seres Humanos
Longevidade/genética
Atividade Motora/genética
Neurônios/metabolismo
Neurônios/patologia
Doença de Parkinson/patologia
Interferência de RNA
alfa-Sinucleína/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Atg6 protein, Drosophila); 0 (Beclin-1); 0 (Drosophila Proteins); 0 (alpha-Synuclein); EC 4.1.1.- (Dopa Decarboxylase)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170221
[Lr] Data última revisão:
170221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE
[do] DOI:10.4238/gmr15048953


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[PMID]:27658936
[Au] Autor:Lee NC; Lee YM; Chen PW; Byrne BJ; Hwu WL
[Ad] Endereço:Department of Medical Genetics, National Taiwan University Hospital, Taipei, Taiwan.
[Ti] Título:Mutation-adapted U1 snRNA corrects a splicing error of the dopa decarboxylase gene.
[So] Source:Hum Mol Genet;25(23):5142-5147, 2016 Dec 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aromatic l-amino acid decarboxylase (AADC) deficiency is an inborn error of monoamine neurotransmitter synthesis, which results in dopamine, serotonin, epinephrine and norepinephrine deficiencies. The DDC gene founder mutation IVS6 + 4A > T is highly prevalent in Chinese patients with AADC deficiency. In this study, we designed several U1 snRNA vectors to adapt U1 snRNA binding sequences of the mutated DDC gene. We found that only the modified U1 snRNA (IVS-AAA) that completely matched both the intronic and exonic U1 binding sequences of the mutated DDC gene could correct splicing errors of either the mutated human DDC minigene or the mouse artificial splicing construct in vitro. We further injected an adeno-associated viral (AAV) vector to express IVS-AAA in the brain of a knock-in mouse model. This treatment was well tolerated and improved both the survival and brain dopamine and serotonin levels of mice with AADC deficiency. Therefore, mutation-adapted U1 snRNA gene therapy can be a promising method to treat genetic diseases caused by splicing errors, but the efficiency of such a treatment still needs improvements.
[Mh] Termos MeSH primário: Erros Inatos do Metabolismo dos Aminoácidos/genética
Descarboxilases de Aminoácido-L-Aromático/deficiência
Dopa Descarboxilase/genética
Terapia Genética
RNA Nuclear Pequeno/genética
[Mh] Termos MeSH secundário: Erros Inatos do Metabolismo dos Aminoácidos/terapia
Animais
Descarboxilases de Aminoácido-L-Aromático/genética
Dependovirus/genética
Modelos Animais de Doenças
Éxons/genética
Técnicas de Introdução de Genes
Seres Humanos
Íntrons/genética
Camundongos
Mutação
Neurotransmissores/genética
Processamento de RNA/genética
RNA Nuclear Pequeno/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurotransmitter Agents); 0 (RNA, Small Nuclear); 0 (U1 small nuclear RNA); EC 4.1.1.- (Dopa Decarboxylase); EC 4.1.1.28 (Aromatic-L-Amino-Acid Decarboxylases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160924
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddw323


  5 / 1066 MEDLINE  
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[PMID]:27366756
[Au] Autor:Cataldo LR; Mizgier ML; Busso D; Olmos P; Galgani JE; Valenzuela R; Mezzano D; Aranda E; Cortés VA; Santos JL
[Ad] Endereço:Departamento de Nutrición, Diabetes y Metabolismo, Escuela de Medicina, Pontificia Universidad Católica de Chile, 8331150 Santiago, Chile; Facultad de Medicina, Universidad de los Andes, 7620001 Santiago, Chile.
[Ti] Título:Serotonin- and Dopamine-Related Gene Expression in db/db Mice Islets and in MIN6 ß-Cells Treated with Palmitate and Oleate.
[So] Source:J Diabetes Res;2016:3793781, 2016.
[Is] ISSN:2314-6753
[Cp] País de publicação:Egypt
[La] Idioma:eng
[Ab] Resumo:High circulating nonesterified fatty acids (NEFAs) concentration, often reported in diabetes, leads to impaired glucose-stimulated insulin secretion (GSIS) through not yet well-defined mechanisms. Serotonin and dopamine might contribute to NEFA-dependent ß-cell dysfunction, since extracellular signal of these monoamines decreases GSIS. Moreover, palmitate-treated ß-cells may enhance the expression of the serotonin receptor Htr2c, affecting insulin secretion. Additionally, the expression of monoamine-oxidase type B (Maob) seems to be lower in islets from humans and mice with diabetes compared to nondiabetic islets, which may lead to increased monoamine concentrations. We assessed the expression of serotonin- and dopamine-related genes in islets from db/db and wild-type (WT) mice. In addition, the effect of palmitate and oleate on the expression of such genes, 5HT content, and GSIS in MIN6 ß-cell was determined. Lower Maob expression was found in islets from db/db versus WT mice and in MIN6 ß-cells in response to palmitate and oleate treatment compared to vehicle. Reduced 5HT content and impaired GSIS in response to palmitate (-25%; p < 0.0001) and oleate (-43%; p < 0.0001) were detected in MIN6 ß-cells. In conclusion, known defects of GSIS in islets from db/db mice and MIN6 ß-cells treated with NEFAs are accompanied by reduced Maob expression and reduced 5HT content.
[Mh] Termos MeSH primário: Células Secretoras de Insulina/efeitos dos fármacos
Ilhotas Pancreáticas/metabolismo
Transcriptoma/genética
[Mh] Termos MeSH secundário: Acetilserotonina O-Metiltransferasa/efeitos dos fármacos
Acetilserotonina O-Metiltransferasa/genética
Animais
Arilalquilamina N-Acetiltransferase/efeitos dos fármacos
Arilalquilamina N-Acetiltransferase/genética
Catecol O-Metiltransferase/efeitos dos fármacos
Catecol O-Metiltransferase/genética
Linhagem Celular
Dopa Descarboxilase/efeitos dos fármacos
Dopa Descarboxilase/genética
Proteínas da Membrana Plasmática de Transporte de Dopamina/efeitos dos fármacos
Proteínas da Membrana Plasmática de Transporte de Dopamina/genética
Dopamina beta-Hidroxilase/efeitos dos fármacos
Dopamina beta-Hidroxilase/genética
Insulina/metabolismo
Insulina/secreção
Células Secretoras de Insulina/metabolismo
Camundongos
Monoaminoxidase/efeitos dos fármacos
Monoaminoxidase/genética
Ácido Oleico/farmacologia
Ácido Palmítico/farmacologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Serotonina/metabolismo
Proteínas da Membrana Plasmática de Transporte de Serotonina/efeitos dos fármacos
Proteínas da Membrana Plasmática de Transporte de Serotonina/genética
Transcriptoma/efeitos dos fármacos
Triptofano Hidroxilase/efeitos dos fármacos
Triptofano Hidroxilase/genética
Tirosina 3-Mono-Oxigenase/efeitos dos fármacos
Tirosina 3-Mono-Oxigenase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dopamine Plasma Membrane Transport Proteins); 0 (Insulin); 0 (Serotonin Plasma Membrane Transport Proteins); 0 (Slc6a3 protein, mouse); 0 (Slc6a4 protein, mouse); 2UMI9U37CP (Oleic Acid); 2V16EO95H1 (Palmitic Acid); 333DO1RDJY (Serotonin); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 1.14.16.4 (Tph1 protein, mouse); EC 1.14.16.4 (Tph2 protein, mouse); EC 1.14.16.4 (Tryptophan Hydroxylase); EC 1.14.17.1 (Dopamine beta-Hydroxylase); EC 1.4.3.4 (Monoamine Oxidase); EC 2.1.1.4 (Acetylserotonin O-Methyltransferase); EC 2.1.1.6 (COMT protein, mouse); EC 2.1.1.6 (Catechol O-Methyltransferase); EC 2.3.1.87 (Arylalkylamine N-Acetyltransferase); EC 4.1.1.- (Dopa Decarboxylase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170609
[Lr] Data última revisão:
170609
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160702
[St] Status:MEDLINE
[do] DOI:10.1155/2016/3793781


  6 / 1066 MEDLINE  
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[PMID]:26827723
[Au] Autor:Mitra S; Ghosh N; Sinha P; Chakrabarti N; Bhattacharyya A
[Ad] Endereço:Immunology Lab, Department of Zoology, University of Calcutta, 35, Ballygunge Circular Road, Kolkata 700019, India. Electronic address: soham_envs@yahoo.co.in.
[Ti] Título:Alteration of nuclear factor-kappaB pathway promote neuroinflammation depending on the functions of estrogen receptors in substantia nigra after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treatment.
[So] Source:Neurosci Lett;616:86-92, 2016 Mar 11.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The simultaneous role of neuroprotective estrogen and neurodegenerative inflammation during the progression of Parkinson's disease (PD) is still remaining elusive. The novel importance of the present study in MPTP mediated mouse model of Parkinson's disease (PD) is-to investigate the status of neuronal and glial cells in a time chase experiment; to explore which pathway of NF-kappaB exist to proceed the neuroinflammation; to investigate the status of estrogen and the activation pattern of nuclear or cytosolic estrogen receptors in either sexes of Swiss albino mice during MPTP mediated progressive neurodegeneration in the substantia nigra. After MPTP intoxication, the nigral molecular anatomy was changed differently in separate time interval during the progression of neurodegeneration with/without association of glial cells and functional (via its nuclear and cytosolic receptors) estrogen level. Both the canonical and/or non-canonical pathways of NF-kappaB exist in the substantia nigra of both the sexes after MPTP treatment that is why inspite of presence of estrogen, neuroinflammation progresses. The homodimeric or heterodimeric form of ER-beta binds with NF-kappaB molecules p65 and RelB differently, but the canonical or non-canonical pathways of NF-kappaB molecules could not be stopped or may be promoted.
[Mh] Termos MeSH primário: 1-Metil-4-Fenil-1,2,3,6-Tetra-Hidropiridina
NF-kappa B/metabolismo
Doença de Parkinson/metabolismo
Receptores Estrogênicos/metabolismo
Substância Negra/metabolismo
[Mh] Termos MeSH secundário: Animais
Astrócitos/metabolismo
Proteínas de Ligação ao Cálcio/metabolismo
Contagem de Células
Modelos Animais de Doenças
Dopa Descarboxilase/metabolismo
Estradiol/metabolismo
Receptor alfa de Estrogênio/metabolismo
Receptor beta de Estrogênio/metabolismo
Feminino
Proteína Glial Fibrilar Ácida/metabolismo
Inflamação/metabolismo
Masculino
Camundongos
Proteínas dos Microfilamentos/metabolismo
Microglia/metabolismo
Neurônios/enzimologia
Neurônios/patologia
Doença de Parkinson/etiologia
Fatores Sexuais
Fator de Transcrição RelA/metabolismo
Fator de Transcrição RelB/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aif1 protein, rat); 0 (Calcium-Binding Proteins); 0 (Estrogen Receptor alpha); 0 (Estrogen Receptor beta); 0 (Glial Fibrillary Acidic Protein); 0 (Microfilament Proteins); 0 (NF-kappa B); 0 (Receptors, Estrogen); 0 (Relb protein, rat); 0 (Transcription Factor RelA); 147337-75-5 (Transcription Factor RelB); 4TI98Z838E (Estradiol); 9P21XSP91P (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine); EC 4.1.1.- (Dopa Decarboxylase)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160318
[Lr] Data última revisão:
160318
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160202
[St] Status:MEDLINE


  7 / 1066 MEDLINE  
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[PMID]:26337060
[Au] Autor:Yu H; Liu J; Yang A; Yang G; Yang W; Lei H; Quan J; Zhang Z
[Ad] Endereço:Department of Child and Adolescent Mental Health, Zhejiang Xiaoshan Hospital, Hangzhou, Zhejiang, China.
[Ti] Título:Lack of Association Between Polymorphisms in Dopa Decarboxylase and Dopamine Receptor-1 Genes With Childhood Autism in Chinese Han Population.
[So] Source:J Child Neurol;31(5):560-4, 2016 Apr.
[Is] ISSN:1708-8283
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genetic factors play an important role in childhood autism. This study is to determine the association of single-nucleotide polymorphisms in dopa decarboxylase (DDC) and dopamine receptor-1 (DRD1) genes with childhood autism, in a Chinese Han population. A total of 211 autistic children and 250 age- and gender-matched healthy controls were recruited. The severity of disease was determined by Children Autism Rating Scale scores. TaqMan Probe by real-time polymerase chain reaction was used to determine genotypes and allele frequencies of single-nucleotide polymorphism rs6592961 in DDC and rs251937 in DRD1. Case-control and case-only studies were respectively performed, to determine the contribution of both single-nucleotide polymorphisms to the predisposition of disease and its severity. Our results showed that there was no significant association of the genotypes and allele frequencies of both single-nucleotide polymorphisms concerning childhood autism and its severity. More studies with larger samples are needed to corroborate their predicting roles.
[Mh] Termos MeSH primário: Transtorno Autístico/genética
Dopa Descarboxilase/genética
Polimorfismo de Nucleotídeo Único/genética
Receptores de Dopamina D1/genética
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático/etnologia
Grupo com Ancestrais do Continente Asiático/genética
Transtorno Autístico/etnologia
Criança
Pré-Escolar
Feminino
Frequência do Gene
Estudos de Associação Genética
Genótipo
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Dopamine D1); EC 4.1.1.- (Dopa Decarboxylase)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150905
[St] Status:MEDLINE
[do] DOI:10.1177/0883073815601496


  8 / 1066 MEDLINE  
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[PMID]:26297895
[Au] Autor:Martin HL; Alsaady I; Howell G; Prandovszky E; Peers C; Robinson P; McConkey GA
[Ad] Endereço:Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, United Kingdom.
[Ti] Título:Effect of parasitic infection on dopamine biosynthesis in dopaminergic cells.
[So] Source:Neuroscience;306:50-62, 2015 Oct 15.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Infection by the neurotropic agent Toxoplasma gondii alters rodent behavior and can result in neuropsychiatric symptoms in humans. Little is understood regarding the effects of infection on host neural processes but alterations to dopaminergic neurotransmission are implicated. We have previously reported elevated levels of dopamine (DA) in infected dopaminergic cells however the involvement of the host enzymes and fate of the produced DA were not defined. In order to clarify the effects of infection on host DA biosynthetic enzymes and DA packaging we examined enzyme levels and activity and DA accumulation and release in T. gondii-infected neurosecretory cells. Although the levels of the host tyrosine hydroxylase (TH) and DOPA decarboxylase and AADC (DDC) did not change significantly in infected cultures, DDC was found within the parasitophorous vacuole (PV), the vacuolar compartment where the parasites reside, as well as in the host cytosol in infected dopaminergic cells. Strikingly, DDC was found within the intracellular parasite cysts in infected brain tissue. This finding could provide some explanation for observations of DA within tissue cysts in infected brain as a parasite-encoded enzyme with TH activity was also localized within tissue cysts. In contrast, cellular DA packaging appeared unchanged in single-cell microamperometry experiments and only a fraction of the increased DA was accessible to high potassium-induced release. This study provides some understanding of how this parasite produces elevated DA within dopaminergic cells without the toxic ramifications of free cytosolic DA. The mechanism for synthesis and packaging of DA by T. gondii-infected dopaminergic cells may have important implications for the effects of chronic T. gondii infection on humans and animals.
[Mh] Termos MeSH primário: Encéfalo/parasitologia
Dopamina/biossíntese
Neurônios Dopaminérgicos/metabolismo
Neurônios Dopaminérgicos/parasitologia
Toxoplasmose/metabolismo
[Mh] Termos MeSH secundário: Animais
Descarboxilases de Aminoácido-L-Aromático/metabolismo
Encéfalo/metabolismo
Dopa Descarboxilase/metabolismo
Neurônios Dopaminérgicos/enzimologia
Células PC12
Ratos
Vesículas Sinápticas/metabolismo
Toxoplasmose/enzimologia
Tirosina 3-Mono-Oxigenase/metabolismo
Proteínas Vesiculares de Transporte de Monoamina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Slc18a1 protein, rat); 0 (Vesicular Monoamine Transport Proteins); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 4.1.1.- (Dopa Decarboxylase); EC 4.1.1.28 (Aromatic-L-Amino-Acid Decarboxylases); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:151027
[Lr] Data última revisão:
151027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150823
[St] Status:MEDLINE


  9 / 1066 MEDLINE  
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[PMID]:26084938
[Au] Autor:Liu S; Wang M; Li X
[Ad] Endereço:1] Department of Pesticide Science, College of Plant Science &Technology, Huazhong Agricultural University, Wuhan, 430070, China [2] Department of Entomology and BIO5 Institute, University of Arizona, Tucson, AZ 85721, USA [3] Hubei Insect Resources Utilization and Sustainable Pest Management Key Laboratory, Institute of Insect Resources, Huazhong Agricultural University, Wuhan, 430070, China.
[Ti] Título:Overexpression of Tyrosine hydroxylase and Dopa decarboxylase associated with pupal melanization in Spodoptera exigua.
[So] Source:Sci Rep;5:11273, 2015 Jun 18.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Melanism has been found in a wide range of species, but the molecular mechanisms involved remain largely elusive. In this study, we studied the molecular mechanisms of the pupal melanism in Spodoptera exigua. The full length cDNA sequences of tyrosine hydroxylase (TH) and dopa decarboxylase (DDC), two key enzymes in the biosynthesis pathway of melanin, were cloned, and their temporal expression patterns in the integument were compared during the larval-pupal metamorphosis process of the S. exigua wild type (SEW) and melanic mutant (SEM) strains. No amino acid change in the protein sequence of TH and DDC was found between the two strains. Both DDC and TH were significantly over-expressed in the integument of the SEM strain at late-prepupa and 0 h pupa, respectively, compared with those of the SEW strain. Feeding 5(th) instar larvae of SEM with diets incorporated with 1 mg/g of the DDC inhibitor L-α-Methyl-DOPA and 0.75 mg/g of the TH inhibitor 3-iodo-tyrosine (3-IT) resulted in 20% pupae with partially-rescued phenotype and 68.2% of pupae with partially- or fully-rescued phenotype, respectively. These results indicate that overexpressions of TH and DDC are involved in the pupal melanization of S. exigua.
[Mh] Termos MeSH primário: Dopa Descarboxilase/genética
Expressão Gênica
Melaninas/metabolismo
Pigmentação
Pupa
Spodoptera/genética
Spodoptera/metabolismo
Tirosina 3-Mono-Oxigenase/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Sítios de Ligação
DNA Complementar/genética
DNA Complementar/metabolismo
Dopa Descarboxilase/metabolismo
Dados de Sequência Molecular
Mutação
Fenótipo
Filogenia
Ligação Proteica
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Melanins); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 4.1.1.- (Dopa Decarboxylase)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:150701
[Lr] Data última revisão:
150701
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150619
[St] Status:MEDLINE
[do] DOI:10.1038/srep11273


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[PMID]:25984720
[Au] Autor:DeLoache WC; Russ ZN; Narcross L; Gonzales AM; Martin VJ; Dueber JE
[Ad] Endereço:Department of Bioengineering, University of California, Berkeley, Berkeley, California, USA.
[Ti] Título:An enzyme-coupled biosensor enables (S)-reticuline production in yeast from glucose.
[So] Source:Nat Chem Biol;11(7):465-71, 2015 Jul.
[Is] ISSN:1552-4469
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Benzylisoquinoline alkaloids (BIAs) are a diverse family of plant-specialized metabolites that include the pharmaceuticals codeine and morphine and their derivatives. Microbial synthesis of BIAs holds promise as an alternative to traditional crop-based manufacturing. Here we demonstrate the production of the key BIA intermediate (S)-reticuline from glucose in Saccharomyces cerevisiae. To aid in this effort, we developed an enzyme-coupled biosensor for the upstream intermediate L-3,4-dihydroxyphenylalanine (L-DOPA). Using this sensor, we identified an active tyrosine hydroxylase and improved its L-DOPA yields by 2.8-fold via PCR mutagenesis. Coexpression of DOPA decarboxylase enabled what is to our knowledge the first demonstration of dopamine production from glucose in yeast, with a 7.4-fold improvement in titer obtained for our best mutant enzyme. We extended this pathway to fully reconstitute the seven-enzyme pathway from L-tyrosine to (S)-reticuline. Future work to improve titers and connect these steps with downstream pathway branches, already demonstrated in S. cerevisiae, will enable low-cost production of many high-value BIAs.
[Mh] Termos MeSH primário: Alcaloides/biossíntese
Benzilisoquinolinas/metabolismo
Técnicas Biossensoriais
Di-Hidroxifenilalanina/análise
Proteínas Fúngicas/metabolismo
Regulação Fúngica da Expressão Gênica
Saccharomyces cerevisiae/metabolismo
[Mh] Termos MeSH secundário: Di-Hidroxifenilalanina/metabolismo
Dopa Descarboxilase/genética
Dopa Descarboxilase/metabolismo
Dopamina/biossíntese
Proteínas Fúngicas/genética
Glucose/metabolismo
Engenharia Metabólica
Mutagênese Sítio-Dirigida
Entorpecentes/metabolismo
Saccharomyces cerevisiae/genética
Tirosina 3-Mono-Oxigenase/genética
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Alkaloids); 0 (Benzylisoquinolines); 0 (Fungal Proteins); 0 (Narcotics); 63-84-3 (Dihydroxyphenylalanine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 4.1.1.- (Dopa Decarboxylase); IY9XDZ35W2 (Glucose); VTD58H1Z2X (Dopamine); X35Z551WT4 (reticuline)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150519
[St] Status:MEDLINE
[do] DOI:10.1038/nchembio.1816



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