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[PMID]:28398555
[Au] Autor:Helassa N; Antonyuk SV; Lian LY; Haynes LP; Burgoyne RD
[Ad] Endereço:Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool L69?3BX, UK.
[Ti] Título:Biophysical and functional characterization of hippocalcin mutants responsible for human dystonia.
[So] Source:Hum Mol Genet;26(13):2426-2435, 2017 Jul 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Dystonia is a neurological movement disorder that forces the body into twisting, repetitive movements or sometimes painful abnormal postures. With the advent of next-generation sequencing technologies, the homozygous mutations T71N and A190T in the neuronal calcium sensor (NCS) hippocalcin were identified as the genetic cause of primary isolated dystonia (DYT2 dystonia). However, the effect of these mutations on the physiological role of hippocalcin has not yet been elucidated. Using a multidisciplinary approach, we demonstrated that hippocalcin oligomerises in a calcium-dependent manner and binds to voltage-gated calcium channels. Mutations T71N and A190T in hippocalcin did not affect stability, calcium-binding affinity or translocation to cellular membranes (Ca2+/myristoyl switch). We obtained the first crystal structure of hippocalcin and alignment with other NCS proteins showed significant variability in the orientation of the C-terminal part of the molecule, the region expected to be important for target binding. We demonstrated that the disease-causing mutations did not affect the structure of the protein, however both mutants showed a defect in oligomerisation. In addition, we observed an increased calcium influx in KCl-depolarised cells expressing mutated hippocalcin, mostly driven by N-type voltage-gated calcium channels. Our data demonstrate that the dystonia-causing mutations strongly affect hippocalcin cellular functions which suggest a central role for perturbed calcium signalling in DYT2 dystonia.
[Mh] Termos MeSH primário: Distonia/genética
Hipocalcina/genética
Hipocalcina/metabolismo
[Mh] Termos MeSH secundário: Cálcio/metabolismo
Canais de Cálcio/metabolismo
Sinalização do Cálcio
Proteínas de Ligação ao Cálcio/genética
Técnicas de Cultura de Células
Membrana Celular/metabolismo
Distúrbios Distônicos
Hipocalcina/fisiologia
Seres Humanos
Mutação
Ácido Mirístico/metabolismo
Proteínas do Tecido Nervoso/genética
Neurônios/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (Calcium-Binding Proteins); 0 (HPCA protein, human); 0 (Nerve Tissue Proteins); 0I3V7S25AW (Myristic Acid); 149223-81-4 (Hippocalcin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170412
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx133


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[PMID]:27816759
[Au] Autor:Liang X; Martyniuk CJ; Zha J; Wang Z
[Ad] Endereço:Key Laboratory of Drinking Water Science and Technology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China; College of Environment and Resources, Inner Mongolia University, Hohhot 010021, China.
[Ti] Título:Brain quantitative proteomic responses reveal new insight of benzotriazole neurotoxicity in female Chinese rare minnow (Gobiocypris rarus).
[So] Source:Aquat Toxicol;181:67-75, 2016 Dec.
[Is] ISSN:1879-1514
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Benzotriazole (BT) is a high-production volume chemical which has been ubiquitously detected in aquatic environments. Although adverse effects from acute and chronic exposure to BT have been reported, the neurotoxic effect of BT and the mechanisms of toxicity are not well documented. In this study, adult female Chinese rare minnow (Gobiocypris rarus) were exposed to 0.05, 0.5, and 5mg/L BT for 28days. The brain proteome showed that BT exposure mainly involved in metabolic process, signal transduction, stress response, cytoskeleton, and transport. Pathway analysis revealed that cellular processes affected by BT included cellular respiration, G-protein signal cascades, Ca -dependent signaling, cell cycle and apoptosis. Moreover, data on relative mRNA levels demonstrated that genes related to these toxic pathways were also significantly affected by BT. Furthermore, proteins affected by BT such as CKBB, GS, HPCA, VDAC1, and FLOT1A are associated with neurological disorders. Therefore, our finding suggested that BT induced molecular responses in the brain and could provide new insight into BT neurotoxicity in Chinese rare minnow.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Cyprinidae/metabolismo
Proteoma/efeitos dos fármacos
Triazóis/toxicidade
Poluentes Químicos da Água/toxicidade
[Mh] Termos MeSH secundário: Animais
China
Análise por Conglomerados
Cyprinidae/crescimento & desenvolvimento
Eletroforese em Gel Bidimensional
Feminino
Proteínas de Peixes/genética
Proteínas de Peixes/metabolismo
Hipocalcina/genética
Hipocalcina/metabolismo
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Proteoma/metabolismo
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Canal de Ânion 1 Dependente de Voltagem/genética
Canal de Ânion 1 Dependente de Voltagem/metabolismo
Poluentes Químicos da Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fish Proteins); 0 (Membrane Proteins); 0 (Proteome); 0 (RNA, Messenger); 0 (Triazoles); 0 (Water Pollutants, Chemical); 0 (flotillins); 149223-81-4 (Hippocalcin); 86110UXM5Y (benzotriazole); EC 1.6.- (Voltage-Dependent Anion Channel 1)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170201
[Lr] Data última revisão:
170201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


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[PMID]:27372904
[Au] Autor:Oikawa K; Odero GL; Nafez S; Ge N; Zhang D; Kobayashi H; Sate K; Kimura S; Tateno M; Albensi BC
[Ad] Endereço:Division of Neurodegenerative Disorders, St. Boniface Hospital Research, 351 Tache Ave./Room 4050, Winnipeg, MB, R2H 2A6, Canada.
[Ti] Título:Visinin-Like Protein-3 Modulates the Interaction Between Cytochrome b and NADH-Cytochrome b Reductase in a Ca -Dependent Manner.
[So] Source:Cell Biochem Biophys;74(4):449-457, 2016 Dec.
[Is] ISSN:1559-0283
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Visinin-like proteins (VILIPs) belong to the calcium sensor protein family. VILIP-1 has been examined as a cerebrospinal fluid biomarker and as a potential indicator for cognitive decline in Alzheimer's disease (AD). However, little is known about VILIP-3 protein biochemistry. We performed co-immunoprecipitation experiments to examine whether VILIP-3 can interact with reduced nicotine adenine dinucleotide (NADH)-cytochrome b reductase. We also evaluated the specificity of cytochrome b within the visinin-like protein subfamily and identified cytochrome P450 isoforms in the brain. In this study, we show that cytochrome b has an affinity for hippocalcin, neurocalcin-δ, and VILIP-3, but not visinin-like protein-1. VILIP-3 was also shown to interact with NADH-cytochrome b reductase in a Ca -dependent manner. These results suggest that VILIP-3, hippocalcin, and neurocalcin-δ provide a Ca -dependent modulation to the NADH-dependent microsomal electron transport. The results also suggest that future therapeutic strategies that target calcium-signaling pathways and VILIPs may be of value.
[Mh] Termos MeSH primário: Proteínas de Ligação ao Cálcio/metabolismo
Citocromo-B(5) Redutase/metabolismo
Citocromos b5/metabolismo
Proteínas do Tecido Nervoso/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Encéfalo/metabolismo
Cálcio/química
Cálcio/metabolismo
Proteínas de Ligação ao Cálcio/genética
Citocromo P-450 CYP4A/metabolismo
Citocromo-B(5) Redutase/química
Citocromos b5/química
Células HEK293
Hipocalcina/química
Hipocalcina/metabolismo
Seres Humanos
Imunoprecipitação
Íons/química
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Dados de Sequência Molecular
Proteínas do Tecido Nervoso/genética
Neurocalcina/química
Neurocalcina/metabolismo
Plasmídeos/genética
Plasmídeos/metabolismo
Ligação Proteica
Alinhamento de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium-Binding Proteins); 0 (Ions); 0 (Nerve Tissue Proteins); 0 (Neurocalcin); 0 (VILIP-3 protein, mouse); 149223-81-4 (Hippocalcin); 9035-39-6 (Cytochromes b5); EC 1.14.15.3 (Cytochrome P-450 CYP4A); EC 1.6.2.2 (Cytochrome-B(5) Reductase); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170119
[Lr] Data última revisão:
170119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160704
[St] Status:MEDLINE


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[PMID]:27066884
[Au] Autor:Nazari M; Keshavarz S; Rafati A; Namavar MR; Haghani M
[Ad] Endereço:Department of physiology, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address: nazari_290@yahoo.com.
[Ti] Título:Fingolimod (FTY720) improves hippocampal synaptic plasticity and memory deficit in rats following focal cerebral ischemia.
[So] Source:Brain Res Bull;124:95-102, 2016 Jun.
[Is] ISSN:1873-2747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fingolimod (FTY720) is a known sphingosine-1-phosphate (S1P) receptor agonist. Several studies have shown the therapeutic efficacy of FTY720 in neurodegenerative disorders. However, the neuroprotective mechanisms in brain ischemia have not been adequately studied. Therefore, the present study aimed to investigate the effects of FTY720 on the impairment of learning and memory and hippocampal synaptic plasticity induced by middle cerebral artery occlusion (MCAO) in ischemic brain injury. Twenty eight male rats were randomly divided into four groups of control (n=7), sham (n=8), ischemic-reperfusion+vehicle (I/R+V; n=7), and I/R+FTY720 (n=6). After 1h of the occlusion of artery, the filament was gently withdrawn to allow reperfusion for the next 7 days. The animals first received a dose of FTY720 (0.5mg/Kg) or its vehicle (intra-peritoneal) twenty-four hours before surgery in I/R+FTY720 and I/R+V groups, respectively. The administration of FTY720 or its vehicle continued every other day. The passive avoidance test and field potential recording were used for evaluation of learning, memory and synaptic plasticity. The brain infarct volume was measured by triphenyltetrazolim hydrochloride (TTC) staining. MCAO caused infarct damage in the rat's brain tissue. The administration of FTY720 significantly reduced the size of the lesion, improved the memory impairment of MCAO rats, and increased the STL time. In addition, the field potential recording demonstrated a marked reduction in induction of long-term potentiation of MCAO animals. However, administration of FTY720 recovers the magnitude of the LTP without any effects on presynaptic plasticity and neurotransmitter release probability. The results of this study demonstrated that MCAO in rats impairs the retention of passive avoidance tasks and multiple injection of FTY720 improved the memory performance after MCAO by LTP induction via post-synaptic mechanisms.
[Mh] Termos MeSH primário: Cloridrato de Fingolimode/uso terapêutico
Hipocalcina/efeitos dos fármacos
Imunossupressores/uso terapêutico
Infarto da Artéria Cerebral Média/patologia
Transtornos da Memória/etiologia
Plasticidade Neuronal/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Aprendizagem da Esquiva/efeitos dos fármacos
Infarto Encefálico/tratamento farmacológico
Infarto Encefálico/etiologia
Modelos Animais de Doenças
Infarto da Artéria Cerebral Média/complicações
Potenciação de Longa Duração/efeitos dos fármacos
Linfócitos/efeitos dos fármacos
Masculino
Transtornos da Memória/tratamento farmacológico
Exame Neurológico
Neutrófilos/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Reperfusão
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunosuppressive Agents); 149223-81-4 (Hippocalcin); G926EC510T (Fingolimod Hydrochloride)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160413
[St] Status:MEDLINE


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[PMID]:27001424
[Au] Autor:Krishnan A; Viviano J; Morozov Y; Venkataraman V
[Ad] Endereço:Graduate School of Biomedical Sciences, Rowan University, Stratford, NJ 08084, USA.
[Ti] Título:Single-column purification of the tag-free, recombinant form of the neuronal calcium sensor protein, hippocalcin expressed in Escherichia coli.
[So] Source:Protein Expr Purif;123:35-41, 2016 07.
[Is] ISSN:1096-0279
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hippocalcin is a 193 aa protein that is a member of the neuronal calcium sensor protein family, whose functions are regulated by calcium. Mice that lack the function of this protein are compromised in the long term potentiation aspect of memory generation. Recently, mutations in the gene have been linked with dystonia in human. The protein has no intrinsic enzyme activity but is known to bind to variety of target proteins. Very little information is available on how the protein executes its critical role in signaling pathways, except that it is regulated by binding of calcium. Further delineation of its function requires large amounts of pure protein. In this report, we present a single-step purification procedure that yields high quantities of the bacterially expressed, recombinant protein. The procedure may be adapted to purify the protein from inclusion bodies or cytosol in its myristoylated or non-myristoylated forms. MALDI-MS (in source decay) analyses demonstrates that the myristoylation occurs at the glycine residue. The protein is also biologically active as measured through tryptophan fluorescence, mobility shift and guanylate cyclase activity assays. Thus, further analyses of hippocalcin, both structural and functional, need no longer be limited by protein availability.
[Mh] Termos MeSH primário: Escherichia coli/genética
Hipocalcina/genética
Hipocalcina/isolamento & purificação
[Mh] Termos MeSH secundário: Animais
Cromatografia Líquida
Expressão Gênica
Vetores Genéticos/genética
Hipocalcina/metabolismo
Seres Humanos
Interações Hidrofóbicas e Hidrofílicas
Ratos
Proteínas Recombinantes/genética
Proteínas Recombinantes/isolamento & purificação
Proteínas Recombinantes/metabolismo
Espectrometria de Massas por Ionização e Dessorção a Laser Assistida por Matriz
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hpca protein, rat); 0 (Recombinant Proteins); 149223-81-4 (Hippocalcin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170417
[Lr] Data última revisão:
170417
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160323
[St] Status:MEDLINE


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[PMID]:26958886
[Au] Autor:Kim KS; Duignan KM; Hawryluk JM; Soh H; Tzingounis AV
[Ad] Endereço:Department of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut.
[Ti] Título:The Voltage Activation of Cortical KCNQ Channels Depends on Global PIP2 Levels.
[So] Source:Biophys J;110(5):1089-98, 2016 Mar 08.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The slow afterhyperpolarization (sAHP) is a calcium-activated potassium conductance with critical roles in multiple physiological processes. Pharmacological and genetic data suggest that KCNQ channels partly mediate the sAHP. However, these channels are not typically open within the observed voltage range of the sAHP. Recent work has shown that the sAHP is gated by increased PIP2 levels, which are generated downstream of calcium binding by neuronal calcium sensors such as hippocalcin. Here, we examined whether changes in PIP2 levels could shift the voltage-activation range of KCNQ channels. In HEK293T cells, expression of the PIP5 kinase PIPKIγ90, which increases global PIP2 levels, shifted the KCNQ voltage activation to within the operating range of the sAHP. Further, the sensitivity of this effect on KCNQ3 channels appeared to be higher than that on KCNQ2. Therefore, we predict that KCNQ3 plays an essential role in maintaining the sAHP under low PIP2 conditions. In support of this notion, we find that sAHP inhibition by muscarinic receptors that increase phosphoinositide turnover in neurons is enhanced in Kcnq3-knockout mice. Likewise, the presence of KCNQ3 is essential for maintaining the sAHP when hippocalcin is ablated, a condition that likely impairs PIP2 generation. Together, our results establish the relationship between PIP2 and the voltage dependence of cortical KCNQ channels (KCNQ2/3, KCNQ3/5, and KCNQ5), and suggest a possible mechanism for the involvement of KCNQ channels in the sAHP.
[Mh] Termos MeSH primário: Córtex Cerebral/metabolismo
Ativação do Canal Iônico
Canal de Potássio KCNQ3/metabolismo
Fosfatidilinositol 4,5-Difosfato/metabolismo
[Mh] Termos MeSH secundário: Animais
Carbamatos/farmacologia
Feminino
Células HEK293
Hipocalcina/metabolismo
Seres Humanos
Canal de Potássio KCNQ3/deficiência
Masculino
Potenciais da Membrana
Camundongos Endogâmicos C57BL
Camundongos Knockout
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Fenilenodiaminas/farmacologia
Células Piramidais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Carbamates); 0 (Hpca protein, mouse); 0 (KCNQ3 Potassium Channel); 0 (Phenylenediamines); 0 (Phosphatidylinositol 4,5-Diphosphate); 12G01I6BBU (ezogabine); 149223-81-4 (Hippocalcin)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170309
[Lr] Data última revisão:
170309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160310
[St] Status:MEDLINE


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[PMID]:26521765
[Au] Autor:Pinilla I; Fernández-Sánchez L; Segura FJ; Sánchez-Cano AI; Tamarit JM; Fuentes-Broto L; Eells JT; Lax P; Cuenca N
[Ad] Endereço:Department of Ophthalmology, Lozano Blesa University Hospital, Zaragoza, Spain; Aragon Institute for Health Research (IIS Aragon), Zaragoza, Spain; Department of Surgery, School of Medicine, Zaragoza University, Spain. Electronic address: isabel.pinilla@telefonica.net.
[Ti] Título:Long time remodeling during retinal degeneration evaluated by optical coherence tomography, immunocytochemistry and fundus autofluorescence.
[So] Source:Exp Eye Res;150:122-34, 2016 Sep.
[Is] ISSN:1096-0007
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To characterize the relationship between fundus autofluorescence (FAF), Optical Coherence Tomography (OCT) and immunohistochemistry (IHC) over the course of chronic retinal degeneration in the P23H rat. METHODS: Homozygous albino P23H rats, Sprague-Dawley (SD) rats as controls and pigmented Long Evans (LE) rats were used. A Spectralis HRA OCT system was used for scanning laser ophthalmoscopy (SLO) imaging OCT and angiography. To determine FAF, fluorescence was excited using diode laser at 488 nm. A fast retina map OCT was performed using the optic nerve as a landmark. IHC was performed to correlate with the findings of OCT and FAF changes. RESULTS: During the course of retinal degeneration, the FAF pattern evolved from some spotting at 2 months old to a mosaic of hyperfluorescent dots in rats 6 months and older. Retinal thicknesses progressively diminished over the course of the disease. At later stages of degeneration, OCT documented changes in the retinal layers, however, IHC better identified the cell loss and remodeling changes. Angiography revealed attenuation of the retinal vascular plexus with time. CONCLUSION: We provide for the first time a detailed long-term analysis of the course of retinal degeneration in P23H rats using a combination of SLO and OCT imaging, angiography, FAF and IHC. Although, the application of noninvasive methods enables longitudinal studies and will decrease the number of animals needed for a study, IHC is still an essential tool to identify retinal changes at the cellular level.
[Mh] Termos MeSH primário: Angiofluoresceinografia/métodos
Hipocalcina/metabolismo
Imuno-Histoquímica/métodos
Degeneração Retiniana
Epitélio Pigmentado da Retina/patologia
Tomografia de Coerência Óptica/métodos
Acuidade Visual
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Fundo de Olho
Seres Humanos
Ratos
Degeneração Retiniana/diagnóstico
Degeneração Retiniana/metabolismo
Degeneração Retiniana/fisiopatologia
Epitélio Pigmentado da Retina/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Hpca protein, rat); 149223-81-4 (Hippocalcin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170615
[Lr] Data última revisão:
170615
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151103
[St] Status:MEDLINE


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[PMID]:26435544
[Au] Autor:Choi HS; Lee CH
[Ad] Endereço:Department of Pharmacy, College of Pharmacy, Dankook University, Cheonan 31116, Korea.
[Ti] Título:Time-course changes of hippocalcin expression in the mouse hippocampus following pilocarpine-induced status epilepticus.
[So] Source:J Vet Sci;17(2):137-44, 2016 Jun 30.
[Is] ISSN:1976-555X
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:Hippocalcin participates in the maintenance of neuronal calcium homeostasis. In the present study, we examined the time-course changes of neuronal degeneration and hippocalcin protein level in the mouse hippocampus following pilocarpine-induced status epilepticus (SE). Marked neuronal degeneration was observed in the hippocampus after SE in a time-dependent manner, although neuronal degeneration differed according to the hippocampal subregions. Almost no hippocalcin immunoreactivity was detected in the pyramidal neurons of the cornu ammonis 1 (CA1) region from 6 h after SE. However, many pyramidal neurons in the CA2 region showed hippocalcin immunoreactivity until 24 h after SE. In the CA3 region, only a few hippocalcin immunoreactive cells were observed at 12 h after SE, and almost no hippocalcin immunoreactivity was observed in the pyramidal neurons from 24 h after SE. Hippocalcin immunoreactivity in the polymorphic cells of the dentate gyrus was markedly decreased from 6 h after SE. In addition, hippocalcin protein level in the hippocampus began to decrease from 6 h after SE, and was significantly decreased at 24 h and 48 h after pilocarpine-induced SE. These results indicate that marked reduction of hippocalcin level may be closely related to neuronal degeneration in the hippocampus following pilocarpine-induced SE.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Hipocalcina/genética
Hipocampo/metabolismo
Degeneração Neural/fisiopatologia
Estado Epiléptico/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Regulação da Expressão Gênica/efeitos dos fármacos
Hipocalcina/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos ICR
Degeneração Neural/induzido quimicamente
Pilocarpina/farmacologia
Estado Epiléptico/induzido quimicamente
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
01MI4Q9DI3 (Pilocarpine); 149223-81-4 (Hippocalcin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170426
[Lr] Data última revisão:
170426
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151006
[St] Status:MEDLINE
[do] DOI:10.4142/jvs.2016.17.2.137


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[PMID]:26095160
[Au] Autor:Hopfner F; Schneider SA
[Ad] Endereço:Department of Neurology, University Hospital Schleswig Holstein, Kiel, Germany.
[Ti] Título:Mystery surrounding DYT2 dystonia now solved: HPCA mutations identified in DYT2-like family.
[So] Source:Mov Disord;30(8):1035, 2015 Jul.
[Is] ISSN:1531-8257
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Distonia/genética
Genes Recessivos/genética
Hipocalcina/genética
Mutação/genética
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:COMMENT; JOURNAL ARTICLE
[Nm] Nome de substância:
149223-81-4 (Hippocalcin)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:150716
[Lr] Data última revisão:
150716
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150623
[St] Status:MEDLINE
[do] DOI:10.1002/mds.26288


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[PMID]:26094611
[Au] Autor:Erro R; Klein C
[Ad] Endereço:Sobell Department of Motor Neuroscience and Movement Disorders, University College London (UCL) Institute of Neurology, London, United Kingdom.
[Ti] Título:DYT2 revealed: Hippocalcin mutations cause autosomal-recessive isolated dystonia.
[So] Source:Mov Disord;30(13):1725, 2015 Nov.
[Is] ISSN:1531-8257
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Distonia/genética
Genes Recessivos/genética
Hipocalcina/genética
Mutação/genética
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:COMMENT; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
149223-81-4 (Hippocalcin)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:160115
[Lr] Data última revisão:
160115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150623
[St] Status:MEDLINE
[do] DOI:10.1002/mds.26280



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