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Pesquisa : D12.776.624.664.520.750.900 [Categoria DeCS]
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[PMID]:24741069
[Au] Autor:Gonzalez-Garcia JR; Bradley J; Nomikos M; Paul L; Machaty Z; Lai FA; Swann K
[Ad] Endereço:Institute of Molecular and Experimental Medicine, School of Medicine, Cardiff University, Cardiff CF14 4XN, UK.
[Ti] Título:The dynamics of MAPK inactivation at fertilization in mouse eggs.
[So] Source:J Cell Sci;127(Pt 12):2749-60, 2014 Jun 15.
[Is] ISSN:1477-9137
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Egg activation at fertilization in mammals is initiated by prolonged Ca(2+) oscillations that trigger the completion of meiosis and formation of pronuclei. A fall in mitogen-activated protein kinase (MAPK) activity is essential for pronuclear formation, but the precise timing and mechanism of decline are unknown. Here, we have measured the dynamics of MAPK pathway inactivation during fertilization of mouse eggs using novel chemiluminescent MAPK activity reporters. This reveals that the MAPK activity decrease begins during the Ca(2+) oscillations, but MAPK does not completely inactivate until after pronuclear formation. The MAPKs present in eggs are Mos, MAP2K1 and MAP2K2 (MEK1 and MEK2, respectively) and MAPK3 and MAPK1 (ERK1 and ERK2, respectively). Notably, the MAPK activity decline at fertilization is not explained by upstream destruction of Mos, because a decrease in the signal from a Mos-luciferase reporter is not associated with egg activation. Furthermore, Mos overexpression does not affect the timing of MAPK inactivation or pronuclear formation. However, the late decrease in MAPK could be rapidly reversed by the protein phosphatase inhibitor, okadaic acid. These data suggest that the completion of meiosis in mouse zygotes is driven by an increased phosphatase activity and not by a decline in Mos levels or MEK activity.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por Mitógeno/metabolismo
Óvulo/enzimologia
[Mh] Termos MeSH secundário: Animais
Sinalização do Cálcio
Inibidores Enzimáticos/farmacologia
Feminino
Fertilização
Genes Reporter
Luciferases de Renilla/biossíntese
Luciferases de Renilla/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos CBA
Ácido Okadáico/farmacologia
Proteínas Oncogênicas v-mos/genética
Proteínas Oncogênicas v-mos/metabolismo
Monoéster Fosfórico Hidrolases/antagonistas & inibidores
Monoéster Fosfórico Hidrolases/metabolismo
Fosforilação
Processamento de Proteína Pós-Traducional
Espermatozoides/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Oncogene Proteins v-mos); 1W21G5Q4N2 (Okadaic Acid); EC 1.13.12.5 (Luciferases, Renilla); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.1.3.2 (Phosphoric Monoester Hydrolases)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140418
[St] Status:MEDLINE
[do] DOI:10.1242/jcs.145045


  2 / 93 MEDLINE  
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[PMID]:23475563
[Au] Autor:Rabi T; Huwiler A; Zangemeister-Wittke U
[Ad] Endereço:Institute of Pharmacology, University of Bern, Bern, Switzerland; K.R. Sterling Cancer and Aids Hospital, Chennai, Tamilnadu, India.
[Ti] Título:AMR-Me inhibits PI3K/Akt signaling in hormone-dependent MCF-7 breast cancer cells and inactivates NF-κB in hormone-independent MDA-MB-231 cells.
[So] Source:Mol Carcinog;53(7):578-88, 2014 Jul.
[Is] ISSN:1098-2744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AMR-Me, a C-28 methylester derivative of triterpenoid compound Amooranin isolated from Amoora rohituka stem bark and the plant has been reported to possess multitude of medicinal properties. Our previous studies have shown that AMR-Me can induce apoptosis through mitochondrial apoptotic and MAPK signaling pathways by regulating the expression of apoptosis related genes in human breast cancer MCF-7 cells. However, the molecular mechanism of AMR-Me induced apoptotic cell death remains unclear. Our results showed that AMR-Me dose-dependently inhibited the proliferation of MCF-7 and MDA-MB-231 cells under serum-free conditions supplemented with 1 nM estrogen (E2) with an IC50 value of 0.15 µM, 0.45 µM, respectively. AMR-Me had minimal effects on human normal breast epithelial MCF-10A + ras and MCF-10A cells with IC50 value of 6 and 6.5 µM, respectively. AMR-Me downregulated PI3K p85, Akt1, and p-Akt in an ERα-independent manner in MCF-7 cells and no change in expression levels of PI3K p85 and Akt were observed in MDA-MB-231 cells treated under similar conditions. The PI3K inhibitor LY294002 suppressed Akt activation similar to AMR-Me and potentiated AMR-Me induced apoptosis in MCF-7 cells. EMSA revealed that AMR-Me inhibited nuclear factor-kappaB (NF-κB) DNA binding activity in MDA-MB-231 cells in a time-dependent manner and abrogated EGF induced NF-κB activation. From these studies we conclude that AMR-Me decreased ERα expression and effectively inhibited Akt phosphorylation in MCF-7 cells and inactivate constitutive nuclear NF-κB and its regulated proteins in MDA-MB-231 cells. Due to this multifactorial effect in hormone-dependent and independent breast cancer cells AMR-Me deserves attention for use in breast cancer prevention and therapy.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Neoplasias da Mama/metabolismo
NF-kappa B/antagonistas & inibidores
Ácido Oleanólico/análogos & derivados
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Fator de Transcrição RelA/antagonistas & inibidores
[Mh] Termos MeSH secundário: Mama/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular
Sobrevivência Celular/efeitos dos fármacos
Cromonas/farmacologia
Proteínas de Ligação a DNA/antagonistas & inibidores
Proteínas de Ligação a DNA/farmacologia
Inibidores Enzimáticos/farmacologia
Estrogênios/farmacologia
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Células MCF-7
Mitocôndrias/efeitos dos fármacos
Morfolinas/farmacologia
Proteínas Nucleares/antagonistas & inibidores
Ácido Oleanólico/farmacologia
Proteínas Oncogênicas v-mos/biossíntese
Fosfatidilinositol 3-Quinases/biossíntese
Fosforilação
Extratos Vegetais/farmacologia
Proteínas Proto-Oncogênicas c-akt/biossíntese
Proteínas Proto-Oncogênicas c-rel
Fator de Transcrição RelB/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Chromones); 0 (DNA-Binding Proteins); 0 (Enzyme Inhibitors); 0 (Estrogens); 0 (HIVEN86A protein, human); 0 (Morpholines); 0 (NF-kappa B); 0 (Nuclear Proteins); 0 (Oncogene Proteins v-mos); 0 (Plant Extracts); 0 (Proto-Oncogene Proteins c-rel); 0 (RELA protein, human); 0 (RELB protein, human); 0 (Transcription Factor RelA); 0 (methyl 25-hydroxy-3-oxoolean-12-en-28-oate); 147337-75-5 (Transcription Factor RelB); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); 6SMK8R7TGJ (Oleanolic Acid); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1408
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130312
[St] Status:MEDLINE
[do] DOI:10.1002/mc.22012


  3 / 93 MEDLINE  
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[PMID]:23851486
[Au] Autor:Chaigne A; Campillo C; Gov NS; Voituriez R; Azoury J; Umaña-Diaz C; Almonacid M; Queguiner I; Nassoy P; Sykes C; Verlhac MH; Terret ME
[Ad] Endereço:1] CIRB, Collège de France, and CNRS-UMR7241 and INSERM-U1050, Equipe Labellisée Ligue Contre le Cancer, Paris F-75005, France.
[Ti] Título:A soft cortex is essential for asymmetric spindle positioning in mouse oocytes.
[So] Source:Nat Cell Biol;15(8):958-66, 2013 Aug.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:At mitosis onset, cortical tension increases and cells round up, ensuring correct spindle morphogenesis and orientation. Thus, cortical tension sets up the geometric requirements of cell division. On the contrary, cortical tension decreases during meiotic divisions in mouse oocytes, a puzzling observation because oocytes are round cells, stable in shape, that actively position their spindles. We investigated the pathway leading to reduction in cortical tension and its significance for spindle positioning. We document a previously uncharacterized Arp2/3-dependent thickening of the cortical F-actin essential for first meiotic spindle migration to the cortex. Using micropipette aspiration, we show that cortical tension decreases during meiosis I, resulting from myosin-II exclusion from the cortex, and that cortical F-actin thickening promotes cortical plasticity. These events soften and relax the cortex. They are triggered by the Mos-MAPK pathway and coordinated temporally. Artificial cortex stiffening and theoretical modelling demonstrate that a soft cortex is essential for meiotic spindle positioning.
[Mh] Termos MeSH primário: Meiose/fisiologia
Oócitos/metabolismo
Fuso Acromático/fisiologia
[Mh] Termos MeSH secundário: Complexo 2-3 de Proteínas Relacionadas à Actina/metabolismo
Actinas/metabolismo
Animais
Feminino
Camundongos
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Modelos Biológicos
Miosinas/metabolismo
Proteínas Oncogênicas v-mos/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actin-Related Protein 2-3 Complex); 0 (Actins); 0 (Oncogene Proteins v-mos); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases); EC 3.6.4.1 (Myosins)
[Em] Mês de entrada:1310
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130716
[St] Status:MEDLINE
[do] DOI:10.1038/ncb2799


  4 / 93 MEDLINE  
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[PMID]:21701776
[Au] Autor:Wen G; Hong M; Li B; Liao W; Cheng SK; Hu B; Calaf GM; Lu P; Partridge MA; Tong J; Hei TK
[Ad] Endereço:Center for Radiological Research, College of Physicians & Surgeons, Columbia University Medical Center, New York, NY, USA.
[Ti] Título:Transforming growth factor-ß-induced protein (TGFBI) suppresses mesothelioma progression through the Akt/mTOR pathway.
[So] Source:Int J Oncol;39(4):1001-9, 2011 Oct.
[Is] ISSN:1791-2423
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:As an uncommon cancer, mesothelioma is very hard to treat with a low average survival rate owing to its usual late detection and being highly invasive. The link between asbestos exposure and the development of mesothelioma in humans is unequivocal. TGFBI, a secreted protein that is induced by transforming growth factor-ß in various human cell types, has been shown to be associated with tumorigenesis in various types of tumors. It has been demonstrated that TGFBI expression is markedly suppressed in asbestos-induced tumorigenic cells, while an ectopic expression of TGFBI significantly suppresses tumorigenicity and progression in human bronchial epithelial cells. In order to delineate a potential role of TGFBI in mediating the molecular events that occur in mesothelioma tumorigenesis, we generated stable TGFBI knockdown mutants from the mesothelium cell line Met-5A by using an shRNA approach, and secondly created ectopic TGFBI overexpression mutants from the mesothelioma cell line H28 in which TGFBI is absent. We observed that in the absence of TGFBI, the knockdown mesothelial and mesothelioma cell lines exhibited an elevated proliferation rate, enhanced plating efficiency, increased anchorage-independent growth, as well as an increased cellular protein synthesis rate as compared with their respective controls. Furthermore, cell cycle regulatory proteins c-myc/cyclin D1/phosphor-Rb were upregulated; a more active PI3K/Akt/mTOR signaling pathway was also detected in TGFBI-depleted cell lines. These findings suggest that TGFBI may repress mesothelioma tumorigenesis and progression via the PI3K/Akt signaling pathway.
[Mh] Termos MeSH primário: Processos de Crescimento Celular/efeitos dos fármacos
Proteínas da Matriz Extracelular/metabolismo
Mesotelioma/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Serina-Treonina Quinases TOR/metabolismo
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Asbestos/toxicidade
Ciclo Celular/efeitos dos fármacos
Linhagem Celular
Linhagem Celular Tumoral
Ciclina D1/metabolismo
Proteínas de Ligação a DNA/metabolismo
Progressão da Doença
Fator de Crescimento Epidérmico/metabolismo
Proteínas da Matriz Extracelular/antagonistas & inibidores
Proteínas da Matriz Extracelular/genética
Técnicas de Silenciamento de Genes/métodos
Seres Humanos
Mesotelioma/etiologia
Mesotelioma/genética
Mesotelioma/patologia
Mutação
Neoplasias Mesoteliais/genética
Neoplasias Mesoteliais/metabolismo
Neoplasias Mesoteliais/patologia
Proteínas Oncogênicas v-mos/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Biossíntese de Proteínas/efeitos dos fármacos
RNA Interferente Pequeno/administração & dosagem
RNA Interferente Pequeno/genética
Transdução de Sinais/efeitos dos fármacos
Fatores de Transcrição/metabolismo
Fator de Crescimento Transformador beta/antagonistas & inibidores
Fator de Crescimento Transformador beta/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (CCND1 protein, human); 0 (DNA-Binding Proteins); 0 (Extracellular Matrix Proteins); 0 (MYCBP protein, human); 0 (Oncogene Proteins v-mos); 0 (RNA, Small Interfering); 0 (Transcription Factors); 0 (Transforming Growth Factor beta); 1332-21-4 (Asbestos); 136601-57-5 (Cyclin D1); 148710-76-3 (betaIG-H3 protein); 62229-50-9 (Epidermal Growth Factor); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1201
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110625
[St] Status:MEDLINE
[do] DOI:10.3892/ijo.2011.1097


  5 / 93 MEDLINE  
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[PMID]:19169828
[Au] Autor:Kabanov AV; Kirpichnikov MP; Khokhlov AR
[Ad] Endereço:Center for Drug Delivery and Nanomedicine, Department of Pharmaceutical Sciences, College of Pharmacy, University of Nebraska Medical Center, 985830 Nebraska Medical Center, Omaha, NE 68198-5830, USA. akabanov@unmc.edu
[Ti] Título:Nanobiology for the pharmacology of cellular ion channels.
[So] Source:J Neuroimmune Pharmacol;4(1):7-9, 2009 Mar.
[Is] ISSN:1557-1904
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Writing this editorial is especially pleasing. First, it provides us an opportunity to introduce new directives to the field of Neuroimmune Pharmacology and to explain why the field of nanomedicine is likely an important part of its future growth and development. Second, it is an opportunity to showcase research in this area currently operative in Russia that may not be readily accessible to the readership. Third, it is a platform to better explain why the Journal Editorial leadership was enthusiastic about the science and its relationship to the Society on NeuroImmune Pharmacology strategic goals. All are brought to bear in this issue of the Journal of Neuroimmune Pharmacology. The issue includes articles presented at a recent joint US-Russian workshop entitled, "Health in the 21st Century: Nanomedicine and Self-Organization of Biological Systems" held at M.V. Lomonosov Moscow State University (MSU), Moscow, Russia, December 10-11, 2007. The conjoint meeting was organized through the Departments of Biology, Chemistry, and Physics, MSU and by the Center for Drug Delivery and Nanomedicine and Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center (Omaha, NE). The speakers included established internationally regarded scientists from these institutions as well as graduate students and faculties at MSU. In addition to selected papers by workshop contributors, we have included several papers closely aligned to the theme of nanomedicine and nanopharmacology of the central nervous system in order to provide a biological anchor for this research. We understand that such works are new to many but hope that its organization and interdisciplinary approaches will appeal to this audience. All together, it is our hope that, by gathering basic and clinical scientists with the common interest of using nanotechnology in the delivery of therapeutic agents with a focus on nanopharmacology and complex supramolecular biological assembly, the papers included will provide a platform for thought, discussion, and future translational research.
[Mh] Termos MeSH primário: Canais Iônicos/efeitos dos fármacos
Nanotecnologia/tendências
Neuroimunomodulação/fisiologia
[Mh] Termos MeSH secundário: Infecções por HIV/metabolismo
Seres Humanos
Proteínas do Tecido Nervoso/biossíntese
Neurociências/tendências
Proteínas Oncogênicas v-mos/metabolismo
Canais de Potássio/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ion Channels); 0 (Nerve Tissue Proteins); 0 (Oncogene Proteins v-mos); 0 (Potassium Channels)
[Em] Mês de entrada:0905
[Cu] Atualização por classe:171104
[Lr] Data última revisão:
171104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090127
[St] Status:MEDLINE
[do] DOI:10.1007/s11481-008-9144-0


  6 / 93 MEDLINE  
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[PMID]:18671273
[Au] Autor:Priyadarshini A; Basu D; Navneet AK; Bhattacharya A; Bhattacharya S; Maitra S; Bhattacharya S
[Ad] Endereço:Department of Zoology, School of Life Science, Visva-Bharati (A Central University), Santiniketan, India.
[Ti] Título:Activation of both Mos and Cdc25 is required for G2-M transition in perch oocyte.
[So] Source:Mol Reprod Dev;76(3):289-300, 2009 Mar.
[Is] ISSN:1098-2795
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Resumption of meiosis from diplotene arrest during the first meiotic prophase in vertebrate oocytes is universally controlled by MPF, a heterodimer of Cdk1 and cyclin B. Activation of MPF depends on the withdrawal of Cdk1 inhibition by Wee1/Myt1 kinase on the one hand and the activation of Cdk1 by Cdc25 phosphatase on the other. It is relevant to know whether both these pathways are necessary to rescue diplotene arrest or if either one of them is sufficient. In MIH (17alpha, 20beta dihydroxy-4-pregnen-3-one) incubated perch (Anabas testudineus) oocytes we have examined these possibilities. Perch oocyte extract following MIH incubation showed a significant increase in Myt1 phosphorylation from 12 to 16 hr indicating its progressive deactivation. MIH induced Mos expression markedly increased at 16 hr effecting 95% GVBD. Cycloheximide inhibited MIH induced Mos expression and its phosphorylation, which in turn reduced Myt1 phosphorylation and GVBD. Myt1 phosphorylation was blocked in Mos immunodepleted oocytes. All these suggest the involvement of Mos in Myt1 phosphorylation. Oocytes incubated in MIH for 16 hr activated Cdc25, but such activation could not rescue the inhibition of GVBD due to Myt1 in Mos immunodepleted oocytes. Blocking Cdc25 with an antisense oligo significantly inhibited GVBD even though Myt1 remained deactivated during this period. Taken together, our findings indicate that MIH requires both pathways for perch oocyte maturation: the expression and activation of Mos, which is linked to Myt1 deactivation on the one hand, and the activation of Cdc25 on the other, as blocking either pathway compromised G2-M transition in perch oocytes.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/metabolismo
Fase G2/fisiologia
Proteínas Oncogênicas v-mos/metabolismo
Oócitos/crescimento & desenvolvimento
Percas/fisiologia
[Mh] Termos MeSH secundário: Animais
Ciclo Celular/genética
Ciclo Celular/fisiologia
Proteínas de Ciclo Celular/genética
Cicloeximida/farmacologia
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Feminino
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Regulação da Expressão Gênica no Desenvolvimento/fisiologia
Hidroxiprogesteronas/metabolismo
Fator Promotor de Maturação/genética
Fator Promotor de Maturação/metabolismo
Proteínas Oncogênicas v-mos/genética
Oogênese/efeitos dos fármacos
Oogênese/fisiologia
Fosforilação/efeitos dos fármacos
Fosforilação/fisiologia
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Fosfatases cdc25/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (DNA-Binding Proteins); 0 (Hydroxyprogesterones); 0 (Oncogene Proteins v-mos); 0 (Transcription Factors); 10456-50-5 (17,20-dihydroxy-4-pregnen-3-one); 98600C0908 (Cycloheximide); EC 2.7.11.22 (Maturation-Promoting Factor); EC 3.1.3.48 (cdc25 Phosphatases)
[Em] Mês de entrada:0908
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080802
[St] Status:MEDLINE
[do] DOI:10.1002/mrd.20952


  7 / 93 MEDLINE  
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[PMID]:17418138
[Au] Autor:Hiipakka M; Saksela K
[Ad] Endereço:Institute of Medical Technology, University of Tampere and Tampere University Hospital, Tampere, Finland.
[Ti] Título:Versatile retargeting of SH3 domain binding by modification of non-conserved loop residues.
[So] Source:FEBS Lett;581(9):1735-41, 2007 May 01.
[Is] ISSN:0014-5793
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Src-homology (SH3) domain belongs to a class of ubiquitous modular protein domains found in nature. SH3 domains have a conserved surface that recognises proline-rich peptides in ligand proteins, but additional contacts also contribute to binding. Using the SH3 domain of hematopoietic cell kinase as a test case, we show that SH3 binding properties can be profoundly altered by modifications within a hexapeptide sequence in the RT-loop region that is not involved in recognition of currently known consensus SH3 target peptides. These results highlight the role of non-conserved regions in SH3 target selection, and introduce a strategy that may be generally feasible for generating artificial SH3 domains with desired ligand binding properties.
[Mh] Termos MeSH primário: Engenharia de Proteínas/métodos
Domínios de Homologia de src
[Mh] Termos MeSH secundário: Proteínas ADAM/química
Proteínas ADAM/metabolismo
Sequência de Aminoácidos
Sítios de Ligação
Complexo CD3/química
Complexo CD3/metabolismo
Sequência Conservada
Produtos do Gene nef/química
Produtos do Gene nef/metabolismo
Imunoensaio/métodos
Proteínas de Membrana/química
Proteínas de Membrana/metabolismo
Modelos Biológicos
Modelos Moleculares
Proteínas Oncogênicas v-mos/química
Proteínas Oncogênicas v-mos/metabolismo
Ligação Proteica
Estrutura Secundária de Proteína
Transporte Proteico
Proteínas Serina-Treonina Quinases/química
Proteínas Serina-Treonina Quinases/metabolismo
Proteína SOS1/química
Proteína SOS1/metabolismo
Quinases Ativadas por p21
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD3 Complex); 0 (Gene Products, nef); 0 (Membrane Proteins); 0 (Oncogene Proteins v-mos); 0 (SOS1 Protein); EC 2.7.11.1 (PAK1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (p21-Activated Kinases); EC 3.4.24.- (ADAM Proteins); EC 3.4.24.- (ADAM15 protein, human)
[Em] Mês de entrada:0706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070410
[St] Status:MEDLINE


  8 / 93 MEDLINE  
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[PMID]:17055699
[Au] Autor:LaChapelle AM; Ruygrok ML; Toomer M; Oost JJ; Monnie ML; Swenson JA; Compton AA; Stebbins-Boaz B
[Ad] Endereço:Department of Biology, Willamette University, Salem, OR 97301, USA.
[Ti] Título:The hormonal herbicide, 2,4-dichlorophenoxyacetic acid, inhibits Xenopus oocyte maturation by targeting translational and post-translational mechanisms.
[So] Source:Reprod Toxicol;23(1):20-31, 2007 Jan.
[Is] ISSN:0890-6238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The widely used hormonal herbicide, 2,4-dichlorophenoxyacetic acid, blocks meiotic maturation in vitro and is thus a potential environmental endocrine disruptor with early reproductive effects. To test whether maturation inhibition was dependent on protein kinase A, an endogenous maturation inhibitor, oocytes were microinjected with PKI, a specific PKA inhibitor, and exposed to 2,4-D. Oocytes failed to mature, suggesting that 2,4-D is not dependent on PKA activity and likely acts on a downstream target, such as Mos. De novo synthesis of Mos, which is triggered by mRNA poly(A) elongation, was examined. Oocytes were microinjected with radiolabelled in vitro transcripts of Mos RNA and exposed to progesterone and 2,4-D. RNA analysis showed progesterone-induced polyadenylation as expected but none with 2,4-D. 2,4-D-activated MAPK was determined to be cytoplasmic in localization studies but poorly induced Rsk2 phosphorylation and activation. In addition to inhibition of the G2/M transition, 2,4-D caused abrupt reduction of H1 kinase activity in MII phase oocytes. Attempts to rescue maturation in oocytes transiently exposed to 2,4-D failed, suggesting that 2,4-D induces irreversible dysfunction of the meiotic signaling mechanism.
[Mh] Termos MeSH primário: Ácido 2,4-Diclorofenoxiacético/toxicidade
Herbicidas/toxicidade
Meiose/efeitos dos fármacos
Oócitos/efeitos dos fármacos
Biossíntese de Proteínas/efeitos dos fármacos
Xenopus laevis
[Mh] Termos MeSH secundário: Animais
Ciclo Celular/efeitos dos fármacos
Quimioterapia Combinada
Feminino
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Meiose/fisiologia
Proteínas Oncogênicas v-mos/biossíntese
Proteínas Oncogênicas v-mos/genética
Oócitos/crescimento & desenvolvimento
Oócitos/metabolismo
Progesterona/farmacologia
Inibidores de Proteínas Quinases/farmacologia
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
RNA Mensageiro/metabolismo
RNA Mensageiro/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Herbicides); 0 (Oncogene Proteins v-mos); 0 (Protein Kinase Inhibitors); 0 (RNA, Messenger); 2577AQ9262 (2,4-Dichlorophenoxyacetic Acid); 4G7DS2Q64Y (Progesterone)
[Em] Mês de entrada:0703
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:061024
[St] Status:MEDLINE


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[PMID]:17027076
[Au] Autor:Ito J; Shimada M; Hochi S; Hirabayashi M
[Ad] Endereço:Section of Molecular Genetics, Center for Brain Experiment, National Institute for Physiological Sciences, Okazaki, Aichi 444-8787, Japan. jito@vasci.umass.edu
[Ti] Título:Involvement of Ca2+-dependent proteasome in the degradation of both cyclin B1 and Mos during spontaneous activation of matured rat oocytes.
[So] Source:Theriogenology;67(3):475-85, 2007 Feb.
[Is] ISSN:0093-691X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In matured rat oocytes, spontaneous activation from the metaphase-II (MII) stage occurred after collection from the oviducts. It is well known that the mitogen-activated protein kinase (MAPK) pathway and p34(cdc2) kinase play an important role in the arrest at MII in other species. However, there is no information about the difference in these factors among strains of rats. In the present study, in spontaneously activated oocytes from the Wistar rat, the Mos protein level and the activity of MAPK kinase (MEK)/MAPK were decreased at 120 min (13.8, 25.7, and 19.3, respectively, P<0.05), whereas Sprague-Dawley (SD) oocytes, which were not spontaneously activated, had a high level of Mos protein and MEK/MAPK activity (75.9, 76.2, and 87.9, respectively, P<0.05). Phosphorylation of MAPK in the SD oocytes was significantly suppressed by MEK inhibitor, U0126 at 60 min; this treatment decreased p34(cdc2) kinase activity via cyclin B1 degradation in a time-dependent manner. The treatment with proteasome inhibitor, MG132 or Ca2+-chelator, BAPTA-AM, overcame the spontaneous degradation of both Mos and cyclin B1 in a dose-dependent manner in Wistar oocytes. More than 90% of Wistar oocytes treated with BAPTA-AM were arrested at MII until 120 min. In conclusion, SD oocytes carrying Mos/MEK/MAPK, maintained a high activity of p34(cdc2) kinase by stabilizing cyclin B1, thus involved in their meiotic arrest. In contrast, Wistar oocytes had a relatively low cytostatic factor activity; rapid decrease of Mos/MEK/MAPK failed to stabilize both cyclin B1 and Mos, and these oocytes were likely to spontaneously activate.
[Mh] Termos MeSH primário: Ciclina B/metabolismo
Proteínas Oncogênicas v-mos/metabolismo
Oócitos/metabolismo
Complexo de Endopeptidases do Proteassoma/metabolismo
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Proliferação Celular
Ciclina B1
Quinases Ciclina-Dependentes/metabolismo
Inibidores de Cisteína Proteinase/farmacologia
Feminino
Leupeptinas/farmacologia
Quinases de Proteína Quinase Ativadas por Mitógeno/antagonistas & inibidores
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Oócitos/efeitos dos fármacos
Complexo de Endopeptidases do Proteassoma/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Ratos Wistar
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ccnb1 protein, rat); 0 (Cyclin B); 0 (Cyclin B1); 0 (Cysteine Proteinase Inhibitors); 0 (Leupeptins); 0 (Oncogene Proteins v-mos); EC 2.7.11.22 (Cyclin-Dependent Kinases); EC 2.7.11.22 (cyclin-dependent kinase-activating kinase); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases); EC 3.4.25.1 (Proteasome Endopeptidase Complex); RF1P63GW3K (benzyloxycarbonylleucyl-leucyl-leucine aldehyde); SY7Q814VUP (Calcium)
[Em] Mês de entrada:0809
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:061010
[St] Status:MEDLINE


  10 / 93 MEDLINE  
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[PMID]:16378104
[Au] Autor:Gong MM; Meng L; Liu WB; Zhang JZ; Shou CC
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Peking University School of Oncology, Peking University Centre for Cancer Research, Beijing 100034, China.
[Ti] Título:[Establishment of a stable and regulable 293 cell line expressing mycoplasma hyorhinis protein P37].
[So] Source:Beijing Da Xue Xue Bao Yi Xue Ban;37(6):575-8, 2005 Dec 18.
[Is] ISSN:1671-167X
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To establish a stable cell line, which can express P37 protein of mycoplasma hyorhinis and be regulated by tetracycline, for investigating the effect of p37 on phenotype of cells and its mechanism. METHODS: Recombinant plasmid PcDNA5/FRT/TO-p37 was constructed and cotransfected with pOG44 into Flp-In-T-REx-293 cells by lipofectamine. Positive clones were screened with Hygromycin and Blasticidin. RT-PCR and Western blot were used to exam the mRNA and protein expression in selected clones. The expression level at different inducing times and concentrations of tetracycline were examined. MTT assay was used to observe the effect of P37 on proliferation of 293 cells. RESULTS: P37 protein, which is 43.5x10(3), was expressed in the selected clone as well as secreted from cells. Tetracycline showed a good regulation on the expression of P37 protein, which was not detectable without tetracycline induction. When induced with 2 mg/L tetracycline for 60 hours, the P37 protein expression reached maximum level. Cell growth was promoted after being transfected with p37. CONCLUSION: A stable cell line expressing P37 regularly was established, which provides a good cell model for studying p37 function and its molecular mechanism.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
Mycoplasma hyorhinis/metabolismo
Proteínas Oncogênicas v-mos/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Bactérias/genética
Linhagem Celular
Proliferação Celular
Cinamatos/farmacologia
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Higromicina B/análogos & derivados
Higromicina B/farmacologia
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Mycoplasma hyorhinis/genética
Nucleosídeos/farmacologia
Proteínas Oncogênicas v-mos/genética
Plasmídeos
Tetraciclina/farmacologia
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Cinnamates); 0 (Membrane Proteins); 0 (Nucleosides); 0 (Oncogene Proteins v-mos); 3XQ2233B0B (Hygromycin B); 3YJY415DDI (hygromycin A); 83U64J9U23 (blasticidin S); F8VB5M810T (Tetracycline)
[Em] Mês de entrada:0806
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:051227
[St] Status:MEDLINE



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