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[PMID]: 29342173 [Au] Autor: Gautam M; Bhattacharya I; Rai U; Majumdar SS [Ad] Endereço: Department of Zoology, University of Delhi, Delhi, India. [Ti] Título: Hormone induced differential transcriptome analysis of Sertoli cells during postnatal maturation of rat testes. [So] Source: PLoS One;13(1):e0191201, 2018. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Sertoli cells (Sc) are unique somatic cells of testis that are the target of both FSH and testosterone (T) and regulate spermatogenesis. Although Sc of neonatal rat testes are exposed to high levels of FSH and T, robust differentiation of spermatogonial cells becomes conspicuous only after 11-days of postnatal age. We have demonstrated earlier that a developmental switch in terms of hormonal responsiveness occurs in rat Sc at around 12 days of postnatal age during the rapid transition of spermatogonia A to B. Therefore, such "functional maturation" of Sc, during pubertal development becomes prerequisite for the onset of spermatogenesis. However, a conspicuous difference in robust hormone (both T and FSH) induced gene expression during the different phases of Sc maturation restricts our understanding about molecular events necessary for the spermatogenic onset and maintenance. Here, using microarray technology, we for the first time have compared the differential transcriptional profile of Sc isolated and cultured from immature (5 days old), maturing (12 days old) and mature (60 days old) rat testes. Our data revealed that immature Sc express genes involved in cellular growth, metabolism, chemokines, cell division, MAPK and Wnt pathways, while mature Sc are more specialized expressing genes involved in glucose metabolism, phagocytosis, insulin signaling and cytoskeleton structuring. Taken together, this differential transcriptome data provide an important resource to reveal the molecular network of Sc maturation which is necessary to govern male germ cell differentiation, hence, will improve our current understanding of the etiology of some forms of idiopathic male infertility. [Mh] Termos MeSH primário: Células de Sertoli/metabolismo Testículo/crescimento & desenvolvimento Testículo/metabolismo [Mh] Termos MeSH secundário: Animais Apoptose/genética Diferenciação Celular/efeitos dos fármacos Quimiocinas/genética Citocinas/genética Citoesqueleto/genética Hormônio Foliculoestimulante/metabolismo Hormônio Foliculoestimulante/farmacologia Perfilação da Expressão Gênica Substâncias de Crescimento/genética Sistema de Sinalização das MAP Quinases/genética Masculino Proteínas Monoméricas de Ligação ao GTP/genética Análise de Sequência com Séries de Oligonucleotídeos Fagocitose/genética Ratos Ratos Wistar Células de Sertoli/citologia Células de Sertoli/efeitos dos fármacos Espermatogênese/efeitos dos fármacos Espermatogênese/genética Espermatogênese/fisiologia Testículo/efeitos dos fármacos Testosterona/metabolismo Testosterona/farmacologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Chemokines); 0 (Cytokines); 0 (Growth Substances); 3XMK78S47O (Testosterone); 9002-68-0 (Follicle Stimulating Hormone); EC 3.6.5.2 (Monomeric GTP-Binding Proteins) [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: 180118 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0191201

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[PMID]: 29193479 [Au] Autor: Xu X; Iwasa H; Hossain S; Sarkar A; Maruyama J; Arimoto-Matsuzaki K; Hata Y [Ad] Endereço: Department of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan. [Ti] Título: BCL-XL binds and antagonizes RASSF6 tumor suppressor to suppress p53 expression. [So] Source: Genes Cells;22(12):993-1003, 2017 Dec. [Is] ISSN: 1365-2443 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: RASSF6, a member of the tumor suppressor Ras-association domain family proteins, induces apoptosis in the caspase-dependent and caspase-independent manners. RASSF6 interacts with MDM2 and stabilizes p53. BCL-XL is a prosurvival member of BCL-2 family proteins. BCL-XL directly inhibits proapoptotic BAX and BAK. BCL-XL also traps tBID, a proapoptotic activator BH3-only protein, and sequesters p53. In addition, BCL-XL regulates the mitochondrial membrane permeability via voltage-dependent anion channel. In these manners, BCL-XL plays an antiapoptotic role. We report the interaction of BCL-XL with RASSF6. BCL-XL inhibits the interaction between RASSF6 and MDM2 and suppresses p53 expression. Consequently, BCL-XL antagonizes RASSF6-mediated apoptosis. Thus, the inhibition of RASSF6-mediated apoptosis also underlies the prosurvival role of BCL-XL. [Mh] Termos MeSH primário: Apoptose Proteínas Monoméricas de Ligação ao GTP/antagonistas & inibidores Proteína Supressora de Tumor p53/metabolismo Proteínas Supressoras de Tumor/metabolismo Proteína bcl-X/metabolismo [Mh] Termos MeSH secundário: Células Cultivadas Seres Humanos Transdução de Sinais [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (BCL2L1 protein, human); 0 (RASSF6 protein, human); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 0 (Tumor Suppressor Proteins); 0 (bcl-X Protein); EC 3.6.5.2 (Monomeric GTP-Binding Proteins) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180130 [Lr] Data última revisão: 180130 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171202 [St] Status: MEDLINE [do] DOI: 10.1111/gtc.12541

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[PMID]: 29060967 [Au] Autor: Mao YN; Zeng LX; Li YH; Liu YZ; Wu JY; Li L; Wang Q [Ad] Endereço: Laboratory of Early Prevention and Treatment for Regional High Frequence Tumor Ministry of Education Key Laboratory, Affiliated Tumor Hospital, Guangxi Medical University, Nanning 530021, China. [Ti] Título: [Significance and expression of PAX8, PAX2, p53 and RAS in ovary and fallopian tubes to origin of ovarian high grade serous carcinoma]. [So] Source: Zhonghua Fu Chan Ke Za Zhi;52(10):687-696, 2017 Oct 25. [Is] ISSN: 0529-567X [Cp] País de publicação: China [La] Idioma: chi [Ab] Resumo: To explore the origin of ovarian high grade serous carcinoma (HGSC) through analysing the expression and significance of PAX8, PAX2, p53 and RAS in the ovary and fallopian tube of different types and grades of serous carcinoma. A total of 44 cases tissue samples of ovarian tumor including 34 malignant ovarian tumor and 10 normal normal tissue (as control group) were collected from the admitted patients in Affiliated Tumor Hospital of Guangxi Medical University from January 2015 to January 2016. Fallopian tube tissues were segmented in accordance with the fimbria, ampulla, isthmus and the corresponding ovarian tissues were by the side. There were 34 cases of patients with ovarian cancer including 29 cases of epithelial ovarian cancer (27 serous carcinoma, 1 mucinous carcinoma,1 endometrioid adenocarcinoma) and 5 non-epithelial ovarian cancer (sex cord-interstitial tumor). Among 27 cases of patients with ovarian serous cancer, there were 23 HGSC and 4 low-grade ovarian serous cancer (LGSC). One hundred fifty-three cases of samples were diagnosed as ovarian serous cancer by Shandong University Affiliated Qilu Hospital from 2005 to 2013 and these samples were made tissue microarray. (1) To analyze the expression and differences of PAX8, PAX2, p53 and RAS in the above tissues and tissue microarray from ovarian and tubal of HGSC and control women by immunohistochemistry methods. (2) To compare the expression levels of PAX8, PAX2, p53 and RAS in ovarian and fallopian tubes of ovarian cancer patients with different pathological types. (3) To analyze the correlations of tubal and ovarian tissue in PAX8, PAX2, p53 and RAS expression of HGSC. (4) To analyze the factors of the prognosis of ovarian serous cancer in tissue microarray by single factor analysis method. (1) PAX8, PAX2, p53 and RAS expression was negative in normal ovarian epithelium of control group, but the expression of PAX8, PAX2, p53 and RAS were strongly positive brown in secrete cells of normal fallopian tube epithelium. (2) p53 and RAS expression of fallopian tube epithelium in the epithelial ovarian cancer group were significantly higher than those in the non-epithelial ovarian cancer groups ( 0.05), but the expression of PAX8 and PAX2 in fallopian tube and the expression of PAX8, PAX2, p53 and RAS in ovarian tissue was not statistically significant in the groups ( 0.05). PAX8, PAX2 and p53 expression of the ovarian in HGSC group were significantly higher than those in LGSC group ( 0.05), while the expression of RAS was lower in the ovarian of the high-grade group ( 0.05), while the expression of PAX8, PAX2, p53 and RAS in fallopian tube was not statistically significant in the groups ( 0.05). (3) There was a significantly positive correlation between fallopian tube and the corresponding ovary of HGSC in PAX8 and PAX2 expression ( 0.422, 0.045; 0.693, 0.000), but not correlation in p53 and RAS expression ( 0.058, 0.793; 0.190, 0.384). (4) Univariate survival analysis showed that the progression free survival time in patients with ovarian serous cancer group was significantly correlated with the protein expression of PAX8, PAX2 and RAS ( 0.05), but there were not correlated with age, surgical staging, cell differentiation, lymph node metastasis and preoperative chemotherapy and p53 protein expression ( 0.05). The total survival time in patients with ovarian serous cancer group was significantly correlated with the protein expression of PAX8 ( 0.05), but there were not correlated with age,surgical staging, cell differentiation, lymph node metastasis and preoperative chemotherapy and the protein expression of PAX2, RAS and p53 ( 0.05). PAX8, PAX2, p53, RAS are of great significance for the study of origin of HGSC. HGSC may be derived from fallopian tube, but further investigation would be necessary to confirm this. PAX8, PAX2, p53, RAS could be expected to be used as predictors of survival prognosis in patients with ovarian serous cancer. [Mh] Termos MeSH primário: Cistadenocarcinoma Seroso/patologia Neoplasias das Tubas Uterinas/patologia Tubas Uterinas/patologia Proteínas Monoméricas de Ligação ao GTP/metabolismo Neoplasias Epiteliais e Glandulares/patologia Neoplasias Ovarianas/patologia Fator de Transcrição PAX2/metabolismo Fator de Transcrição PAX8/metabolismo Proteína Supressora de Tumor p53/metabolismo [Mh] Termos MeSH secundário: Carcinoma Endometrioide China Cistadenocarcinoma Seroso/genética Cistadenocarcinoma Seroso/metabolismo Epitélio Neoplasias das Tubas Uterinas/genética Neoplasias das Tubas Uterinas/metabolismo Tubas Uterinas/metabolismo Feminino Regulação Neoplásica da Expressão Gênica Seres Humanos Imuno-Histoquímica Proteínas Monoméricas de Ligação ao GTP/genética Proteínas de Neoplasias/genética Proteínas de Neoplasias/metabolismo Neoplasias Epiteliais e Glandulares/genética Neoplasias Epiteliais e Glandulares/metabolismo Neoplasias Ovarianas/genética Neoplasias Ovarianas/metabolismo Fator de Transcrição PAX2/genética Fator de Transcrição PAX8/genética Proteína Supressora de Tumor p53/genética [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Neoplasm Proteins); 0 (PAX2 Transcription Factor); 0 (PAX2 protein, human); 0 (PAX8 Transcription Factor); 0 (PAX8 protein, human); 0 (Tumor Suppressor Protein p53); EC 3.6.5.2 (Monomeric GTP-Binding Proteins); EC 3.6.5.2 (REM2 protein, human) [Em] Mês de entrada: 1711 [Cu] Atualização por classe: 171109 [Lr] Data última revisão: 171109 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171025 [St] Status: MEDLINE [do] DOI: 10.3760/cma.j.issn.0529-567X.2017.10.008

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[PMID]: 28931551 [Au] Autor: Reboll MR; Korf-Klingebiel M; Klede S; Polten F; Brinkmann E; Reimann I; Schönfeld HJ; Bobadilla M; Faix J; Kensah G; Gruh I; Klintschar M; Gaestel M; Niessen HW; Pich A; Bauersachs J; Gogos JA; Wang Y; Wollert KC [Ad] Endereço: From Division of Molecular and Translational Cardiology, Department of Cardiology and Angiology (M.R.R., M.K.-K., S.K., E.B., I.R., Y.W., K.C.W.), Core Unit Proteomics, Institute of Toxicology (F.P., A.P.), Department of Biophysical Chemistry (J.F.), Leibniz Research Laboratories for Biotechnology a [Ti] Título: EMC10 (Endoplasmic Reticulum Membrane Protein Complex Subunit 10) Is a Bone Marrow-Derived Angiogenic Growth Factor Promoting Tissue Repair After Myocardial Infarction. [So] Source: Circulation;136(19):1809-1823, 2017 Nov 07. [Is] ISSN: 1524-4539 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: BACKGROUND: Clinical trials of bone marrow cell-based therapies after acute myocardial infarction (MI) have produced mostly neutral results. Treatment with specific bone marrow cell-derived secreted proteins may provide an alternative biological approach to improving tissue repair and heart function after MI. We recently performed a bioinformatic secretome analysis in bone marrow cells from patients with acute MI and discovered a poorly characterized secreted protein, EMC10 (endoplasmic reticulum membrane protein complex subunit 10), showing activity in an angiogenic screen. METHODS: We investigated the angiogenic potential of EMC10 and its mouse homolog (Emc10) in cultured endothelial cells and infarcted heart explants. We defined the cellular sources and function of Emc10 after MI using wild-type, -deficient, and bone marrow-chimeric mice subjected to transient coronary artery ligation. Furthermore, we explored the therapeutic potential of recombinant Emc10 delivered by osmotic minipumps after MI in heart failure-prone FVB/N mice. RESULTS: Emc10 signaled through small GTPases, p21-activated kinase, and the p38 mitogen-activated protein kinase (MAPK)-MAPK-activated protein kinase 2 (MK2) pathway to promote actin polymerization and endothelial cell migration. Confirming the importance of these signaling events in the context of acute MI, Emc10 stimulated endothelial cell outgrowth from infarcted mouse heart explants via p38 MAPK-MK2. Emc10 protein abundance was increased in the infarcted region of the left ventricle and in the circulation of wild-type mice after MI. Emc10 expression was also increased in left ventricular tissue samples from patients with acute MI. Bone marrow-derived monocytes and macrophages were the predominant sources of Emc10 in the infarcted murine heart. KO mice showed no cardiovascular phenotype at baseline. After MI, however, capillarization of the infarct border zone was impaired in KO mice, and the animals developed larger infarct scars and more pronounced left ventricular remodeling compared with wild-type mice. Transplanting KO mice with wild-type bone marrow cells rescued the angiogenic defect and ameliorated left ventricular remodeling. Treating FVB/N mice with recombinant Emc10 enhanced infarct border-zone capillarization and exerted a sustained beneficial effect on left ventricular remodeling. CONCLUSIONS: We have identified Emc10 as a previously unknown angiogenic growth factor that is produced by bone marrow-derived monocytes and macrophages as part of an endogenous adaptive response that can be enhanced therapeutically to repair the heart after MI. [Mh] Termos MeSH primário: Proteínas Angiogênicas/metabolismo Células da Medula Óssea/metabolismo Proteínas de Membrana/metabolismo Infarto do Miocárdio/metabolismo Miocárdio/metabolismo Neovascularização Fisiológica Cicatrização [Mh] Termos MeSH secundário: Proteínas Angiogênicas/administração & dosagem Proteínas Angiogênicas/deficiência Proteínas Angiogênicas/genética Animais Transplante de Medula Óssea Células Cultivadas Modelos Animais de Doenças Células Endoteliais/metabolismo Genótipo Peptídeos e Proteínas de Sinalização Intracelular/metabolismo Macrófagos/metabolismo Proteínas de Membrana/administração & dosagem Proteínas de Membrana/deficiência Proteínas de Membrana/genética Camundongos Endogâmicos C57BL Camundongos Knockout Monócitos/metabolismo Proteínas Monoméricas de Ligação ao GTP/metabolismo Infarto do Miocárdio/tratamento farmacológico Infarto do Miocárdio/genética Infarto do Miocárdio/patologia Miocárdio/patologia Neovascularização Fisiológica/efeitos dos fármacos Fenótipo Proteínas Serina-Treonina Quinases/metabolismo Transdução de Sinais Fatores de Tempo Cicatrização/efeitos dos fármacos Quinases Ativadas por p21/metabolismo Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Angiogenic Proteins); 0 (Emc10 protein, mouse); 0 (Intracellular Signaling Peptides and Proteins); 0 (Membrane Proteins); EC 2.7.1.- (MAP-kinase-activated kinase 2); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (p21-Activated Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 3.6.5.2 (Monomeric GTP-Binding Proteins) [Em] Mês de entrada: 1711 [Cu] Atualização por classe: 171113 [Lr] Data última revisão: 171113 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 170922 [St] Status: MEDLINE [do] DOI: 10.1161/CIRCULATIONAHA.117.029980

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[PMID]: 28911119 [Au] Autor: Huang C; Shi J; Guo Y; Huang W; Huang S; Ming S; Wu X; Zhang R; Ding J; Zhao W; Jia J; Huang X; Xiang AP; Shi Y; Yao C [Ad] Endereço: Center for Stem Cell Biology and Tissue Engineering, Key Laboratory for Stem Cells and Tissue Engineering, Ministry of Education, Sun Yat-Sen University, Guangzhou 510080, China. [Ti] Título: A snoRNA modulates mRNA 3' end processing and regulates the expression of a subset of mRNAs. [So] Source: Nucleic Acids Res;45(15):8647-8660, 2017 Sep 06. [Is] ISSN: 1362-4962 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: mRNA 3' end processing is an essential step in gene expression. It is well established that canonical eukaryotic pre-mRNA 3' processing is carried out within a macromolecular machinery consisting of dozens of trans-acting proteins. However, it is unknown whether RNAs play any role in this process. Unexpectedly, we found that a subset of small nucleolar RNAs (snoRNAs) are associated with the mammalian mRNA 3' processing complex. These snoRNAs primarily interact with Fip1, a component of cleavage and polyadenylation specificity factor (CPSF). We have functionally characterized one of these snoRNAs and our results demonstrated that the U/A-rich SNORD50A inhibits mRNA 3' processing by blocking the Fip1-poly(A) site (PAS) interaction. Consistently, SNORD50A depletion altered the Fip1-RNA interaction landscape and changed the alternative polyadenylation (APA) profiles and/or transcript levels of a subset of genes. Taken together, our data revealed a novel function for snoRNAs and provided the first evidence that non-coding RNAs may play an important role in regulating mRNA 3' processing. [Mh] Termos MeSH primário: Processamento de Terminações 3´ de RNA/genética RNA Mensageiro/metabolismo RNA Nucleolar Pequeno/fisiologia [Mh] Termos MeSH secundário: Fator de Especificidade de Clivagem e Poliadenilação/metabolismo Regulação da Expressão Gênica Células HeLa Seres Humanos Proteínas Monoméricas de Ligação ao GTP/metabolismo Poli A/metabolismo Ligação Proteica RNA Nucleolar Pequeno/metabolismo Fatores de Poliadenilação e Clivagem de mRNA/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Cleavage And Polyadenylation Specificity Factor); 0 (RNA, Messenger); 0 (RNA, Small Nucleolar); 0 (mRNA Cleavage and Polyadenylation Factors); 24937-83-5 (Poly A); EC 3.6.1.- (RRAGA protein, human); EC 3.6.5.2 (Monomeric GTP-Binding Proteins) [Em] Mês de entrada: 1711 [Cu] Atualização por classe: 171107 [Lr] Data última revisão: 171107 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170916 [St] Status: MEDLINE [do] DOI: 10.1093/nar/gkx651

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[PMID]: 28882589 [Au] Autor: Choi H; Son JB; Kang J; Kwon J; Kim JH; Jung M; Kim SK; Kim S; Mun JY [Ad] Endereço: BK21 Plus Program, Department of Senior Healthcare, Graduate School, Eulji University, South Korea. [Ti] Título: Leucine-induced localization of Leucyl-tRNA synthetase in lysosome membrane. [So] Source: Biochem Biophys Res Commun;493(2):1129-1135, 2017 Nov 18. [Is] ISSN: 1090-2104 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Leucyl-tRNA synthetase (LRS) plays major roles in providing leucine-tRNA and activating mechanistic target of rapamycin complex 1 (mTORC1) through intracellular leucine sensing. mTORC1 activated by amino acids affects the influence on physiology functions including cell proliferation, protein synthesis and autophagy in various organisms. Biochemical results demonstrating leucine sensing have been published, but visual results are lacking. Therefore, we observed the location of LRS with and without leucine using stimulated emission depletion (STED) microscopy one of the super-resolution microscopy and transmission electron microscopy (TEM). This revealed that LRS was translocated to the lysosome on addition of leucine. The translocation was inhibited by treatment with compound BC-LI-0186, disrupting the interaction between RagD and LRS. Immuno-TEM revealed a clear decrease in LRS translocation to the lysosome on addition of the inhibitor. This direct visualization of leucine sensing and LRS translocation to the lysosome was related to mTORC1 activation. To study the relationship between mTORC1 activation and LRS translocation, we monitored the change in autophagy for each condition using TEM and CLSM. The results showed a decrease in autophagy on addition of leucine, demonstrating crosstalk between leucine sensing, LRS translocation, RagD interaction, and mTORC1 activation. [Mh] Termos MeSH primário: Leucina-tRNA Ligase/metabolismo Leucina/metabolismo Lisossomos/metabolismo [Mh] Termos MeSH secundário: Autofagia Células HEK293 Células HeLa Seres Humanos Leucina-tRNA Ligase/análise Proteína 2 de Membrana Associada ao Lisossomo/análise Proteína 2 de Membrana Associada ao Lisossomo/metabolismo Lisossomos/ultraestrutura Alvo Mecanístico do Complexo 1 de Rapamicina Proteínas Monoméricas de Ligação ao GTP/análise Proteínas Monoméricas de Ligação ao GTP/metabolismo Complexos Multiproteicos/análise Complexos Multiproteicos/metabolismo Serina-Treonina Quinases TOR/análise Serina-Treonina Quinases TOR/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (LAMP2 protein, human); 0 (Lysosomal-Associated Membrane Protein 2); 0 (Multiprotein Complexes); 0 (RRAGD protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1); EC 3.6.5.2 (Monomeric GTP-Binding Proteins); EC 6.1.1.4 (Leucine-tRNA Ligase); GMW67QNF9C (Leucine) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171116 [Lr] Data última revisão: 171116 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170909 [St] Status: MEDLINE

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[PMID]: 28869817 [Au] Autor: Younesian S; Shahkarami S; Ghaffari P; Alizadeh S; Mehrasa R; Ghavamzadeh A; Ghaffari SH [Ad] Endereço: Hematology, Oncology and Stem Cell Transplantation Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran; Department of Hematology, School of Allied Medical Sciences, International Campus, Tehran University of Medical Sciences, Tehran, Iran. [Ti] Título: DNA hypermethylation of tumor suppressor genes RASSF6 and RASSF10 as independent prognostic factors in adult acute lymphoblastic leukemia. [So] Source: Leuk Res;61:33-38, 2017 Oct. [Is] ISSN: 1873-5835 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: BACKGROUND: The Hypermethylation of Ras association domain family (RASSF) often plays a key role in malignant progression of solid tumors; however, their impact on the prognosis and survival of adult ALL patients remain elusive. METHODS: The frequency of the promoter methylation pattern of RASSF6 and RASSF10 were analyzed in the peripheral blood (PB) samples taken at the time of diagnosis of 45 ALL patients. The methylation-specific PCR (MSP) assay was used to detect the DNA methylation patterns. RESULTS: RASSF6 was frequently hypermethylated in patients diagnosed with pre-B-ALL (90.9%) and B-ALL (87.5%), followed by T-ALL (66.7%); whereas, RASSF10 methylation was more confined to T-ALL (80%) as compared to B-ALL (25%) and pre-B ALL (9.1%) patients. Moreover, hypermethylation of RASSF6 was significantly associated with a poor prognosis and shorter overall survival (OS) in patients with pre-B-ALL (log-rank test; P=0.041). CONCLUSION: RASSF6 and RASSF10 were frequently hypermethylated in the samples at the time of diagnosis of adult ALL patients. Our study represents the first report of methylation of RASSF6 at a high frequency in patients with pre-B ALL. Furthermore, hypermethylation of RASSF6 was significantly associated with inferior overall survival in pre-B ALL patients. It may suggest that the frequent epigenetic inactivation of RASSF6 plays an important role in the pathogenesis and progression of pre-B-ALL. [Mh] Termos MeSH primário: Metilação de DNA/genética Proteínas Monoméricas de Ligação ao GTP/genética Leucemia-Linfoma Linfoblástico de Células Precursoras B/genética Leucemia-Linfoma Linfoblástico de Células T Precursoras/genética Proteínas Supressoras de Tumor/genética [Mh] Termos MeSH secundário: Adolescente Adulto Idoso Idoso de 80 Anos ou mais Feminino Seres Humanos Estimativa de Kaplan-Meier Masculino Meia-Idade Leucemia-Linfoma Linfoblástico de Células Precursoras B/mortalidade Leucemia-Linfoma Linfoblástico de Células T Precursoras/mortalidade Prognóstico Adulto Jovem [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (RASSF10 protein, human); 0 (RASSF6 protein, human); 0 (Tumor Suppressor Proteins); EC 3.6.5.2 (Monomeric GTP-Binding Proteins) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171017 [Lr] Data última revisão: 171017 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170905 [St] Status: MEDLINE

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[PMID]: 28768685 [Au] Autor: MacDonald C; Piper RC [Ad] Endereço: Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA. [Ti] Título: Genetic dissection of early endosomal recycling highlights a TORC1-independent role for Rag GTPases. [So] Source: J Cell Biol;216(10):3275-3290, 2017 Oct 02. [Is] ISSN: 1540-8140 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Endocytosed cell surface membrane proteins rely on recycling pathways for their return to the plasma membrane. Although endosome-to-plasma membrane recycling is critical for many cellular processes, much of the required machinery is unknown. We discovered that yeast has a recycling route from endosomes to the cell surface that functions efficiently after inactivation of the allele of Sec7, which controls transit through the Golgi. A genetic screen based on an engineered synthetic reporter that exclusively follows this pathway revealed that recycling was subject to metabolic control through the Rag GTPases Gtr1 and Gtr2, which work downstream of the exchange factor Vam6. Gtr1 and Gtr2 control the recycling pathway independently of TORC1 regulation through the Gtr1 interactor Ltv1. We further show that the early-endosome recycling route and its control though the Vam6>Gtr1/Gtr2>Ltv1 pathway plays a physiological role in regulating the abundance of amino acid transporters at the cell surface. [Mh] Termos MeSH primário: Endossomos Proteínas Monoméricas de Ligação ao GTP Complexos Multiproteicos Proteínas de Saccharomyces cerevisiae Saccharomyces cerevisiae Serina-Treonina Quinases TOR [Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transporte Vesicular/genética Proteínas Adaptadoras de Transporte Vesicular/metabolismo Endossomos/genética Endossomos/metabolismo Fatores de Troca do Nucleotídeo Guanina/genética Fatores de Troca do Nucleotídeo Guanina/metabolismo Alvo Mecanístico do Complexo 1 de Rapamicina Proteínas Monoméricas de Ligação ao GTP/genética Proteínas Monoméricas de Ligação ao GTP/metabolismo Complexos Multiproteicos/metabolismo Saccharomyces cerevisiae/genética Saccharomyces cerevisiae/metabolismo Proteínas de Saccharomyces cerevisiae/genética Proteínas de Saccharomyces cerevisiae/metabolismo Serina-Treonina Quinases TOR/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Adaptor Proteins, Vesicular Transport); 0 (GTR2 protein, S cerevisiae); 0 (Gtr1 protein, S cerevisiae); 0 (Guanine Nucleotide Exchange Factors); 0 (LTV1 protein, S cerevisiae); 0 (Multiprotein Complexes); 0 (Saccharomyces cerevisiae Proteins); 0 (Sec7 guanine nucleotide exchange factors); 0 (VAM6 protein, S cerevisiae); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1); EC 3.6.5.2 (Monomeric GTP-Binding Proteins) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171121 [Lr] Data última revisão: 171121 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170804 [St] Status: MEDLINE [do] DOI: 10.1083/jcb.201702177

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[PMID]: 28716730 [Au] Autor: Lee CY; Choi JW; Shin S; Lee J; Seo HH; Lim S; Lee S; Joo HC; Kim SW; Hwang KC [Ad] Endereço: Department of Integrated Omics for Biomedical Sciences, Graduate School, Yonsei University, Seoul, 03722, Republic of Korea. [Ti] Título: Interaction of small G protein signaling modulator 3 with connexin 43 contributes to myocardial infarction in rat hearts. [So] Source: Biochem Biophys Res Commun;491(2):429-435, 2017 Sep 16. [Is] ISSN: 1090-2104 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Connexin 43 (Cx43), a ubiquitous connexin expressed in the heart and skin, is associated with a variety of hereditary conditions. Therefore, the characterization of Cx43-interacting proteins and their dynamics is important to understand not only the molecular mechanisms underlying pathological malfunction of gap junction-mediated intercellular communication but also to identify novel and unanticipated biological functions of Cx43. In the present study, we observed potential targets of Cx43 to determine new molecular functions in cardio-protection. MALDI-TOF mass spectrometry analysis of Cx43 co-immunoprecipitated proteins showed that Cx43 interacts with several proteins related to metabolism. In GeneMANIA network analysis, SGSM3, which has not been previously associated with Cx43, was highly correlated with Cx43 in heart functions, and high levels of SGSM3 appeared to induce the turnover of Cx43 through lysosomal degradation in myocardial infarcted rat hearts. Moreover, we confirmed that lysosomal degradation of Cx43 is dependent upon the interaction between SGSM3 and Cx43 in H9c2 cardiomyocytes. The functional importance of the interaction between SGSM3 and Cx43 was confirmed by results showing that Cx43 expression was enhanced by SGSM3 siRNA knockdown in H9c2 cells. In summary, the results of this study elucidate the molecular mechanisms in which Cx43 with SGSM3 is degraded in myocardial infarcted rat hearts, which may contribute to the establishment of new therapeutic targets to modulate cardiac function in physiological and pathological conditions. [Mh] Termos MeSH primário: Conexina 43/metabolismo Junções Comunicantes/metabolismo Proteínas Monoméricas de Ligação ao GTP/metabolismo Infarto do Miocárdio/metabolismo Miocárdio/metabolismo Miócitos Cardíacos/metabolismo [Mh] Termos MeSH secundário: Animais Comunicação Celular Linhagem Celular Conexina 43/genética Vasos Coronários/patologia Vasos Coronários/cirurgia Junções Comunicantes/patologia Junções Comunicantes/ultraestrutura Perfilação da Expressão Gênica Regulação da Expressão Gênica Ligadura Lisossomos/metabolismo Masculino Proteínas Monoméricas de Ligação ao GTP/antagonistas & inibidores Proteínas Monoméricas de Ligação ao GTP/genética Infarto do Miocárdio/genética Infarto do Miocárdio/patologia Miocárdio/patologia Miócitos Cardíacos/patologia Miócitos Cardíacos/ultraestrutura Ligação Proteica Mapeamento de Interação de Proteínas Proteólise RNA Interferente Pequeno/genética RNA Interferente Pequeno/metabolismo Ratos Ratos Sprague-Dawley Transdução de Sinais Proteína da Zônula de Oclusão-1/genética Proteína da Zônula de Oclusão-1/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Connexin 43); 0 (RNA, Small Interfering); 0 (Tjp1 protein, rat); 0 (Zonula Occludens-1 Protein); 0 (connexin 43 protein, rat); EC 3.6.5.2 (Monomeric GTP-Binding Proteins); EC 3.6.5.2 (Sgsm3 protein, rat) [Em] Mês de entrada: 1708 [Cu] Atualização por classe: 170829 [Lr] Data última revisão: 170829 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170719 [St] Status: MEDLINE

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[PMID]: 28546426 [Au] Autor: Emery AC; Xu W; Eiden MV; Eiden LE [Ad] Endereço: From the Section on Molecular Neuroscience and. [Ti] Título: Guanine nucleotide exchange factor Epac2-dependent activation of the GTP-binding protein Rap2A mediates cAMP-dependent growth arrest in neuroendocrine cells. [So] Source: J Biol Chem;292(29):12220-12231, 2017 Jul 21. [Is] ISSN: 1083-351X [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: First messenger-dependent activation of MAP kinases in neuronal and endocrine cells is critical for cell differentiation and function and requires guanine nucleotide exchange factor (GEF)-mediated activation of downstream Ras family small GTPases, which ultimately lead to ERK, JNK, and p38 phosphorylation. Because there are numerous GEFs and also a host of Ras family small GTPases, it is important to know which specific GEF-small GTPase dyad functions in a given cellular process. Here we investigated the upstream activators and downstream effectors of signaling via the GEF Epac2 in the neuroendocrine NS-1 cell line. Three cAMP sensors, Epac2, PKA, and neuritogenic cAMP sensor-Rapgef2, mediate distinct cellular outputs: p38-dependent growth arrest, cAMP response element-binding protein-dependent cell survival, and ERK-dependent neuritogenesis, respectively, in these cells. Previously, we found that cAMP-induced growth arrest of PC12 and NS-1 cells requires Epac2-dependent activation of p38 MAP kinase, which posed the important question of how Epac2 engages p38 without simultaneously activating other MAP kinases in neuronal and endocrine cells. We now show that the small GTP-binding protein Rap2A is the obligate effector for, and GEF substrate of, Epac2 in mediating growth arrest through p38 activation in NS-1 cells. This new pathway is distinctly parcellated from the G protein-coupled receptor → G → adenylate cyclase → cAMP → PKA → cAMP response element-binding protein pathway mediating cell survival and the G protein-coupled receptor → G → adenylate cyclase → cAMP → neuritogenic cAMP sensor-Rapgef2 → B-Raf → MEK → ERK pathway mediating neuritogenesis in NS-1 cells. [Mh] Termos MeSH primário: AMP Cíclico/metabolismo Fatores de Troca do Nucleotídeo Guanina/metabolismo Sistema de Sinalização das MAP Quinases Células Neuroendócrinas/metabolismo Processamento de Proteína Pós-Traducional Proteínas rap de Ligação ao GTP/agonistas [Mh] Termos MeSH secundário: Animais Linhagem Celular Tumoral Ativação Enzimática Proteínas de Ligação ao GTP/química Proteínas de Ligação ao GTP/genética Proteínas de Ligação ao GTP/metabolismo Proteínas de Fluorescência Verde/genética Proteínas de Fluorescência Verde/metabolismo Ligantes Proteínas Monoméricas de Ligação ao GTP/antagonistas & inibidores Proteínas Monoméricas de Ligação ao GTP/genética Proteínas Monoméricas de Ligação ao GTP/metabolismo Proteínas do Tecido Nervoso/agonistas Proteínas do Tecido Nervoso/antagonistas & inibidores Proteínas do Tecido Nervoso/genética Proteínas do Tecido Nervoso/metabolismo Neuritos/metabolismo Células Neuroendócrinas/citologia Neurogênese Fosforilação Prenilação de Proteína Interferência de RNA Ratos Proteínas Recombinantes/metabolismo Proteínas rap de Ligação ao GTP/antagonistas & inibidores Proteínas rap de Ligação ao GTP/genética Proteínas rap de Ligação ao GTP/metabolismo Proteínas ras/antagonistas & inibidores Proteínas ras/genética Proteínas ras/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Epac-2 protein, rat); 0 (Guanine Nucleotide Exchange Factors); 0 (Ligands); 0 (Nerve Tissue Proteins); 0 (Rap2a protein, rat); 0 (Recombinant Proteins); 147336-22-9 (Green Fluorescent Proteins); E0399OZS9N (Cyclic AMP); EC 3.6.1.- (GTP-Binding Proteins); EC 3.6.5.2 (Monomeric GTP-Binding Proteins); EC 3.6.5.2 (Rit1 protein, rat); EC 3.6.5.2 (rap GTP-Binding Proteins); EC 3.6.5.2 (ras Proteins) [Em] Mês de entrada: 1708 [Cu] Atualização por classe: 170808 [Lr] Data última revisão: 170808 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170527 [St] Status: MEDLINE [do] DOI: 10.1074/jbc.M117.790329

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