Base de dados : MEDLINE
Pesquisa : D12.776.260.655.500 [Categoria DeCS]
Referências encontradas : 185 [refinar]
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  1 / 185 MEDLINE  
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[PMID]:29309627
[Au] Autor:Kharade SS; Parekh VI; Agarwal SK
[Ad] Endereço:Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland.
[Ti] Título:Functional Defects From Endocrine Disease-Associated Mutations in HLXB9 and Its Interacting Partner, NONO.
[So] Source:Endocrinology;159(2):1199-1212, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The insulin-secreting pancreatic neuroendocrine tumors, insulinomas, characterized by increased pancreatic islet ß-cell proliferation, express the phosphorylated isoform of the ß-cell differentiation factor HLXB9 that interacts with NONO/p54NRB, a survival factor. Interestingly, two different homozygous germline mutations in HLXB9, p.F248L and p.F272L, were reported in neonatal diabetes, a condition with functional ß-cell deficiency. Also, two somatic heterozygous NONO mutations were found in endocrine-related tumors, p.H146R (parathyroid) and p.R293H (small intestine neuroendocrine tumor). However, the biological consequence of the mutations, and the role of HLXB9-NONO interaction in normal or abnormal ß cells, is not known. Expression, localization, and functional analysis of the clinically relevant HLXB9 and NONO mutants showed that HLXB9/p.F248L mutant localized in the nucleus but lacked phosphorylation, and NONO/p.R293H mutant was structurally impaired. The HLXB9 and NONO mutants retained the ability to interact, and overexpression of wild-type or mutant HXLB9 in MIN6 cells suppressed cell proliferation. To further understand the biological consequence of the HLXB9-NONO interaction, we mapped the NONO-interacting region in HLXB9. An 80-amino acid conserved region of HLXB9 could compete with full-length HLXB9 to interact with NONO; however, in functional assays, nuclear expression of this HLXB9-conserved region in MIN6 cells did not interfere with cell proliferation. Overall, our results highlight the importance of HLXB9 in conditions of ß-cell excess (insulinomas) and in conditions of ß-cell loss or dysfunction (diabetes). Our studies implicate therapeutic strategies for either reducing ß-cell proliferation in insulinomas or alleviating normal ß-cell deficiency in diabetes through the modulation of HLXB9 phosphorylation.
[Mh] Termos MeSH primário: Doenças do Sistema Endócrino/genética
Proteínas de Homeodomínio/genética
Proteínas de Homeodomínio/metabolismo
Proteínas Associadas à Matriz Nuclear/genética
Proteínas Associadas à Matriz Nuclear/metabolismo
Fatores de Transcrição de Octâmero/genética
Fatores de Transcrição de Octâmero/metabolismo
Proteínas de Ligação a RNA/genética
Proteínas de Ligação a RNA/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Diabetes Mellitus/genética
Doenças do Sistema Endócrino/metabolismo
Mutação em Linhagem Germinativa
Seres Humanos
Recém-Nascido
Células Secretoras de Insulina/metabolismo
Células Secretoras de Insulina/patologia
Camundongos
Camundongos Transgênicos
Mutação
Ligação Proteica
Proteínas Proto-Oncogênicas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (MNX1 protein, human); 0 (Men1 protein, mouse); 0 (NONO protein, human); 0 (Nuclear Matrix-Associated Proteins); 0 (Octamer Transcription Factors); 0 (Proto-Oncogene Proteins); 0 (RNA-Binding Proteins); 0 (Transcription Factors)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03155


  2 / 185 MEDLINE  
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[PMID]:29216297
[Au] Autor:Yamashita J; Ohmoto M; Yamaguchi T; Matsumoto I; Hirota J
[Ad] Endereço:Department of Life Science and Technology, Graduate School of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.
[Ti] Título:Skn-1a/Pou2f3 functions as a master regulator to generate Trpm5-expressing chemosensory cells in mice.
[So] Source:PLoS One;12(12):e0189340, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transient receptor potential channel M5 (Trpm5)-expressing cells, such as sweet, umami, and bitter taste cells in the oropharyngeal epithelium, solitary chemosensory cells in the nasal respiratory epithelium, and tuft cells in the small intestine, that express taste-related genes function as chemosensory cells. Previous studies demonstrated that Skn-1a/Pou2f3, a POU homeodomain transcription factor is expressed in these Trpm5-expressing chemosensory cells, and is necessary for their generation. Trpm5-expressing cells have recently been found in trachea, auditory tube, urethra, thymus, pancreatic duct, stomach, and large intestine. They are considered to be involved in protective responses to potential hazardous compounds as Skn-1a-dependent bitter taste cells, respiratory solitary chemosensory cells, and intestinal tuft cells are. In this study, we examined the expression and function of Skn-1a/Pou2f3 in Trpm5-expressing cells in trachea, auditory tube, urethra, thymus, pancreatic duct, stomach, and large intestine. Skn-1a/Pou2f3 is expressed in a majority of Trpm5-expressing cells in all tissues examined. In Skn-1a/Pou2f3-deficient mice, the expression of Trpm5 as well as marker genes for Trpm5-expressing cells were absent in all tested tissues. Immunohistochemical analyses demonstrated that two types of microvillous cells exist in trachea, urethra, and thymus, Trpm5-positive and Trpm5-negative cells. In Skn-1a/Pou2f3-deficient mice, a considerable proportion of Trpm5-negative and villin-positive microvillous cells remained present in these tissues. Thus, we propose that Skn-1a/Pou2f3 is the master regulator for the generation of the Trpm5-expressing microvillous cells in multiple tissues.
[Mh] Termos MeSH primário: Fatores de Transcrição de Octâmero/fisiologia
Canais de Cátion TRPM/fisiologia
[Mh] Termos MeSH secundário: Animais
Sistema Digestório/citologia
Sistema Digestório/metabolismo
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Traqueia/citologia
Traqueia/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Octamer Transcription Factors); 0 (Pou2f3 protein, mouse); 0 (TRPM Cation Channels); 0 (Trpm5 protein, mouse)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189340


  3 / 185 MEDLINE  
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[PMID]:28846091
[Au] Autor:Jiang L; Shao C; Wu QJ; Chen G; Zhou J; Yang B; Li H; Gou LT; Zhang Y; Wang Y; Yeo GW; Zhou Y; Fu XD
[Ad] Endereço:State Key Laboratory of Virology and Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, China.
[Ti] Título:NEAT1 scaffolds RNA-binding proteins and the Microprocessor to globally enhance pri-miRNA processing.
[So] Source:Nat Struct Mol Biol;24(10):816-824, 2017 Oct.
[Is] ISSN:1545-9985
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNA (miRNA) biogenesis is known to be modulated by a variety of RNA-binding proteins (RBPs), but in most cases, individual RBPs appear to influence the processing of a small subset of target miRNAs. Here, we report that the RNA-binding NONO-PSF heterodimer binds a large number of expressed pri-miRNAs in HeLa cells to globally enhance pri-miRNA processing by the Drosha-DGCR8 Microprocessor. NONO and PSF are key components of paraspeckles organized by the long noncoding RNA (lncRNA) NEAT1. We further demonstrate that NEAT1 also has a profound effect on global pri-miRNA processing. Mechanistic dissection reveals that NEAT1 broadly interacts with the NONO-PSF heterodimer as well as many other RBPs and that multiple RNA segments in NEAT1, including a 'pseudo pri-miRNA' near its 3' end, help attract the Microprocessor. These findings suggest a 'bird nest' model in which an lncRNA orchestrates efficient processing of potentially an entire class of small noncoding RNAs in the nucleus.
[Mh] Termos MeSH primário: MicroRNAs/metabolismo
Proteínas Associadas à Matriz Nuclear/metabolismo
Fatores de Transcrição de Octâmero/metabolismo
Fator de Processamento Associado a PTB/metabolismo
Processamento Pós-Transcricional do RNA
RNA Longo não Codificante/metabolismo
Proteínas de Ligação a RNA/metabolismo
Ribonuclease III/metabolismo
[Mh] Termos MeSH secundário: Células HeLa
Seres Humanos
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DGCR8 protein, human); 0 (MicroRNAs); 0 (NEAT1 long non-coding RNA, human); 0 (NONO protein, human); 0 (Nuclear Matrix-Associated Proteins); 0 (Octamer Transcription Factors); 0 (PTB-Associated Splicing Factor); 0 (RNA, Long Noncoding); 0 (RNA-Binding Proteins); EC 3.1.26.3 (DROSHA protein, human); EC 3.1.26.3 (Ribonuclease III)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE
[do] DOI:10.1038/nsmb.3455


  4 / 185 MEDLINE  
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[PMID]:28712728
[Au] Autor:Morchikh M; Cribier A; Raffel R; Amraoui S; Cau J; Severac D; Dubois E; Schwartz O; Bennasser Y; Benkirane M
[Ad] Endereço:Institut de Génétique Humaine, Laboratoire de Virologie Moléculaire, Université de Montpellier, CNRS UMR9002, 34000 Montpellier, France. Electronic address: mehdi.morchikh@igh.cnrs.fr.
[Ti] Título:HEXIM1 and NEAT1 Long Non-coding RNA Form a Multi-subunit Complex that Regulates DNA-Mediated Innate Immune Response.
[So] Source:Mol Cell;67(3):387-399.e5, 2017 Aug 03.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The DNA-mediated innate immune response underpins anti-microbial defenses and certain autoimmune diseases. Here we used immunoprecipitation, mass spectrometry, and RNA sequencing to identify a ribonuclear complex built around HEXIM1 and the long non-coding RNA NEAT1 that we dubbed the HEXIM1-DNA-PK-paraspeckle components-ribonucleoprotein complex (HDP-RNP). The HDP-RNP contains DNA-PK subunits (DNAPKc, Ku70, and Ku80) and paraspeckle proteins (SFPQ, NONO, PSPC1, RBM14, and MATRIN3). We show that binding of HEXIM1 to NEAT1 is required for its assembly. We further demonstrate that the HDP-RNP is required for the innate immune response to foreign DNA, through the cGAS-STING-IRF3 pathway. The HDP-RNP interacts with cGAS and its partner PQBP1, and their interaction is remodeled by foreign DNA. Remodeling leads to the release of paraspeckle proteins, recruitment of STING, and activation of DNAPKc and IRF3. Our study establishes the HDP-RNP as a key nuclear regulator of DNA-mediated activation of innate immune response through the cGAS-STING pathway.
[Mh] Termos MeSH primário: DNA/imunologia
Herpesvirus Humano 8/imunologia
Imunidade Inata
RNA Longo não Codificante/imunologia
Proteínas de Ligação a RNA/imunologia
[Mh] Termos MeSH secundário: Proteínas de Ligação ao Cálcio/genética
Proteínas de Ligação ao Cálcio/imunologia
Proteínas de Ligação ao Cálcio/metabolismo
DNA/genética
DNA/metabolismo
Células HEK293
Células HeLa
Interações Hospedeiro-Patógeno
Células Endoteliais da Veia Umbilical Humana/imunologia
Células Endoteliais da Veia Umbilical Humana/metabolismo
Células Endoteliais da Veia Umbilical Humana/virologia
Seres Humanos
Fator Regulador 3 de Interferon/genética
Fator Regulador 3 de Interferon/imunologia
Fator Regulador 3 de Interferon/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/genética
Peptídeos e Proteínas de Sinalização Intracelular/imunologia
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Autoantígeno Ku/genética
Autoantígeno Ku/imunologia
Autoantígeno Ku/metabolismo
Proteínas de Membrana/genética
Proteínas de Membrana/imunologia
Proteínas de Membrana/metabolismo
Complexos Multiproteicos
Proteínas Associadas à Matriz Nuclear/genética
Proteínas Associadas à Matriz Nuclear/imunologia
Proteínas Associadas à Matriz Nuclear/metabolismo
Proteínas Nucleares/genética
Proteínas Nucleares/imunologia
Proteínas Nucleares/metabolismo
Nucleotidiltransferases/genética
Nucleotidiltransferases/imunologia
Nucleotidiltransferases/metabolismo
Fatores de Transcrição de Octâmero/genética
Fatores de Transcrição de Octâmero/imunologia
Fatores de Transcrição de Octâmero/metabolismo
Fator de Processamento Associado a PTB/genética
Fator de Processamento Associado a PTB/imunologia
Fator de Processamento Associado a PTB/metabolismo
Ligação Proteica
Interferência de RNA
RNA Longo não Codificante/genética
RNA Longo não Codificante/metabolismo
Proteínas de Ligação a RNA/genética
Proteínas de Ligação a RNA/metabolismo
Transdução de Sinais
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CIB1 protein, human); 0 (Calcium-Binding Proteins); 0 (HEXIM1 protein, human); 0 (IRF3 protein, human); 0 (Interferon Regulatory Factor-3); 0 (Intracellular Signaling Peptides and Proteins); 0 (MATR3 protein, human); 0 (MPYS protein, human); 0 (Membrane Proteins); 0 (Multiprotein Complexes); 0 (NEAT1 long non-coding RNA, human); 0 (NONO protein, human); 0 (Nuclear Matrix-Associated Proteins); 0 (Nuclear Proteins); 0 (Octamer Transcription Factors); 0 (PSPC1 protein, human); 0 (PTB-Associated Splicing Factor); 0 (RBM14 protein, human); 0 (RNA, Long Noncoding); 0 (RNA-Binding Proteins); 9007-49-2 (DNA); EC 2.7.7.- (MB21D1 protein, human); EC 2.7.7.- (Nucleotidyltransferases); EC 3.6.4.12 (XRCC5 protein, human); EC 3.6.4.12 (Xrcc6 protein, human); EC 4.2.99.- (Ku Autoantigen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE


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[PMID]:28359935
[Au] Autor:Maeda N; Narukawa M; Ishimaru Y; Yamamoto K; Misaka T; Abe K
[Ad] Endereço:Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
[Ti] Título:A large increase of sour taste receptor cells in Skn-1-deficient mice does not alter the number of their sour taste signal-transmitting gustatory neurons.
[So] Source:Neurosci Lett;648:53-58, 2017 May 01.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The connections between taste receptor cells (TRCs) and innervating gustatory neurons are formed in a mutually dependent manner during development. To investigate whether a change in the ratio of cell types that compose taste buds influences the number of innervating gustatory neurons, we analyzed the proportion of gustatory neurons that transmit sour taste signals in adult Skn-1a mice in which the number of sour TRCs is greatly increased. We generated polycystic kidney disease 1 like 3-wheat germ agglutinin (pkd1l3-WGA)/Skn-1a and pkd1l3-WGA/Skn-1a mice by crossing Skn-1a mice and pkd1l3-WGA transgenic mice, in which neural pathways of sour taste signals can be visualized. The number of WGA-positive cells in the circumvallate papillae is 3-fold higher in taste buds of pkd1l3-WGA/Skn-1a mice relative to pkd1l3-WGA/Skn-1a mice. Intriguingly, the ratio of WGA-positive neurons to P2X -expressing gustatory neurons in nodose/petrosal ganglia was similar between pkd1l3-WGA/Skn-1a and pkd1l3-WGA/Skn-1a mice. In conclusion, an alteration in the ratio of cell types that compose taste buds does not influence the number of gustatory neurons that transmit sour taste signals.
[Mh] Termos MeSH primário: Neurônios/citologia
Fatores de Transcrição de Octâmero/fisiologia
Papilas Gustativas/citologia
Paladar
[Mh] Termos MeSH secundário: Animais
Camundongos
Camundongos Knockout
Neurônios/metabolismo
Fatores de Transcrição de Octâmero/genética
Transdução de Sinais
Papilas Gustativas/metabolismo
Aglutininas do Germe de Trigo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Octamer Transcription Factors); 0 (Pou2f3 protein, mouse); 0 (Wheat Germ Agglutinins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170401
[St] Status:MEDLINE


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[PMID]:28334947
[Au] Autor:Pham DH; Tan CC; Homan CC; Kolc KL; Corbett MA; McAninch D; Fox AH; Thomas PQ; Kumar R; Gecz J
[Ad] Endereço:Adelaide Medical School, The University of Adelaide, Adelaide 5000, Australia.
[Ti] Título:Protocadherin 19 (PCDH19) interacts with paraspeckle protein NONO to co-regulate gene expression with estrogen receptor alpha (ERα).
[So] Source:Hum Mol Genet;26(11):2042-2052, 2017 Jun 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:De novo and inherited mutations of X-chromosome cell adhesion molecule protocadherin 19 (PCDH19) cause frequent, highly variable epilepsy, autism, cognitive decline and behavioural problems syndrome. Intriguingly, hemizygous null males are not affected while heterozygous females are, contradicting established X-chromosome inheritance. The disease mechanism is not known. Cellular mosaicism is the likely driver. We have identified p54nrb/NONO, a multifunctional nuclear paraspeckle protein with known roles in nuclear hormone receptor gene regulation, as a PCDH19 protein interacting partner. Using breast cancer cells we show that PCDH19-NONO complex is a positive co-regulator of ERα-mediated gene expression. Expression of mutant PCDH19 affects at least a subset of known ERα-regulated genes. These data are consistent with our findings that genes regulated by nuclear hormone receptors and those involved in the metabolism of neurosteroids in particular are dysregulated in PCDH19-epilepsy girls and affected mosaic males. Overall we define and characterize a novel mechanism of gene regulation driven by PCDH19, which is mediated by paraspeckle constituent NONO and is ERα-dependent. This PCDH19-NONO-ERα axis is of relevance not only to PCDH19-epilepsy and its comorbidities but likely also to ERα and generally nuclear hormone receptor-associated cancers.
[Mh] Termos MeSH primário: Caderinas/metabolismo
Proteínas Associadas à Matriz Nuclear/metabolismo
Fatores de Transcrição de Octâmero/metabolismo
Proteínas de Ligação a RNA/metabolismo
[Mh] Termos MeSH secundário: Neoplasias da Mama/metabolismo
Caderinas/genética
Linhagem Celular Tumoral
Epilepsia/genética
Receptor alfa de Estrogênio/genética
Receptor alfa de Estrogênio/metabolismo
Expressão Gênica
Regulação Neoplásica da Expressão Gênica/genética
Células HEK293
Seres Humanos
Deficiência Intelectual/genética
Mutação
Proteínas Associadas à Matriz Nuclear/genética
Fatores de Transcrição de Octâmero/genética
Linhagem
Proteínas de Ligação a RNA/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (Estrogen Receptor alpha); 0 (NONO protein, human); 0 (Nuclear Matrix-Associated Proteins); 0 (Octamer Transcription Factors); 0 (PCDH19 protein, human); 0 (RNA-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:170324
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx094


  7 / 185 MEDLINE  
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[PMID]:28288210
[Au] Autor:Shen W; Liang XH; Sun H; De Hoyos CL; Crooke ST
[Ad] Endereço:Department of Core Antisense Research, IONIS Pharmaceuticals, Inc. 2855 Gazelle Court, Carlsbad, CA, United States of America.
[Ti] Título:Depletion of NEAT1 lncRNA attenuates nucleolar stress by releasing sequestered P54nrb and PSF to facilitate c-Myc translation.
[So] Source:PLoS One;12(3):e0173494, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Altered expression of NEAT1, the architectural long non-coding RNA (lncRNA) of nuclear paraspeckles, has been reported during tumorigenesis, as well as under various cellular stress conditions. Here we report that the depletion of NEAT1 lncRNA alleviates nucleolar stress during RNAP I inhibition through releasing sequestered P54nrb and PSF to facilitate the IRES-dependent translation of c-Myc. RNAP I inhibitor CX5461 disrupts the SL1-rDNA interaction and induces nucleolar disruption, demonstrated by the accumulation of fibrillarin-containing nucleoplasmic foci and nucleolar clearance of ribosomal proteins in HeLa cells. Antisense oligonucleotide-mediated depletion of NEAT1 lncRNA significantly attenuated the RNAP I inhibition and its related nucleolar disruption. Interestingly, induction in the levels of c-Myc protein was observed in NEAT1-depeleted cells under RNAP I inhibition. NEAT1-associated paraspeckle proteins P54nrb and PSF have been reported as positive regulators of c-Myc translation through interaction with c-Myc IRES. Indeed, an increased association of P54nrb and PSF with c-Myc mRNA was observed in NEAT1-depleted cells. Moreover, apoptosis was observed in HeLa cells depleted of P54nrb and PSF, further confirming the positive involvement of P54nrb and PSF in cell proliferation. Together, our results suggest that NEAT1 depletion rescues CX5461-induced nucleolar stress through facilitating c-Myc translation by relocating P54nrb/PSF from nuclear paraspeckles to c-Myc mRNAs.
[Mh] Termos MeSH primário: Genes myc
Proteínas Associadas à Matriz Nuclear/metabolismo
Fatores de Transcrição de Octâmero/metabolismo
Fator de Processamento Associado a PTB/metabolismo
Biossíntese de Proteínas
RNA Longo não Codificante/fisiologia
Proteínas de Ligação a RNA/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Seres Humanos
RNA Mensageiro/genética
RNA Ribossômico/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NEAT1 long non-coding RNA, human); 0 (NONO protein, human); 0 (Nuclear Matrix-Associated Proteins); 0 (Octamer Transcription Factors); 0 (PTB-Associated Splicing Factor); 0 (RNA, Long Noncoding); 0 (RNA, Messenger); 0 (RNA, Ribosomal); 0 (RNA-Binding Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0173494


  8 / 185 MEDLINE  
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[PMID]:28139300
[Au] Autor:Ren F; Yu S; Chen R; Lv X; Pan C
[Ad] Endereço:College of Animal Science and Technology, Northwest A&F University, Shaanxi Key Laboratory of Molecular Biology for Agriculture, Yangling, Shaanxi 712100, PR China. Electronic address: renfa0306@126.com.
[Ti] Título:Identification of a novel 12-bp insertion/deletion (indel) of iPS-related Oct4 gene and its association with reproductive traits in male piglets.
[So] Source:Anim Reprod Sci;178:55-60, 2017 Mar.
[Is] ISSN:1873-2232
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:As a key factor of cellular reprogramming, Oct4 is one of vital transcription factors for induced pluripotent stem cells (iPSCs). Loss of its function or deletion causes apoptosis in primordial germ cells (PGCs), which affect reproductive traits in mammals. In this study, a novel 12-bp insertion/deletion (indel) polymorphism (NC_010449:g.2759-2760insGGTTTTTGTCTA) within the Oct4 gene was identified in 442 pigs of Large White (LW) and Landrace (LD) breeds, showing three genotypes designated as II, ID, and DD. The frequencies of allele "I" in LW and LD pigs were 0.587 and 0.648, respectively. The male piglets with homozygous II or DD genotypes of Oct4 gene exhibited better reproductive traits than those with heterozygous ID genotype. Moreover, there were two significant associations between this 12-bp indel polymorphism and testis long circumference (TLC) (P=0.005) and testis short girth (TSG) (P=0.003) as well as 15-day testis weight (TW) (P=0.013) in the LW male piglets. These findings suggest that the 12-bp indel polymorphism of the Oct4 gene might be a potential DNA marker for selecting preferred individuals in relation to reproductive traits in pig marker-assisted selection (MAS) breeding, which could contribute to the breeding and genetics in male piglets.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/fisiologia
Células-Tronco Pluripotentes Induzidas/fisiologia
Fatores de Transcrição de Octâmero/metabolismo
Reprodução/genética
Suínos/genética
Suínos/fisiologia
[Mh] Termos MeSH secundário: Animais
Reprogramação Celular/genética
Reprogramação Celular/fisiologia
Marcadores Genéticos
Genótipo
Heterozigoto
Mutação INDEL
Masculino
Fatores de Transcrição de Octâmero/genética
Polimorfismo Genético
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Genetic Markers); 0 (Octamer Transcription Factors)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170303
[Lr] Data última revisão:
170303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170201
[St] Status:MEDLINE


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[PMID]:28009605
[Au] Autor:McGregor SM; Alikhan MB; John RA; Kotler H; Bridge JA; Mujacic I; Kadri S; Segal J; Krausz T
[Ad] Endereço:*Department of Pathology, University of Chicago Medicine §Chicago Otolaryngology Associates, Chicago ‡Dermatopathology, Midwest Diagnostic Pathology, Park Ridge, IL †Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison, Madison, WI ∥Department of Pathology/Microbiology, Pediatrics, and Orthopaedic Surgery, 983135 Nebraska Medical Center, University of Nebraska, Omaha, NE.
[Ti] Título:Melanotic PEComa of the Sinonasal Mucosa With NONO-TFE3 Fusion: An Elusive Mimic of Sinonasal Melanoma.
[So] Source:Am J Surg Pathol;41(5):717-722, 2017 May.
[Is] ISSN:1532-0979
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Perivascular epithelioid cell neoplasms (PEComas) are a family of mesenchymal tumors with features of both smooth muscle and melanocytic differentiation, with or without true melanin pigment. The highly variable morphology of PEComas results in a broad differential diagnosis that is also dependent on anatomic site. A subset demonstrates rearrangements involving the TFE3 (Xp11) locus, which can be used in diagnostically difficult cases. Here we describe a case of a melanotic PEComa with NONO-TFE3 fusion occurring in the sinonasal mucosa, as demonstrated by both next-generation sequencing and molecular cytogenetic studies. This case is the first of its kind in the literature and only the second documented PEComa harboring a NONO-TFE3 rearrangement. In light of unequivocal molecular ancillary studies, this case illustrates that PEComa must enter the differential for pigmented lesions of the sinonasal mucosa, where malignant melanoma would be much more likely to occur.
[Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina e Hélice-Alça-Hélix Básicos/genética
Biomarcadores Tumorais/análise
Biomarcadores Tumorais/genética
Fusão Gênica
Melaninas/análise
Melanoma/genética
Mucosa Nasal/química
Neoplasias Nasais/genética
Proteínas Associadas à Matriz Nuclear/genética
Fatores de Transcrição de Octâmero/genética
Neoplasias de Células Epitelioides Perivasculares/genética
Proteínas de Ligação a RNA/genética
[Mh] Termos MeSH secundário: Biópsia
Diagnóstico Diferencial
Feminino
Seres Humanos
Imuno-Histoquímica
Hibridização in Situ Fluorescente
Melanoma/química
Melanoma/patologia
Meia-Idade
Mucosa Nasal/patologia
Neoplasias Nasais/química
Neoplasias Nasais/patologia
Neoplasias de Células Epitelioides Perivasculares/química
Neoplasias de Células Epitelioides Perivasculares/patologia
Valor Preditivo dos Testes
Análise de Sequência de DNA
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Leucine Zipper Transcription Factors); 0 (Biomarkers, Tumor); 0 (Melanins); 0 (NONO protein, human); 0 (Nuclear Matrix-Associated Proteins); 0 (Octamer Transcription Factors); 0 (RNA-Binding Proteins); 0 (TFE3 protein, human)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170424
[Lr] Data última revisão:
170424
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161224
[St] Status:MEDLINE
[do] DOI:10.1097/PAS.0000000000000778


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[PMID]:28007765
[Au] Autor:Jerabek S; Ng CK; Wu G; Arauzo-Bravo MJ; Kim KP; Esch D; Malik V; Chen Y; Velychko S; MacCarthy CM; Yang X; Cojocaru V; Schöler HR; Jauch R
[Ad] Endereço:Max Planck Institute for Molecular Biomedicine, Münster, Germany.
[Ti] Título:Changing POU dimerization preferences converts Oct6 into a pluripotency inducer.
[So] Source:EMBO Rep;18(2):319-333, 2017 Feb.
[Is] ISSN:1469-3178
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The transcription factor Oct4 is a core component of molecular cocktails inducing pluripotent stem cells (iPSCs), while other members of the POU family cannot replace Oct4 with comparable efficiency. Rather, group III POU factors such as Oct6 induce neural lineages. Here, we sought to identify molecular features determining the differential DNA-binding and reprogramming activity of Oct4 and Oct6. In enhancers of pluripotency genes, Oct4 cooperates with Sox2 on heterodimeric SoxOct elements. By re-analyzing ChIP-Seq data and performing dimerization assays, we found that Oct6 homodimerizes on palindromic OctOct more cooperatively and more stably than Oct4. Using structural and biochemical analyses, we identified a single amino acid directing binding to the respective DNA elements. A change in this amino acid decreases the ability of Oct4 to generate iPSCs, while the reverse mutation in Oct6 does not augment its reprogramming activity. Yet, with two additional amino acid exchanges, Oct6 acquires the ability to generate iPSCs and maintain pluripotency. Together, we demonstrate that cell type-specific POU factor function is determined by select residues that affect DNA-dependent dimerization.
[Mh] Termos MeSH primário: Transdiferenciação Celular/genética
Reprogramação Celular/genética
Proteínas de Transporte de Cátions Orgânicos/genética
Proteínas de Transporte de Cátions Orgânicos/metabolismo
Fatores do Domínio POU/química
Fatores do Domínio POU/metabolismo
Multimerização Proteica
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Animais
Sítios de Ligação
Linhagem Celular
Células-Tronco Embrionárias
Elementos Facilitadores Genéticos
Epigênese Genética
Seres Humanos
Células-Tronco Pluripotentes Induzidas/citologia
Células-Tronco Pluripotentes Induzidas/metabolismo
Camundongos
Modelos Moleculares
Motivos de Nucleotídeos
Fatores de Transcrição de Octâmero/química
Fatores de Transcrição de Octâmero/genética
Fatores de Transcrição de Octâmero/metabolismo
Fatores do Domínio POU/genética
Regiões Promotoras Genéticas
Ligação Proteica
Conformação Proteica
Estabilidade Proteica
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Octamer Transcription Factors); 0 (Organic Cation Transport Proteins); 0 (POU Domain Factors); 0 (SLC22A16 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170815
[Lr] Data última revisão:
170815
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161224
[St] Status:MEDLINE
[do] DOI:10.15252/embr.201642958



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