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[PMID]:28716526
[Au] Autor:Qin F; Zhang Y; Liu J; Li H
[Ad] Endereço:Department of Pathology, University of Virginia, Charlottesville, VA, 22908, USA.
[Ti] Título:SLC45A3-ELK4 functions as a long non-coding chimeric RNA.
[So] Source:Cancer Lett;404:53-61, 2017 Sep 28.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Gene fusions in cancer typically lead to the expression of a fusion protein or disrupt the expression of one of the parental genes. Here we report a new phenomenon whereby a fusion transcript functions as a long non-coding chimeric RNA (lnccRNA). This fusion RNA, SLC45A3-ELK4, generated by cis-splicing between neighboring genes, was found in prostate cancer. The fusion RNA encodes the same protein as ELK4. Intriguingly, we found that the fusion RNA level is less than 1% of wild type ELK4, unlikely to perturb the general pool of ELK4 protein. Nonetheless, when the fusion RNA, but not ELK4 is silenced, cell proliferation is inhibited in both androgen-dependent and castration-resistant prostate cancer cells. This growth arrest can be rescued by exogenous expression of the fusion and a mutant designed to prevent translation of the ELK4 protein. In the same setting, the mutant could also suppress CDKN1A and several other targets of SLC45A3-ELK4. In addition, similar to many long non-coding RNAs, the fusion RNA is enriched in the nuclear fraction. Altogether, these results indicate that SLC45A3-ELK4 regulates cancer cell proliferation by its transcript, not translated protein.
[Mh] Termos MeSH primário: Proliferação Celular
Proteínas de Membrana Transportadoras/fisiologia
Proteínas de Fusão Oncogênicas/fisiologia
Neoplasias da Próstata/metabolismo
RNA Longo não Codificante/fisiologia
Proteínas Elk-4 do Domínio ets/fisiologia
[Mh] Termos MeSH secundário: Núcleo Celular/metabolismo
Regulação Neoplásica da Expressão Gênica/fisiologia
Fusão Gênica
Seres Humanos
Masculino
Proteínas de Fusão Oncogênicas/metabolismo
Neoplasias da Próstata/genética
Neoplasias da Próstata/patologia
RNA Longo não Codificante/metabolismo
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ELK4 protein, human); 0 (Membrane Transport Proteins); 0 (Oncogene Proteins, Fusion); 0 (RNA, Long Noncoding); 0 (SLC45a3 protein, human); 146481-62-1 (ets-Domain Protein Elk-4)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE


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[PMID]:28655758
[Au] Autor:Jiang L; Xiong J; Zhan J; Yuan F; Tang M; Zhang C; Cao Z; Chen Y; Lu X; Li Y; Wang H; Wang L; Wang J; Zhu WG; Wang H
[Ad] Endereço:From the Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Beijing Key Laboratory of Protein Post-translational Modifications and Cell Function, Department of Biochemistry and Molecular Biology, Peking University Health Science Center.
[Ti] Título:Ubiquitin-specific peptidase 7 (USP7)-mediated deubiquitination of the histone deacetylase SIRT7 regulates gluconeogenesis.
[So] Source:J Biol Chem;292(32):13296-13311, 2017 Aug 11.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sirtuin 7 (SIRT7), a member of the NAD -dependent class III histone deacetylases, is involved in the regulation of various cellular processes and in resisting various stresses, such as hypoxia, low glucose levels, and DNA damage. Interestingly, SIRT7 is linked to the control of glycolysis, suggesting a role in glucose metabolism. Given the important roles of SIRT7, it is critical to clarify how SIRT7 activity is potentially regulated. It has been reported that some transcriptional and post-transcriptional regulatory mechanisms are involved. However, little is known how SIRT7 is regulated by the post-translational modifications. Here, we identified ubiquitin-specific peptidase 7 (USP7), a deubiquitinase, as a negative regulator of SIRT7. We showed that USP7 interacts with SIRT7 both and and we further demonstrated that SIRT7 undergoes endogenous Lys-63-linked polyubiquitination, which is removed by USP7. Although the USP7-mediated deubiquitination of SIRT7 had no effect on its stability, the deubiquitination repressed its enzymatic activity. We also showed that USP7 coordinates with SIRT7 to regulate the expression of glucose-6-phosphatase catalytic subunit ( ), a gluconeogenic gene. USP7 depletion by RNA interference increased both expression and SIRT7 enzymatic activity. Moreover, SIRT7 targeted the promoter through the transcription factor ELK4 but not through forkhead box O1 (FoxO1). In summary, SIRT7 is a USP7 substrate and has a novel role as a regulator of gluconeogenesis. Our study may provide the basis for new clinical approaches to treat metabolic disorders related to glucose metabolism.
[Mh] Termos MeSH primário: Regulação Enzimológica da Expressão Gênica
Glucose-6-Fosfatase/metabolismo
Regiões Promotoras Genéticas
Processamento de Proteína Pós-Traducional
Sirtuínas/metabolismo
Ubiquitina Tiolesterase/metabolismo
Proteínas Elk-4 do Domínio ets/metabolismo
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Linhagem Celular Tumoral
Deleção de Genes
Gluconeogênese
Glucose-6-Fosfatase/antagonistas & inibidores
Glucose-6-Fosfatase/genética
Células HEK293
Seres Humanos
Hidrólise
Lisina/metabolismo
Mutação
Fragmentos de Peptídeos/antagonistas & inibidores
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Domínios e Motivos de Interação entre Proteínas
Subunidades Proteicas/genética
Subunidades Proteicas/metabolismo
Interferência de RNA
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Sirtuínas/antagonistas & inibidores
Sirtuínas/genética
Especificidade por Substrato
Ubiquitina Tiolesterase/antagonistas & inibidores
Ubiquitina Tiolesterase/genética
Peptidase 7 Específica de Ubiquitina
Ubiquitinação
Proteínas Elk-4 do Domínio ets/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ELK4 protein, human); 0 (Peptide Fragments); 0 (Protein Subunits); 0 (Recombinant Fusion Proteins); 0 (SIRT7 protein, human); 146481-62-1 (ets-Domain Protein Elk-4); EC 3.1.3.9 (G6PC1 protein, human); EC 3.1.3.9 (Glucose-6-Phosphatase); EC 3.4.19.12 (USP7 protein, human); EC 3.4.19.12 (Ubiquitin Thiolesterase); EC 3.4.19.12 (Ubiquitin-Specific Peptidase 7); EC 3.5.1.- (Sirtuins); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.780130


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[PMID]:28275114
[Au] Autor:Hooker E; Baldwin C; Roodman V; Batra A; Isa NN; Takano T; Lemay S
[Ad] Endereço:Department of Medicine, Division of Nephrology, McGill University Health Centre, Montreal, QC, Canada.
[Ti] Título:Binding and inhibition of the ternary complex factor Elk-4/Sap1 by the adapter protein Dok-4.
[So] Source:Biochem J;474(9):1509-1528, 2017 Apr 19.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The adapter protein Dok-4 (downstream of kinase-4) has been reported as both an activator and inhibitor of Erk and Elk-1, but lack of knowledge about the identity of its partner molecules has precluded any mechanistic insight into these seemingly conflicting properties. We report that Dok-4 interacts with the transactivation domain of Elk-4 through an atypical phosphotyrosine-binding domain-mediated interaction. Dok-4 possesses a nuclear export signal and can relocalize Elk-4 from nucleus to cytosol, whereas Elk-4 possesses two nuclear localization signals that restrict interaction with Dok-4. The Elk-4 protein, unlike Elk-1, is highly unstable in the presence of Dok-4, through both an interaction-dependent mechanism and a pleckstrin homology domain-dependent but interaction-independent mechanism. This is reversed by proteasome inhibition, depletion of endogenous Dok-4 or lysine-to-arginine mutation of putative Elk-4 ubiquitination sites. Finally, Elk-4 transactivation is potently inhibited by Dok-4 overexpression but enhanced by Dok-4 knockdown in MDCK renal tubular cells, which correlates with increased basal and EGF-induced expression of Egr-1, Fos and cylcinD1 mRNA, and cell proliferation despite reduced Erk activation. Thus, Dok-4 can target Elk-4 activity through multiple mechanisms, including binding of the transactivation domain, nuclear exclusion and protein destabilization, without a requirement for inhibition of Erk.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/genética
Sinais de Exportação Nuclear/genética
Sinais de Localização Nuclear/genética
Proteínas Elk-4 do Domínio ets/genética
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular/genética
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Sequência de Aminoácidos
Animais
Células COS
Proliferação Celular/genética
Cães
Regulação da Expressão Gênica
Células HEK293
Seres Humanos
Immunoblotting
Células Madin Darby de Rim Canino
Camundongos
Microscopia Confocal
Ligação Proteica
Interferência de RNA
Homologia de Sequência de Aminoácidos
Técnicas do Sistema de Duplo-Híbrido
Proteínas Elk-4 do Domínio ets/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Dok4 protein, mouse); 0 (Nuclear Export Signals); 0 (Nuclear Localization Signals); 146481-62-1 (ets-Domain Protein Elk-4)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20160832


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[PMID]:28189763
[Au] Autor:Ramialison M; Waardenberg AJ; Schonrock N; Doan T; de Jong D; Bouveret R; Harvey RP
[Ad] Endereço:Victor Chang Cardiac Research Institute, Darlinghurst, NSW 2010, Australia; Australian Regenerative Medicine Institute, Monash University, Clayton, VIC 3800, Australia; Systems Biology Institute, Australia.
[Ti] Título:Analysis of steric effects in DamID profiling of transcription factor target genes.
[So] Source:Genomics;109(2):75-82, 2017 Mar.
[Is] ISSN:1089-8646
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA adenine methyltransferase identification (DamID) is an enzymatic technology for detecting DNA regions targeted by chromatin-associated proteins. Proteins are fused to bacterial DNA adenine methyltransferase (Dam) and expressed in cultured cells or whole organisms. Here, we used DamID to detect DNA regions bound by the cardiac-restricted transcription factors (TFs) NKX2-5 and SRF, and ubiquitously-expressed co-factors ELK1 and ELK4. We compared targets bound by these TFs as N- and C-terminal fusions with Dam, for both wild type (WT) NKX2-5 and mutant proteins mimicking those found in congenital heart disease. Overall, DamID is highly robust: while the orientation of WT Dam fusions can affect the size of the target sets, their signatures remained largely reproducible. Furthermore, a severe NKX2-5 mutant lacking the homeodomain showed strong steric effects negatively impacting target discovery. The extent of steric effect is likely to be dependent on the protein in question and the orientation of Dam fusion.
[Mh] Termos MeSH primário: Cromatina/metabolismo
Regulação da Expressão Gênica
Técnicas Genéticas
Cardiopatias Congênitas/metabolismo
DNA Metiltransferases Sítio Específica (Adenina-Específica)
[Mh] Termos MeSH secundário: Animais
DNA/metabolismo
Cardiopatias Congênitas/genética
Proteína Homeobox Nkx-2.5/metabolismo
Seres Humanos
Camundongos
Fator de Resposta Sérica/metabolismo
Proteínas Elk-1 do Domínio ets/metabolismo
Proteínas Elk-4 do Domínio ets/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromatin); 0 (Elk1 protein, mouse); 0 (Elk4 protein, mouse); 0 (Homeobox Protein Nkx-2.5); 0 (Nkx2-5 protein, mouse); 0 (Serum Response Factor); 0 (ets-Domain Protein Elk-1); 146481-62-1 (ets-Domain Protein Elk-4); 9007-49-2 (DNA); EC 2.1.1.72 (Site-Specific DNA-Methyltransferase (Adenine-Specific))
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170213
[St] Status:MEDLINE


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[PMID]:26938874
[Au] Autor:Qin F; Song Y; Zhang Y; Facemire L; Frierson H; Li H
[Ad] Endereço:Department of Pathology, School of Medicine, University of Virginia, Charlottesville, Virginia, United States of America.
[Ti] Título:Role of CTCF in Regulating SLC45A3-ELK4 Chimeric RNA.
[So] Source:PLoS One;11(3):e0150382, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The chimeric RNA, SLC45A3-ELK4, was found to be a product of cis-splicing between the two adjacent genes (cis-SAGe). Despite the biological and clinical significance of SLC45A3-ELK4, its generating mechanism has not been elucidated. It was shown in one cell line that the binding of transcription factor CTCF to the insulators located at or near the gene boundaries, inversely correlates with the level of the chimera. To investigate the mechanism of such cis-SAGe events, we sequenced potential regions that may play a role in such transcriptional read-through. We could not detect mutations at the transcription termination site, insulator sites, splicing sites, or within CTCF itself in LNCaP cells, thus suggesting a "soft-wired" mechanism in regulating the cis-SAGe event. To investigate the role CTCF plays in regulating the chimeric RNA expression, we compared the levels of CTCF binding to the insulators in different cell lines, as well as clinical samples. Surprisingly, we did not find an inverse correlation between CTCF level, or its bindings to the insulators and SLC45A3-ELK4 expression among different samples. However, in three prostate cancer cell lines, different environmental factors can cause the expression levels of the chimeric RNA to change, and these changes do inversely correlate with CTCF level, and/or its bindings to the insulators. We thus conclude that CTCF and its bindings to the insulators are not the primary reasons for differential SLC45A3-ELK4 expression in different cell lines, or clinical cases. However, they are the likely mechanism for the same cells to respond to different environmental cues, in order to regulate the expression of SLC45A3-ELK4 chimeric RNA. This response to different environmental cues is not general to other cis-SAGe events, as we only found one out of 16 newly identified chimeric RNAs showing a pattern similar to SLC45A3-ELK4.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Proteínas de Membrana Transportadoras/metabolismo
RNA/genética
Proteínas Repressoras/metabolismo
Proteínas Elk-4 do Domínio ets/metabolismo
[Mh] Termos MeSH secundário: Sequência de Bases
Sítios de Ligação
Fator de Ligação a CCCTC
Linhagem Celular Tumoral
Imunoprecipitação da Cromatina
Células HEK293
Seres Humanos
Masculino
Dados de Sequência Molecular
Mutação
Mutação Puntual
Neoplasias da Próstata/metabolismo
Proteínas Repressoras/genética
Homologia de Sequência do Ácido Nucleico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CCCTC-Binding Factor); 0 (CTCF protein, human); 0 (ELK4 protein, human); 0 (Membrane Transport Proteins); 0 (Repressor Proteins); 0 (SLC45a3 protein, human); 146481-62-1 (ets-Domain Protein Elk-4); 63231-63-0 (RNA)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160304
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0150382


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[PMID]:26028036
[Au] Autor:Peng C; Zeng W; Su J; Kuang Y; He Y; Zhao S; Zhang J; Ma W; Bode AM; Dong Z; Chen X
[Ad] Endereço:The Hormel Institute, University of Minnesota, Austin, MN, USA.
[Ti] Título:Cyclin-dependent kinase 2 (CDK2) is a key mediator for EGF-induced cell transformation mediated through the ELK4/c-Fos signaling pathway.
[So] Source:Oncogene;35(9):1170-9, 2016 Mar 03.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cyclin-dependent kinase 2 (CDK2) is a known regulator in the cell cycle control of the G1/S and S/G2 transitions. However, the role of CDK2 in tumorigenesis is controversial. Evidence from knockout mice as well as colon cancer cell lines indicated that CDK2 is dispensable for cell proliferation. In this study, we found that ectopic CDK2 enhances Ras (G12V)-induced foci formation and knocking down CDK2 expression markedly decreases epidermal growth factor (EGF)-induced cell transformation mediated through the downregulation of c-fos expression. Interestingly, CDK2 directly phosphorylates ELK4 at Thr194 and Ser387 and regulates the ELK4 transcriptional activity, which serves as a mechanism to regulate c-fos expression. In addition, ELK4 is overexpressed in melanoma and knocking down the ELK4 or CDK2 expression significantly attenuated the malignant phenotype of melanoma cells. Taken together, our study reveals a novel function of CDK2 in EGF-induced cell transformation and the associated signal transduction pathways. This indicates that CDK2 is a useful molecular target for the chemoprevention and therapy against skin cancer.
[Mh] Termos MeSH primário: Quinase 2 Dependente de Ciclina/genética
Melanoma/genética
Proteínas Proto-Oncogênicas c-fos/biossíntese
Proteínas Elk-4 do Domínio ets/biossíntese
[Mh] Termos MeSH secundário: Animais
Ciclo Celular/genética
Linhagem Celular
Proliferação Celular
Transformação Celular Neoplásica/genética
Quinase 2 Dependente de Ciclina/biossíntese
Fator de Crescimento Epidérmico/genética
Fator de Crescimento Epidérmico/metabolismo
Seres Humanos
Melanoma/patologia
Camundongos
Fosforilação
Ativação Transcricional/genética
Proteínas Elk-4 do Domínio ets/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ELK4 protein, human); 0 (Proto-Oncogene Proteins c-fos); 146481-62-1 (ets-Domain Protein Elk-4); 62229-50-9 (Epidermal Growth Factor); EC 2.7.11.22 (CDK2 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 2)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150602
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2015.175


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[PMID]:25188740
[Au] Autor:Ren G; Zhang Y; Mao X; Liu X; Mercer E; Marzec J; Ding D; Jiao Y; Qiu Q; Sun Y; Zhang B; Yeste-Velasco M; Chelala C; Berney D; Lu YJ
[Ad] Endereço:1 Department of Pathology, The First Affiliated Hospital, Zhejiang University Medical College , Hangzhou, China .
[Ti] Título:Transcription-mediated chimeric RNAs in prostate cancer: time to revisit old hypothesis?
[So] Source:OMICS;18(10):615-24, 2014 Oct.
[Is] ISSN:1557-8100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chromosomal rearrangements and fusion genes play important roles in tumor development and progression. Four high-frequency prostate cancer-specific fusion genes were recently reported in Chinese cases. We attempted to confirm one of the fusion genes, USP9Y-TTTY15, by reverse transcription PCR, but detected the presence of the USP9Y-TTTY15 fusion transcript in cancer samples, nonmalignant prostate tissues, and normal tissues from other organs, demonstrating that it is a transcription-induced chimeric RNA, which is commonly produced in normal tissues. In 105 prostate cancer samples and case-matched adjacent nonmalignant tissues, we determined the expression level of USP9Y-TTTY15 and a previously reported transcription-induced chimeric RNA, SLC45A3-ELK4. The expression levels of both chimeric RNAs vary greatly in cancer and normal cells. USP9Y-TTTY15 expression is neither higher in cancer than adjacent normal tissues, nor correlated with features of advanced prostate cancer. Although the expression level of SLC45A3-ELK4 is higher in cancer than normal cells, and a dramatic increase in its expression from normal to cancer cells is correlated with advanced disease, its expression level in cancer samples alone is not correlated with any clinical parameters. These data show that both chimeric RNAs contribute less to prostate carcinogenesis than previously reported.
[Mh] Termos MeSH primário: Proteínas de Fusão Oncogênicas/genética
Neoplasias da Próstata/metabolismo
RNA não Traduzido/genética
[Mh] Termos MeSH secundário: Idoso
Seres Humanos
Masculino
Proteínas de Membrana Transportadoras/genética
Proteínas de Membrana Transportadoras/metabolismo
Antígenos de Histocompatibilidade Menor
Estadiamento de Neoplasias
Proteínas de Fusão Oncogênicas/metabolismo
Próstata/metabolismo
Neoplasias da Próstata/genética
Neoplasias da Próstata/patologia
RNA não Traduzido/metabolismo
Transcrição Genética
Transcriptoma
Ubiquitina Tiolesterase/genética
Ubiquitina Tiolesterase/metabolismo
Proteínas Elk-4 do Domínio ets/genética
Proteínas Elk-4 do Domínio ets/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ELK4 protein, human); 0 (Membrane Transport Proteins); 0 (Minor Histocompatibility Antigens); 0 (Oncogene Proteins, Fusion); 0 (RNA, Untranslated); 0 (SLC45a3 protein, human); 146481-62-1 (ets-Domain Protein Elk-4); EC 3.1.2.15 (USP9Y protein, human); EC 3.4.19.12 (Ubiquitin Thiolesterase)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140905
[St] Status:MEDLINE
[do] DOI:10.1089/omi.2014.0042


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[PMID]:24758171
[Au] Autor:Xie L
[Ad] Endereço:Medical Systems Biology Research Center, Department of Biomedical Engineering, Tsinghua University School of Medicine, Beijing 100084, China. xielan@tsinghua.edu.cn.
[Ti] Título:MKL1/2 and ELK4 co-regulate distinct serum response factor (SRF) transcription programs in macrophages.
[So] Source:BMC Genomics;15:301, 2014 Apr 23.
[Is] ISSN:1471-2164
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Serum response factor (SRF) is a widely expressed transcription factor involved in multiple regulatory programs. It is believed that SRF can toggle between disparate programs of gene expression through association with different cofactors. However, the direct evidence as to how these factors function on a genome-wide level is still lacking. RESULTS: In the present study, I explored the functions of SRF and its representative cofactors, megakaryoblastic leukemia 1/2 (MKL1/2) and ETS-domain protein 4 (ELK4), during fungal infection challenge in macrophages. The knockdown study, combined with gene expression array analysis, revealed that MKL1/2 regulated SRF-dependent genes were related to actin cytoskeleton organization, while ELK4 regulated SRF-dependent genes were related to external stimulus responses. Subsequent chromatin immunoprecipitation coupled with massively parallel sequencing (ChIP-seq) suggested that many of these regulations were mediated directly in cis. CONCLUSIONS: I conclude that SRF utilizes MKL1/2 to fulfill steady state cellular functions, including cytoskeletal organization, and utilizes ELK4 to facilitate acute responses to external infection. Together, these findings indicate that SRF, along with its two cofactors, are important players in both cellular homeostasis and stress responses in macrophages.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Macrófagos/metabolismo
Fator de Resposta Sérica/genética
Transativadores/metabolismo
Fatores de Transcrição/metabolismo
Transcrição Genética
Proteínas Elk-4 do Domínio ets/metabolismo
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Linhagem Celular
Regulação da Expressão Gênica/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Macrófagos/efeitos dos fármacos
Masculino
Camundongos
Motivos de Nucleotídeos
Matrizes de Pontuação de Posição Específica
Regiões Promotoras Genéticas
Ligação Proteica
Transporte Proteico
Reprodutibilidade dos Testes
Transativadores/genética
Fatores de Transcrição/genética
Zimosan/farmacologia
Proteínas Elk-4 do Domínio ets/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Elk4 protein, mouse); 0 (MKL1 protein, mouse); 0 (Serum Response Factor); 0 (Trans-Activators); 0 (Transcription Factors); 0 (myocardin-like protein 2, mouse); 146481-62-1 (ets-Domain Protein Elk-4); 9010-72-4 (Zymosan)
[Em] Mês de entrada:1411
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140425
[St] Status:MEDLINE
[do] DOI:10.1186/1471-2164-15-301


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[PMID]:23540573
[Au] Autor:French JD; Ghoussaini M; Edwards SL; Meyer KB; Michailidou K; Ahmed S; Khan S; Maranian MJ; O'Reilly M; Hillman KM; Betts JA; Carroll T; Bailey PJ; Dicks E; Beesley J; Tyrer J; Maia AT; Beck A; Knoblauch NW; Chen C; Kraft P; Barnes D; González-Neira A; Alonso MR; Herrero D; Tessier DC; Vincent D; Bacot F; Luccarini C; Baynes C; Conroy D; Dennis J; Bolla MK; Wang Q; Hopper JL; Southey MC; Schmidt MK; Broeks A; Verhoef S; Cornelissen S; Muir K; Lophatananon A; Stewart-Brown S; Siriwanarangsan P; Fasching PA; Loehberg CR; Ekici AB; Beckmann MW; Peto J; dos Santos Silva I; GENICA Network; kConFab Investigators
[Ad] Endereço:School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, Queensland 4072, Australia.
[Ti] Título:Functional variants at the 11q13 risk locus for breast cancer regulate cyclin D1 expression through long-range enhancers.
[So] Source:Am J Hum Genet;92(4):489-503, 2013 Apr 04.
[Is] ISSN:1537-6605
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Analysis of 4,405 variants in 89,050 European subjects from 41 case-control studies identified three independent association signals for estrogen-receptor-positive tumors at 11q13. The strongest signal maps to a transcriptional enhancer element in which the G allele of the best candidate causative variant rs554219 increases risk of breast cancer, reduces both binding of ELK4 transcription factor and luciferase activity in reporter assays, and may be associated with low cyclin D1 protein levels in tumors. Another candidate variant, rs78540526, lies in the same enhancer element. Risk association signal 2, rs75915166, creates a GATA3 binding site within a silencer element. Chromatin conformation studies demonstrate that these enhancer and silencer elements interact with each other and with their likely target gene, CCND1.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Cromossomos Humanos Par 11/genética
Ciclina D1/genética
Elementos Facilitadores Genéticos/genética
Polimorfismo de Nucleotídeo Único/genética
[Mh] Termos MeSH secundário: Sítios de Ligação
Estudos de Casos e Controles
Linhagem Celular Tumoral
Cromatina/química
Cromatina/genética
Imunoprecipitação da Cromatina
Ciclina D1/metabolismo
Ensaio de Desvio de Mobilidade Eletroforética
Feminino
Fator de Transcrição GATA3/antagonistas & inibidores
Fator de Transcrição GATA3/genética
Fator de Transcrição GATA3/metabolismo
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Luciferases/metabolismo
Regiões Promotoras Genéticas/genética
RNA Mensageiro/genética
RNA Interferente Pequeno/genética
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Elementos Silenciadores Transcricionais/genética
Proteínas Elk-4 do Domínio ets/antagonistas & inibidores
Proteínas Elk-4 do Domínio ets/genética
Proteínas Elk-4 do Domínio ets/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCND1 protein, human); 0 (Chromatin); 0 (ELK4 protein, human); 0 (GATA3 Transcription Factor); 0 (GATA3 protein, human); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 136601-57-5 (Cyclin D1); 146481-62-1 (ets-Domain Protein Elk-4); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:1306
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130402
[St] Status:MEDLINE


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[PMID]:23348503
[Au] Autor:Horn S; Figl A; Rachakonda PS; Fischer C; Sucker A; Gast A; Kadel S; Moll I; Nagore E; Hemminki K; Schadendorf D; Kumar R
[Ad] Endereço:Division of Molecular Genetic Epidemiology, German Cancer Research Center, Im Neuenheimer Feld 580, 69120 Heidelberg, Germany.
[Ti] Título:TERT promoter mutations in familial and sporadic melanoma.
[So] Source:Science;339(6122):959-61, 2013 Feb 22.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cutaneous melanoma occurs in both familial and sporadic forms. We investigated a melanoma-prone family through linkage analysis and high-throughput sequencing and identified a disease-segregating germline mutation in the promoter of the telomerase reverse transcriptase (TERT) gene, which encodes the catalytic subunit of telomerase. The mutation creates a new binding motif for Ets transcription factors and ternary complex factors (TCFs) near the transcription start and, in reporter gene assays, caused up to twofold increase in transcription. We then screened the TERT promoter in sporadic melanoma and observed recurrent ultraviolet signature somatic mutations in 125 of 168 (74%) of human cell lines derived from metastatic melanomas, 45 of 53 corresponding metastatic tumor tissues (85%), and 25 of 77 (33%) primary melanomas. The majority of those mutations occurred at two positions in the TERT promoter and also generated binding motifs for Ets/TCF transcription factors.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Mutação em Linhagem Germinativa
Melanoma/genética
Regiões Promotoras Genéticas
Neoplasias Cutâneas/genética
Telomerase/genética
[Mh] Termos MeSH secundário: Sítios de Ligação
Linhagem Celular Tumoral
Feminino
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Masculino
Melanoma/secundário
Linhagem
Polimorfismo de Nucleotídeo Único
Proteínas Proto-Oncogênicas c-ets/metabolismo
Análise de Sequência de DNA
Neoplasias Cutâneas/patologia
Telomerase/química
Telomerase/metabolismo
Sítio de Iniciação de Transcrição
Transcrição Genética
Proteínas Elk-1 do Domínio ets/metabolismo
Proteínas Elk-4 do Domínio ets/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-ets); 0 (ets-Domain Protein Elk-1); 146481-62-1 (ets-Domain Protein Elk-4); EC 2.7.7.49 (TERT protein, human); EC 2.7.7.49 (Telomerase)
[Em] Mês de entrada:1303
[Cu] Atualização por classe:130222
[Lr] Data última revisão:
130222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130126
[St] Status:MEDLINE
[do] DOI:10.1126/science.1230062



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