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[PMID]:28472346
[Au] Autor:Fuglerud BM; Lemma RB; Wanichawan P; Sundaram AYM; Eskeland R; Gabrielsen OS
[Ad] Endereço:Department of Biosciences, University of Oslo, P.O.Box 1066 Blindern, N-0316 Oslo, Norway.
[Ti] Título:A c-Myb mutant causes deregulated differentiation due to impaired histone binding and abrogated pioneer factor function.
[So] Source:Nucleic Acids Res;45(13):7681-7696, 2017 Jul 27.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The transcription factor c-Myb is involved in early differentiation and proliferation of haematopoietic cells, where it operates as a regulator of self-renewal and multi-lineage differentiation. Deregulated c-Myb plays critical roles in leukaemias and other human cancers. Due to its role as a master regulator, we hypothesized it might function as a pioneer transcription factor. Our approach to test this was to analyse a mutant of c-Myb, D152V, previously reported to cause haematopoietic defects in mice by an unknown mechanism. Our transcriptome data from K562 cells indicates that this mutation specifically affects c-Myb's ability to regulate genes involved in differentiation, causing failure in c-Myb's ability to block differentiation. Furthermore, we see a major effect of this mutation in assays where chromatin opening is involved. We show that each repeat in the minimal DNA-binding domain of c-Myb binds to histones and that D152V disrupts histone binding of the third repeat. ATAC-seq data indicates this mutation impairs the ability of c-Myb to cause chromatin opening at specific sites. Taken together, our findings support that c-Myb acts as a pioneer factor and show that D152V impairs this function. The D152V mutant is the first mutant of a transcription factor specifically destroying pioneer factor function.
[Mh] Termos MeSH primário: Diferenciação Celular/genética
Genes myb
Histonas/metabolismo
Mutação
Proteínas Proto-Oncogênicas c-myb/genética
Proteínas Proto-Oncogênicas c-myb/metabolismo
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Animais
Cromatina/genética
Cromatina/metabolismo
Eritropoese/genética
Técnicas de Silenciamento de Genes
Seres Humanos
Células K562
Camundongos
Modelos Moleculares
Proteínas Mutantes/química
Proteínas Mutantes/genética
Proteínas Mutantes/metabolismo
Ligação Proteica
Domínios Proteicos
Proteínas Proto-Oncogênicas c-myb/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromatin); 0 (Histones); 0 (Mutant Proteins); 0 (Proto-Oncogene Proteins c-myb)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx364


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[PMID]:28260788
[Au] Autor:Li Z; Abraham BJ; Berezovskaya A; Farah N; Liu Y; Leon T; Fielding A; Tan SH; Sanda T; Weintraub AS; Li B; Shen S; Zhang J; Mansour MR; Young RA; Look AT
[Ad] Endereço:Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
[Ti] Título:APOBEC signature mutation generates an oncogenic enhancer that drives LMO1 expression in T-ALL.
[So] Source:Leukemia;31(10):2057-2064, 2017 Oct.
[Is] ISSN:1476-5551
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Oncogenic driver mutations are those that provide a proliferative or survival advantage to neoplastic cells, resulting in clonal selection. Although most cancer-causing mutations have been detected in the protein-coding regions of the cancer genome; driver mutations have recently also been discovered within noncoding genomic sequences. Thus, a current challenge is to gain precise understanding of how these unique genomic elements function in cancer pathogenesis, while clarifying mechanisms of gene regulation and identifying new targets for therapeutic intervention. Here we report a C-to-T single nucleotide transition that occurs as a somatic mutation in noncoding sequences 4 kb upstream of the transcriptional start site of the LMO1 oncogene in primary samples from patients with T-cell acute lymphoblastic leukaemia. This single nucleotide alteration conforms to an APOBEC-like cytidine deaminase mutational signature, and generates a new binding site for the MYB transcription factor, leading to the formation of an aberrant transcriptional enhancer complex that drives high levels of expression of the LMO1 oncogene. Since APOBEC-signature mutations are common in a broad spectrum of human cancers, we suggest that noncoding nucleotide transitions such as the one described here may activate potent oncogenic enhancers not only in T-lymphoid cells but in other cell lineages as well.
[Mh] Termos MeSH primário: Desaminases APOBEC/metabolismo
Proteínas de Ligação a DNA/biossíntese
Elementos Facilitadores Genéticos/genética
Regulação Leucêmica da Expressão Gênica/genética
Proteínas com Domínio LIM/biossíntese
Proteínas de Neoplasias/biossíntese
Mutação Puntual
Leucemia-Linfoma Linfoblástico de Células T Precursoras/genética
Fatores de Transcrição/biossíntese
Transcriptoma
[Mh] Termos MeSH secundário: Regiões 5' não Traduzidas/genética
Sequência de Bases
Sítios de Ligação
Linhagem Celular Tumoral
Criança
Imunoprecipitação da Cromatina
DNA de Neoplasias/genética
Proteínas de Ligação a DNA/genética
Genes myb
Seres Humanos
Células Jurkat
Proteínas com Domínio LIM/genética
Proteínas de Neoplasias/genética
Polimorfismo de Nucleotídeo Único
Leucemia-Linfoma Linfoblástico de Células T Precursoras/metabolismo
Proteínas Proto-Oncogênicas c-myb/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-myb/genética
Proteínas Proto-Oncogênicas c-myb/metabolismo
Interferência de RNA
RNA Interferente Pequeno/genética
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5' Untranslated Regions); 0 (DNA, Neoplasm); 0 (DNA-Binding Proteins); 0 (LIM Domain Proteins); 0 (LMO1 protein, human); 0 (Neoplasm Proteins); 0 (Proto-Oncogene Proteins c-myb); 0 (RNA, Small Interfering); 0 (Transcription Factors); EC 3.5.4.5 (APOBEC Deaminases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170307
[St] Status:MEDLINE
[do] DOI:10.1038/leu.2017.75


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[PMID]:28234982
[Au] Autor:Tak H; Negi S; Ganapathi TR
[Ad] Endereço:Plant Cell Culture Technology Section, Nuclear Agriculture and Biotechnology Division, Bhabha Atomic Research Centre, Trombay, Mumbai, India.
[Ti] Título:Overexpression of MusaMYB31, a R2R3 type MYB transcription factor gene indicate its role as a negative regulator of lignin biosynthesis in banana.
[So] Source:PLoS One;12(2):e0172695, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lignin and polyphenols are important cellular components biosynthesized through phenylpropanoid pathway. Phenylpropanoid pathway in plants is regulated by some important transcription factors including R2R3 MYB transcription factors. In this study, we report the cloning and functional characterization of a banana R2R3-MYB transcription factor (MusaMYB31) by overexpression in transgenic banana plants and evaluated its potential role in regulating biosynthesis of lignin and polyphenols. Sequence analysis of MusaMYB31 indicated its clustering with members of subgroup 4 (Sg4) of R2R3MYB family which are well known for their role as repressors of lignin biosynthesis. Expression analysis indicated higher expression of MusaMYB31 in corm and root tissue, known for presence of highly lignified tissue than other organs of banana. Overexpression of MusaMYB31 in banana cultivar Rasthali was carried out and four transgenic lines were confirmed by GUS histochemical staining, PCR analysis and Southern blot. Histological and biochemical analysis suggested reduction of cell wall lignin in vascular elements of banana. Transgenic lines showed alteration in transcript levels of general phenylpropanoid pathway genes including lignin biosynthesis pathway genes. Reduction of total polyphenols content in transgenic lines was in line with the observation related to repression of general phenylpropanoid pathway genes. This study suggested the potential role of MusaMYB31 as repressor of lignin and polyphenols biosynthesis in banana.
[Mh] Termos MeSH primário: Parede Celular/genética
Regulação da Expressão Gênica de Plantas
Genes myb
Musa/genética
Proteínas de Plantas/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Parede Celular/metabolismo
Parede Celular/ultraestrutura
Lignina/biossíntese
Musa/metabolismo
Fenilpropionatos/metabolismo
Filogenia
Folhas de Planta/genética
Folhas de Planta/metabolismo
Proteínas de Plantas/metabolismo
Plantas Geneticamente Modificadas
Polifenóis/biossíntese
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phenylpropionates); 0 (Plant Proteins); 0 (Polyphenols); 0 (RNA, Messenger); 0 (Transcription Factors); 9005-53-2 (Lignin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0172695


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[PMID]:27899693
[Au] Autor:Weissinger SE; Frick M; Möller P; Horst BA; Lennerz JK
[Ad] Endereço:1 University of Ulm, Ulm, Germany.
[Ti] Título:Performance Testing of RREB1, MYB, and CCND1 Fluorescence In Situ Hybridization in Spindle-Cell and Desmoplastic Melanoma Argues for a Two-Step Test Algorithm.
[So] Source:Int J Surg Pathol;25(2):148-157, 2017 Apr.
[Is] ISSN:1940-2465
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Diagnostic confirmation of spindle-cell melanoma (SM) or desmoplastic melanoma (DM) as a melanoma can be challenging. In conventional melanoma (CM), a recently established fluorescence in situ hybridization (FISH) assay for RREB1, MYB, CCND1 can be helpful. Here, we determined the presence of RREB1, MYB, and CCND1 abnormalities in an SM/DM/mixed cohort. METHODS: We assembled 49 cases and performed 3 separate hybridizations for RREB1/MYB/CCND1. We assessed clinical utility in diagnostically challenging cases and performed a cost and turnaround time analysis. RESULTS: With regard to the diagnosis of melanoma, the FISH assay is 76% sensitive (n = 31/41 true positives melanomas) and 88% specific (n = 1/8 false positive desmoplastic nevi). The prevalence of abnormalities in DM is lower (12/19 cases, 63%; P = .03) than in SM (15/18 cases, 83%; P = .27), mixed (4 of 4 cases), or the reported sensitivity in CM (345/411 cases, 84%). The implied genetic differences in DM result in a higher false negative rate in DM (37%). Despite these limitations, when restricted to diagnostically challenging cases (n = 23), the FISH assay and, in particular, RREB1 was able to confirm melanoma in 70% (n = 16/23). Individual probe sensitivities ( RREB1 > MYB > CCND1) and a cost and turnaround time analysis argues for a 2-step test algorithm that reduces the economic impact of FISH testing considerably (~55%; n = 69 vs 123 hybridizations). CONCLUSION: We propose a step-by-step genetic testing algorithm to support the diagnosis of melanoma in the setting of SM/DM and show that FISH testing is useful in diagnostically challenging cases.
[Mh] Termos MeSH primário: Algoritmos
Biomarcadores Tumorais/análise
Melanoma/diagnóstico
Neoplasias Cutâneas/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Idoso
Ciclina D1/análise
Ciclina D1/genética
Proteínas de Ligação a DNA/análise
Proteínas de Ligação a DNA/genética
Feminino
Dosagem de Genes
Genes myb/genética
Seres Humanos
Imuno-Histoquímica
Hibridização in Situ Fluorescente
Masculino
Meia-Idade
Sensibilidade e Especificidade
Fatores de Transcrição/análise
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CCND1 protein, human); 0 (DNA-Binding Proteins); 0 (RREB1 protein, human); 0 (Transcription Factors); 136601-57-5 (Cyclin D1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161201
[St] Status:MEDLINE
[do] DOI:10.1177/1066896916680072


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[PMID]:27859477
[Au] Autor:Prieto-Granada CN; Zhang L; Antonescu CR; Henneberry JM; Messina JL
[Ad] Endereço:Department of Pathology, University of Alabama at Birmingham (UAB), Birmingham, AL, USA.
[Ti] Título:Primary cutaneous adenoid cystic carcinoma with MYB aberrations: report of three cases and comprehensive review of the literature.
[So] Source:J Cutan Pathol;44(2):201-209, 2017 Feb.
[Is] ISSN:1600-0560
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adenoid cystic carcinoma (ACC) is a relatively rare slow-growing and often-aggressive epithelial-myoepithelial neoplasm that arises in multiple organs including the skin. The t(6;9) (q22-23;p23-24) translocation, resulting in a MYB-NFIB gene fusion has been found in ACCs from the salivary glands and other organs. Recently, MYB aberrations occurring in a subset (40%) of primary cutaneous ACC (PCACC) examples was described. Herein, we report three additional cases of PCACC harboring MYB aberrations. The tumors presented in three males aged 43, 81 and 55 years old and affected the extremities in the first two patients and the scalp in the third one. None of the patients had history of prior or concurrent ACC elsewhere. Lesions exhibited the classic ACC morphology of nests of basaloid cells arranged in cribriform and adenoid patterns. Sentinel lymph node biopsy was performed in two cases with one case showing lymph node positivity. Fluorescence in situ hybridization with break-apart probes for MYB and NFIB loci revealed that two cases showed MYB rearrangements while one case showed loss of one MYB signal. None of the cases showed NFIB rearrangements. We contribute with three additional cases of PCACC exhibiting MYB aberrations, the apparent driving genetic abnormality in these tumors.
[Mh] Termos MeSH primário: Carcinoma Adenoide Cístico/genética
Carcinoma Adenoide Cístico/patologia
Genes myb/genética
Neoplasias Cutâneas/genética
Neoplasias Cutâneas/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso de 80 Anos ou mais
Seres Humanos
Hibridização in Situ Fluorescente
Masculino
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170916
[Lr] Data última revisão:
170916
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161119
[St] Status:MEDLINE
[do] DOI:10.1111/cup.12856


  6 / 329 MEDLINE  
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[PMID]:27220777
[Au] Autor:Zhang B; Yuan F; Liu J; Li Y; Zhou F; Liu X; Hao Z; Li Q; Zheng Y; Wang W
[Ad] Endereço:Department of Neurology, The Second Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
[Ti] Título:Hsa-miR-495 acts as a tumor suppressor gene in glioma via the negative regulation of MYB.
[So] Source:Mol Med Rep;14(1):977-82, 2016 Jul.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:MicroRNAs (miRNAs) are small non-coding RNA molecules that regulate gene expression at the post-transcriptional level. Previous studies have reported that there are causative links between the abnormal regulation of miRNAs and cancer development. Hsa­miR­495 has previously been demonstrated to be downregulated, and to function as a tumor suppressor, in numerous types of human cancer. However, the function and molecular mechanism of hsa­miR­495 in glioma remains unclear. In the current study, the expression and effects of hsa­miR­495 on glioma were evaluated. It was identified that the expression levels of hsa-miR-495 were downregulated in glioma tissues and cell lines. Furthermore, restoration of hsa-miR-495 inhibited glioma cell proliferation and invasion in vitro. Notably, a luciferase reporter assay revealed that hsa­miR­495 was able to directly target v­myb avian myeloblastosis viral oncogene homolog (MYB) in glioma cells. In addition, an RNA interference assay indicated that MYB knockdown inhibited glioma cell proliferation and invasion in vitro. In conclusion, the results of the present study suggested that hsa­miR­495 may act as a tumor suppressor gene in glioma by directly inhibiting MYB expression, which may provide a novel therapeutic strategy for the treatment of glioma.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Genes Supressores de Tumor
Genes myb
Glioma/genética
MicroRNAs/genética
Interferência de RNA
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Sítios de Ligação
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Expressão Gênica
Técnicas de Silenciamento de Genes
Seres Humanos
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (MIRN495 microRNA, human); 0 (MicroRNAs)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170406
[Lr] Data última revisão:
170406
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160526
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2016.5327


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[PMID]:27174194
[Au] Autor:Broz M; Steiner P; Salzman R; Hauer L; Starek I
[Ad] Endereço:Department of Otorhinolaryngology, University Hospital Olomouc and Faculty of Medicine and Dentistry, Palacky University Olomouc, Czech Republic.
[Ti] Título:The incidence of MYB gene breaks in adenoid cystic carcinoma of the salivary glands and its prognostic significance.
[So] Source:Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub;160(3):417-22, 2016 Sep.
[Is] ISSN:1213-8118
[Cp] País de publicação:Czech Republic
[La] Idioma:eng
[Ab] Resumo:AIMS: To detect MYB gene breaks in adenoid cystic carcinoma (ACC) of the salivary glands and its correlation with prognosis and selected clinical parameters METHODS: MYB gene break was detected by FISH assay in 23 adenoid cystic carcinomas using formalin-fixed paraffin-embedded blocks. The Kaplan-Meier survival analysis was used to estimate prognosis. RESULTS: Fifteen of 23 evaluated tumours were MYB positive and 8 MYB negative. The 10-year cumulative survival, respectively disease free interval, was 60.0%, respectively 59.3%, in MYB positive patients and 88.5%, respectively 80.0%, in MYB negative patients (long rank test, P=0.23). There were no significant differences in age, gender, perineural invasion, the presence of hematogenic or nodal metastases or degree of histopathological grading between MYB positive and MYB negative patients. CONCLUSION: A tendency to differences in the survival of patients with ACC, depending on their MYB status. MYB negative patients were predisposed to better prognosis.
[Mh] Termos MeSH primário: Carcinoma Adenoide Cístico/genética
Genes myb/genética
Neoplasias das Glândulas Salivares/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Carcinoma Adenoide Cístico/mortalidade
Feminino
Predisposição Genética para Doença/genética
Seres Humanos
Hibridização in Situ Fluorescente
Masculino
Meia-Idade
Prognóstico
Neoplasias das Glândulas Salivares/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170418
[Lr] Data última revisão:
170418
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160514
[St] Status:MEDLINE
[do] DOI:10.5507/bp.2016.027


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[PMID]:27129581
[Au] Autor:Casaretto JA; El-Kereamy A; Zeng B; Stiegelmeyer SM; Chen X; Bi YM; Rothstein SJ
[Ad] Endereço:Department of Molecular and Cellular Biology, University of Guelph, Guelph, ON, N1G 2W1, Canada. jcasaret@uoguelph.ca.
[Ti] Título:Expression of OsMYB55 in maize activates stress-responsive genes and enhances heat and drought tolerance.
[So] Source:BMC Genomics;17:312, 2016 Apr 29.
[Is] ISSN:1471-2164
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Plant response mechanisms to heat and drought stresses have been considered in strategies for generating stress tolerant genotypes, but with limited success. Here, we analyzed the transcriptome and improved tolerance to heat stress and drought of maize plants over-expressing the OsMYB55 gene. RESULTS: Over-expression of OsMYB55 in maize decreased the negative effects of high temperature and drought resulting in improved plant growth and performance under these conditions. This was evidenced by the higher plant biomass and reduced leaf damage exhibited by the transgenic lines compared to wild type when plants were subjected to individual or combined stresses and during or after recovery from stress. A global transcriptomic analysis using RNA sequencing revealed that several genes induced by heat stress in wild type plants are constitutively up-regulated in OsMYB55 transgenic maize. In addition, a significant number of genes up-regulated in OsMYB55 transgenic maize under control or heat treatments have been associated with responses to abiotic stresses including high temperature, dehydration and oxidative stress. The latter is a common and major consequence of imposed heat and drought conditions, suggesting that this altered gene expression may be associated with the improved stress tolerance in these transgenic lines. Functional annotation and enrichment analysis of the transcriptome also pinpoint the relevance of specific biological processes for stress responses. CONCLUSIONS: Our results show that expression of OsMYB55 can improve tolerance to heat stress and drought in maize plants. Enhanced expression of stress-associated genes may be involved in OsMYB55-mediated stress tolerance. Possible implications for the improved tolerance to heat stress and drought of OsMYB55 transgenic maize are discussed.
[Mh] Termos MeSH primário: Genes myb
Oryza/genética
Proteínas de Plantas/genética
Estresse Fisiológico/genética
Zea mays/fisiologia
[Mh] Termos MeSH secundário: Secas
Regulação da Expressão Gênica de Plantas
Sequenciamento de Nucleotídeos em Larga Escala
Temperatura Alta
Fenótipo
Plantas Geneticamente Modificadas/genética
Análise de Sequência de RNA
Transcriptoma
Regulação para Cima
Zea mays/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Plant Proteins)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160501
[St] Status:MEDLINE
[do] DOI:10.1186/s12864-016-2659-5


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[PMID]:27098811
[Au] Autor:Upadhye D; Jain D; Trivedi Y; Nadkarni A; Ghosh K; Colah R
[Ad] Endereço:National Institute of Immunohaematology, (Indian Council of Medical Research), 13th floor, New Multistoried Building, K.E.M. Hospital Campus, Parel, Mumbai, 400012, India.
[Ti] Título:Influence of single nucleotide polymorphisms in the BCL11A and HBS1L-MYB gene on the HbF levels and clinical severity of sickle cell anaemia patients.
[So] Source:Ann Hematol;95(7):1201-3, 2016 Jun.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Mh] Termos MeSH primário: Anemia Falciforme/genética
Proteínas de Transporte/genética
Hemoglobina Fetal/genética
Proteínas de Ligação ao GTP/genética
Genes myb/genética
Proteínas de Choque Térmico HSP70/genética
Proteínas Nucleares/genética
Fatores de Alongamento de Peptídeos/genética
Polimorfismo de Nucleotídeo Único/genética
[Mh] Termos MeSH secundário: Adulto
Anemia Falciforme/diagnóstico
Estudos de Coortes
Feminino
Seguimentos
Seres Humanos
Masculino
Índice de Gravidade de Doença
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (BCL11A protein, human); 0 (Carrier Proteins); 0 (HSP70 Heat-Shock Proteins); 0 (Hbs1 protein, human); 0 (Nuclear Proteins); 0 (Peptide Elongation Factors); 9034-63-3 (Fetal Hemoglobin); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170127
[Lr] Data última revisão:
170127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160422
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-016-2675-1


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[PMID]:27009386
[Au] Autor:He Q; Jones DC; Li W; Xie F; Ma J; Sun R; Wang Q; Zhu S; Zhang B
[Ad] Endereço:Department of Biology, East Carolina University, Greenville, NC 27858, United States of America.
[Ti] Título:Genome-Wide Identification of R2R3-MYB Genes and Expression Analyses During Abiotic Stress in Gossypium raimondii.
[So] Source:Sci Rep;6:22980, 2016 Mar 24.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The R2R3-MYB is one of the largest families of transcription factors, which have been implicated in multiple biological processes. There is great diversity in the number of R2R3-MYB genes in different plants. However, there is no report on genome-wide characterization of this gene family in cotton. In the present study, a total of 205 putative R2R3-MYB genes were identified in cotton D genome (Gossypium raimondii), that are much larger than that found in other cash crops with fully sequenced genomes. These GrMYBs were classified into 13 groups with the R2R3-MYB genes from Arabidopsis and rice. The amino acid motifs and phylogenetic tree were predicted and analyzed. The sequences of GrMYBs were distributed across 13 chromosomes at various densities. The results showed that the expansion of the G. Raimondii R2R3-MYB family was mainly attributable to whole genome duplication and segmental duplication. Moreover, the expression pattern of 52 selected GrMYBs and 46 GaMYBs were tested in roots and leaves under different abiotic stress conditions. The results revealed that the MYB genes in cotton were differentially expressed under salt and drought stress treatment. Our results will be useful for determining the precise role of the MYB genes during stress responses with crop improvement.
[Mh] Termos MeSH primário: Expressão Gênica
Genes myb
Gossypium/crescimento & desenvolvimento
Gossypium/genética
Proteínas de Plantas/genética
[Mh] Termos MeSH secundário: Secas
Duplicação Gênica
Regulação da Expressão Gênica de Plantas
Genoma de Planta
Família Multigênica
Filogenia
Salinidade
Duplicações Segmentares Genômicas
Análise de Sequência de Proteína
Estresse Fisiológico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Plant Proteins)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160325
[St] Status:MEDLINE
[do] DOI:10.1038/srep22980



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