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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human MCF7 cells infected with adenovirus expressing c-Myb, v-Myb or the hybrid construct, 3MutC

ABSTRACT: The transcriptional activities of c-Myb and its oncogenic variant v-Myb were compared by expressing them in human MCF7 cells using recombinant adenovirus vectors. A hybrid construct, 3Mutc, which is a variant of c-Myb harboring three v-Myb-derived DNA binding domain mutations was also analyzed. All the samples were compared to cells infected with a control adenovirus. The results showed that v-Myb, which differs from c-Myb only by N- and C-terminal deletions and eleven amino acid substitutions, has a qualitatively different transcriptional activity. Experiment Overall Design: 2 replicates of each type were analyzed. Replicates were performed independently, more than a week apart.

ORGANISM(S): Homo sapiens

SUBMITTER: Scott Ness

PROVIDER: E-GEOD-2815 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Oncogenic mutations cause dramatic, qualitative changes in the transcriptional activity of c-Myb.

Liu F F Lei W W O'Rourke J P JP Ness S A SA

Oncogene 20060201 5

The v-Myb oncoprotein encoded by Avian Myeloblastosis Virus is highly oncogenic, induces leukemias in chickens and mice and transforms immature hematopoietic cells in vitro. The v-Myb protein is a mutated and truncated version of c-Myb, a DNA-binding transcription factor expressed in many cell types that is essential for normal hematopoiesis. Previous studies suggested that two types of differences, DNA binding domain mutations and the deletion of a C-terminal negative regulatory domain were imp ...[more]

PMID: 16205643

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Transcription profiling of human monocytes infected with adenovirus expressing either c-Myb or v-Myb

Project description:The transcriptional activities of c-Myb and its oncogenic variant v-Myb were compared by expressing them in primary human monocytes using recombinant adenovirus vectors. All the samples were compared to cells infected with a control adenovirus expressing only GFP. The results showed that v-Myb, which differs from c-Myb only by N- and C-terminal deletions and eleven amino acid substitutions, has a qualitatively different transcriptional activity. Experiment Overall Design: 2 replicates of each type were analyzed. Replicates were performed independently, more than a week apart.

2007-12-12 | E-GEOD-2816 | biostudies-arrayexpress

c-Myb inhibits myoblast fusion

Project description:The study of the effects of modification of c-Myb expression on differenatiation of C2C12 cells

2013-10-21 | E-MTAB-1376 | biostudies-arrayexpress

MicroRNA-15/16 Antagonizes c-Myb to Control Natural Killer Cell Maturation (c-Myb overexpression)

Project description:NK cells develop in the bone marrow and complete their maturation in peripheral organs, but the molecular events controlling maturation are incompletely understood. Utilizing an NK cell-specific miR-15/16 deficient genetic model (15aKO), we identified a critical role for miR-15/16 family microRNAs in the normal maturation of NK cells in vivo, with a specific reduction in mature CD11b+CD27- NK cells in multiple tissues. The mechanism responsible was a block in differentiation, since accelerated NK cell death was not evident, and earlier intermediates of NK cell maturation were expanded. Further, we identified Myb as a direct target of miR-15/16 in NK cells, with Myb expression increased in immature 15aKO NK cells. Following adoptive transfer, immature 15aKO NK cells exhibited defective maturation, which was rescued by ectopic miR-15/16 expression or Myb knockdown. Moreover, Myb overexpression resulted in defective NK cell maturation. Thus, miR-15/16 regulation of Myb controls the normal NK cell maturation program. KY-1 and KY-2 cell lines overexpressing c-Myb

2015-09-03 | E-GEOD-58268 | biostudies-arrayexpress

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Project description:Earlier we have shown important roles of MYB in pancreatic tumor pathobiology. To better understand the role of MYB in the tumor microenvironment and identify MYB-associated secreted biomarker proteins, we conducted mass spectrometry analysis of the secretome from MYB-modulated and control pancreatic cancer cell lines. We also performed in silico analyses to determine MYB-associated biofunctions, gene networks and altered biological pathways. We further investigated the secreted proteins for their potential biomarker properties.

2021-09-08 | PXD015126 | Pride

Transcription profiling by array of human p73 over-expressing H1299 cells

Project description:The integral role of p53 in tumor suppression has promted many laboratories to perform extensive analyses of signaling pathways downstream of the p53 family of sequence-specific DNA binding transcription factors (p53 and its homologs p63 and p73). Despite the ability of p73 to regulate many p53 family target genes, little is known about the specific pathways that modulate p73 during development, tumorigenesis and tumor therapy. In this study we present a gene signature-based approach for connecting signaling pathways to transcription factors, as exemplified by p73. We generated a p73 gene signature by integrating whole-genome chromatin immunoprecipitation and expression profiling. Experiment Overall Design: H1299 lung carcinoma cells were infected with p73 expressing or control adenovirus for 5 h and then harvested.

2008-10-20 | E-GEOD-11626 | biostudies-arrayexpress

Microarray analysis of BHLHB2 and BHLHB3 target genes in human skeletal muscle cells

Project description:In this study we have identified the target genes of BHLHB2 and BHLHB3 in primary cultures of human skeletal muscle cells using adenoviral vectors expressing either BHLHB2 or BHLHB3, and oligonucleotide microarrays. Human myotubes were prepared from 4 different skeletal muscle biopsies. After 7 days of differentiation, myotubes were infected for 48 hours with recombinant adenovirus expressing either GFP, BHLHB2 or BHLHB3. Each BHLHB2- or BHLHB3-infected myotubes culture was compared to GFP-infected myotubes culture. GFP-infected myotubes were considered the control. Four biological replicates were processed.

2010-04-11 | E-GEOD-12947 | biostudies-arrayexpress

Genome-wide Myb chromatin occupancy in murine myeloid progenitor cells

Project description:We report genome-wide pattern of Myb chromatin occupancy in vivo. We used ERMYB, a myeloid progenitor cell line derived by transformation of primary cells by ER-Myb fusion protein, as our model system. In these cells, activation of the ER-Myb fusion protein by estrogen is required to maintain a proliferative progenitor-like phenotype. We performed ChIP-seq with biological duplicate samples from ERMYB cells with Myb either “on” or “off” (i.e. + or - ?-E2 for 6 hr). By comparing enrichment signals between Myb-on, Myb-off and isotype control samples, we identified 7,646 high-confidence Myb binding regions, which can be assigned to 4,892 annotated genes according to their distances to the nearest transcriptional start sites. Examination of Myb chromatin occupany in myeloid cells transformed by a switchable form of Myb

2011-02-23 | E-GEOD-22095 | biostudies-arrayexpress

Definition of aberrant MYB CBP/P300 complex in AML

Project description:Dysregulated gene expression is one of the most prevalent features in human cancers. Here, we show that most subtypes of acute myeloid leukemia (AML) depend on the aberrant assembly of the MYB transcriptional co-activator complex. By rapid and selective peptidomimetic interference with the binding of CBP/P300 to MYB, but not CREB or MLL1, we find that the leukemic functions of MYB are mediated by CBP/P300-mediated co-activation of a distinct set of transcriptional factor complexes that are aberrantly assembled with MYB in AML cells. This therapeutic remodeling is accompanied by dynamic redistribution of CBP/P300 complexes to genes that control cellular differentiation and growth. Thus, aberrantly organized transcription factor complexes control convergent gene expression programs in AML cells. These findings establish a compelling strategy for pharmacologic reprogramming of oncogenic gene expression that supports its targeting for leukemias and other human cancers caused by dysregulated gene control.

2020-12-17 | PXD019708 | Pride

Tri-KIX +/- c-Myb MEFs

Project description:Transcription profiling by array of wild type and p300 KIX/KIX; CBP +/KIX primary mouse embryonic fibroblasts (MEFs) transduced with either MSCV-c-Myb_IRES-GFP or MSCV-IRES-GFP retrovirus to determine the effect of mutating the KIX domain of CBP and p300 on c-Myb regulated gene expression. CBP KIX mutation (MGI:3578129) and p300 KIX mutation (MGI:3578128).

2014-02-10 | E-MTAB-1973 | biostudies-arrayexpress

Cardiac transcription factors in HL-1 cells: gene expression and genome binding profiling

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2011-03-02 | E-GEOD-21529 | biostudies-arrayexpress

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