We used a combination of genome-wide and promoter-specific DNA binding and expression analyses to assess the functional roles of Myod and Myog in regulating the program of skeletal muscle gene expression. Our findings indicate that Myod and Myog have distinct regulatory roles at a similar set of target genes. At genes expressed throughout the program of myogenic differentiation, Myod can bind and recruit histone acetyltransferases. At early targets, Myod is sufficient for near full expression; whereas, at late expressed genes Myod initiates regional histone modification but is not sufficient for gene expression. At these late genes, Myog does not bind efficiently without Myod, however, transcriptional activation requires the combined activity of Myod and Myog. Therefore, the role of Myog in mediating terminal differentiation is, in part, to enhance expression of a subset of genes previously initiated by Myod.
Global and gene-specific analyses show distinct roles for Myod and Myog at a common set of promoters.
No sample metadata fields
View SamplesPbx homeodomain proteins have been implicated in the regulation of gene expression during muscle development. Whether Pbx proteins are required broadly for the regulation of muscle gene expression or are required for the expression of a specific subset of muscle gene expression is not known. We employed microarrays to determine the requirements for Pbx proteins during zebrafish development.
Pbx homeodomain proteins direct Myod activity to promote fast-muscle differentiation.
No sample metadata fields
View SamplesInvestigate the genome-wide gene expression profiles of 50% and 95% confluent C2C12 myoblasts and C2C12 myotubes differentiated for 24 and 48 hours.
Genome-wide MyoD binding in skeletal muscle cells: a potential for broad cellular reprogramming.
Specimen part, Cell line, Time
View SamplesRhabdomyosarcomas (RMS) are characterized by expression of myogenic specification genes, such as MyoD and/or Myf5, as well as their bHLH partners for heterodimerization, the E-proteins. We have shown that expression of a forced heterodimer of MyoD with one of the E2A proteins, E12, leads to differentiation in a RMS cell culture model when exposed to low serum conditions.
MyoD and E-protein heterodimers switch rhabdomyosarcoma cells from an arrested myoblast phase to a differentiated state.
Cell line
View SamplesAmplification of large chromosomal regions (gene amplification) is a common somatic alteration in human cancer cells and often is associated with advanced disease. A critical event initiating gene amplification is a DNA double strand break (DSB), which is immediately followed by the formation of a large DNA palindrome. Large DNA palindromes are frequent and non-randomly distributed in the genomes of cancer cells and facilitate further increase in copy number. Although the importance of the formation of large DNA palindromes as a very early event in gene amplification is widely recognized, it is not known 1) how a DSB is resolved to form a large DNA palindrome; and 2) whether any local DNA structure determines the location of large DNA palindromes. We show here that intra-strand annealing following a DNA double-strand break leads to the formation of large DNA palindromes and that DNA inverted repeats in the genome determines the efficiency of this event. Furthermore, in human Colo320DM cancer cells, a DNA inverted repeat in the genome marks the border between amplified and non-amplified DNA. Therefore, an early step of gene amplification is a regulated process that is facilitated by DNA inverted repeats in the genome.
Intrastrand annealing leads to the formation of a large DNA palindrome and determines the boundaries of genomic amplification in human cancer.
No sample metadata fields
View SamplesPurpose: We generated extensive transcriptional and proteomic profiles from a Her2-driven mouse model of breast cancer that closely recapitulates human breast cancer. This report makes these data publicly available in raw and processed forms, as a resource to the community. Importantly, we previously made biospecimens from this same mouse model freely available through a sample repository, so researchers can obtain samples to test biological hypotheses without the need of breeding animals and collecting biospecimens.
Proteome and transcriptome profiles of a Her2/Neu-driven mouse model of breast cancer.
Sex, Specimen part
View SamplesOSCC is associated with substantial mortality and morbidity. To identify potential biomarkers for the early detection of invasive OSCC, we compared the gene expressions of OSCC, oral dysplasia, and normal
Gene expression profiling identifies genes predictive of oral squamous cell carcinoma.
Sex
View SamplesIn MTN-007, a phase 1, randomized, double-blinded rectal microbicide trial, we used systems genomics/proteomics to determine the effect of tenofovir 1% gel, nonoxynol-9 2% gel, placebo gel or no treatment on rectal biopsies taken at baseline, after one application or after seven daily applications (15 subjects/arm). Experiments were repeated using primary vaginal epithelial cells from four healthy women.
Mucosal effects of tenofovir 1% gel.
Specimen part, Treatment
View SamplesThe objectives of this study were to measure effects of an aspirin intervention on gene expression in normal colonic epithelial and stromal tissue in healthy humans and to determine whether response differed by UGT1A6*2 genotype. We also sought to characterize gene expression differences within colonic tissue microenvironments by identifying genes that were differentially expressed between epithelial and stromal tissue.
Tissue-specific patterns of gene expression in the epithelium and stroma of normal colon in healthy individuals in an aspirin intervention trial.
Sex, Specimen part
View SamplesOSCC is associated with substantial mortality and morbidity. In this study, we built on our previous molecular work to identify and validate a prognostic 13-gene signature that showed a higher ability than tumor stage in predicting survival for patients with
A 13-gene signature prognostic of HPV-negative OSCC: discovery and external validation.
Sex, Specimen part, Treatment
View Samples