This SuperSeries is composed of the SubSeries listed below.
The MuvB complex sequentially recruits B-Myb and FoxM1 to promote mitotic gene expression.
Cell line
View SamplesPeriodic expression of cell cycle genes highlights the importance of precise temporal control of transcription in regulating cell cycle events. We used HeLa cells enriched for different phases of the cell cycle to identify genes that are expressed in a periodic fashion in specific cell cycle phases. These data were generated for comparison with ChIP-Sequencing data obtained for two subunits of the B-Myb-MuvB complex, B-Myb and LIN9, in HeLa cells.
No associated publication
Cell line
View SamplesThe mammalian Retinoblastoma (RB) family including pRB, p107, and p130 represses E2F target genes through mechanisms that are not fully understood. In D. melanogaster, RB-dependent repression is mediated in part by the multisubunit protein complex Drosophila RBF, E2F, and Myb (dREAM) that contains homologs of the C. elegans synthetic multivulva class B (synMuvB) gene products. Using an integrated approach combining proteomics, genomics, and bioinformatic analyses, we identified a p130 complex termed DP, RB-like, E2F, and MuvB (DREAM) that contains mammalian homologs of synMuvB proteins LIN-9, LIN-37, LIN-52, LIN-54, and LIN-53/RBBP4. DREAM bound to more than 800 human promoters in G0 and was required for repression of E2F target genes. In S phase, MuvB proteins dissociated from p130 and formed a distinct submodule that bound MYB. This work reveals an evolutionarily conserved multisubunit protein complex that contains p130 and E2F4, but not pRB, and mediates the repression of cell cycle-dependent genes in quiescence.
Evolutionarily conserved multisubunit RBL2/p130 and E2F4 protein complex represses human cell cycle-dependent genes in quiescence.
No sample metadata fields
View SamplesGenotypic differences greatly influence susceptibility and resistance to disease. Understanding genotype-phenotype relationships requires that phenotypes be viewed as manifestations of network properties, rather than simply as the result of individual genomic variations. Genome sequencing efforts have identified numerous germline mutations associated with cancer predisposition and large numbers of somatic genomic alterations. However, it remains challenging to distinguish between background, or passenger and causal, or driver cancer mutations in these datasets. Human viruses intrinsically depend on their host cell during the course of infection and can elicit pathological phenotypes similar to those arising from mutations. To test the hypothesis that genomic variations and tumour viruses may cause cancer via related mechanisms, we systematically examined host interactome and transcriptome network perturbations caused by DNA tumour virus proteins. The resulting integrated viral perturbation data reflects rewiring of the host cell networks, and highlights pathways that go awry in cancer, such as Notch signalling and apoptosis. We show that systematic analyses of host targets of viral proteins can identify cancer genes with a success rate on par with their identification through functional genomics and large-scale cataloguing of tumour mutations. These complementary approaches together result in increased specificity for cancer gene identification. Combining systems-level studies of pathogen-encoded gene products with genomic approaches will facilitate prioritization of cancer-causing driver genes so as to advance understanding of the genetic basis of human cancer.
Interpreting cancer genomes using systematic host network perturbations by tumour virus proteins.
Cell line
View SamplesWe obtained gene expression data and HD-SNP6.0 copy number data from PTL, PCNSL and PMLBCL samples and performed an integrative analysis on them. RNA was whole genome amplified using Nugen.
Targetable genetic features of primary testicular and primary central nervous system lymphomas.
Disease, Disease stage
View SamplesWnt pathway is dysregulated in CLL-We characterized Wnt pathway gene expression in normal B and CLL-B cells and identified Wnt targets in normal B and CLL-B cells through this data set.
Somatic mutation as a mechanism of Wnt/β-catenin pathway activation in CLL.
Specimen part
View SamplesAs part of a large study regarding the epigenetics of CLL we also acquired 3UTR expression arrays.
No associated publication
Specimen part
View SamplesWe performed gene expression profiling of laser capture microdissected normal non-neoplastic prostate (cystoprostatectomies) epithelial tissue and compared it to non-transformed and neoplastic low and high grade prostate epithelial tissue from radical prostatectomies, each with its immediately surrounding stroma.
Stromal and epithelial transcriptional map of initiation progression and metastatic potential of human prostate cancer.
No sample metadata fields
View SamplesTo understand the molecular curcuits perturbed by BET bromodoman inhibtion we obtained gene expression profiling of five DLBCL cell lines, SU-DHL6, OCI-Ly1, OCI-Ly4, Toledo and HBL-1, which were treated with either 500nM JQ1 or DMSO for 0,2,6,12,24 and 48hr.
Discovery and characterization of super-enhancer-associated dependencies in diffuse large B cell lymphoma.
Specimen part, Cell line, Treatment, Time
View SamplesGene Expression profiling of 170 newly diagnosed Multiple Myeloma patients
A small molecule inhibitor of ubiquitin-specific protease-7 induces apoptosis in multiple myeloma cells and overcomes bortezomib resistance.
Disease
View Samples