This SuperSeries is composed of the SubSeries listed below.
Promoter-proximal transcription factor binding is transcriptionally active when coupled with nucleosome repositioning in immediate vicinity.
Specimen part, Disease, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Non-metastatic 2 (NME2)-mediated suppression of lung cancer metastasis involves transcriptional regulation of key cell adhesion factor vinculin.
Specimen part, Cell line
View SamplesNon-metastatic 2 (NME2) is an established metastases suppressor in multiple human cancer types. However, the molecular mechanisms of NME2 action remain insufficiently resolved. We recently validated the transcription regulatory activity of NME2 with respect to control of proto-oncogene c-MYC expression. We hypothesized that large scale transcriptional potential of NME2 may be at the core of metastases suppression by NME2. Using a combination of high throughput genomic assays such as chromatin immunoprecipitation coupled to promoter array hybridization (ChIP-chip) and gene expression profiling, we characterized the transcriptional roles of NME2. Specifically, we found a set of NME2 target genes which changed expression upon selective depletion of NME2 in a lung cancer cell line, A549. The analysis of gene expression suggested control of various biological pathways esp. cell adhesion and apoptosis by NME2 target genes which could be important in regulation of metastases.
Promoter-proximal transcription factor binding is transcriptionally active when coupled with nucleosome repositioning in immediate vicinity.
Specimen part, Cell line
View SamplesIt is widely believed that reorganization of nucleosomes result in availability of binding sites that engage transcription factors during eukaryotic gene regulation. Recent findings, on the other hand, suggest that transcription factors induced as a result of physiological perturbations directly (or in association with chromatin modifiers) may alter nucleosome occupancy to facilitate DNA binding. Although, together these suggest a close relationship between transcription factor binding and nucleosome reorganization, the nature of the inter-dependency, or to what extent it influences regulatory transcription is not clear. Moreover, since most studies used physiolgical pertubations that induced multiple transcription factor chromatin modifiers, the relatively local (or direct) effect of transcription factor binding on nucleosome occupancy remains unclear. With these in mind, we used a single transcription factor to induce physiological changes, representing metastatic (aggressive cancer) and the corresponding non-metastatic state, in human cancer cells. Following characterization of the two states (before and after induction of the transcription factor) we determined: (a) genome wide binding sites of the transcription factor, (b) promoter nucleosome occupancy and (c) transcriptome profiles, independently in both conditions. Interestingly, we find only ~20% of TF binding results from nucleosome reorganization - however, almost all corresponding genes were transcriptionally altered. Whereas, in cases where TF-occupancy was independent of nucleosome repositioning (in close vicinity), or co-occurred with nucleosomes, only a small fraction of the corresponding genes were expressed/repressed. Together, these indicate a model where TF occupancy only when coupled with nucleosome repositioning in close proximity is transcriptionally active. This, to our knowledge, for the first time also helps explain why genome wide TF occupancy (e.g., from ChIP-seq) is typically associated with only a small fraction of genes that change expression.
Promoter-proximal transcription factor binding is transcriptionally active when coupled with nucleosome repositioning in immediate vicinity.
Specimen part, Cell line
View SamplesNGS of IGIB-NIV 01 Hologenome
No associated publication
No sample metadata fields
View SamplesAnalysis of altered level of transcripts in cases of SCA12 patients from peripheral blood samples
No associated publication
Specimen part, Disease, Disease stage
View SamplesMycobacterium tuberculosis(Mtb) is known to reside in cells of innate immune system- macrophages and dendritic cells. A variety of non -conventional cell typeslike adipocytes, mesenchyal stem cells and osteoclasts can also be infected with Mtb. However, cellular transcriptional adapations enabling survival of Mtb in these cells remain known.
No associated publication
Specimen part
View Samples