We have investigated the p53-dependent stress response in medium spiny neurons (MSNs) that degenerate in Huntingtons disease. To induce p53 signaling cascade, we have genetically inactivated by the Cre/loxP system the essential RNA polymerase I (Pol I) transcription factor TIF-IA, leading to stabilization of p53 and induction of p53-dependent apoptosis.
A neuroprotective phase precedes striatal degeneration upon nucleolar stress.
Age, Specimen part
View SamplesBy mapping global transcription start site (TSS) and chromatin dynamics, we observed the activation of thousands of cryptic, currently non-annotated TSSs (TINATS) following DNMTi and/or HDACi treatment. The resulting transcripts encode truncated or chimeric open reading frames that can be translated into products with predicted abnormal functions or immunogenic potential. TINAT activation after DNMTi coincided with DNA hypomethylation and gain in H3K4me3, H3K9ac, and H3K27ac histone marks. In contrast, HDACi induced only canonical TSSs in association with histone acetylation, but TINATs via a yet unknown mechanism. Nevertheless, both inhibitors convergently induced unidirectional transcription from identical sites since TINATs are encoded in solitary long-terminal repeats of the endogenous retrovirus-9 family, epigenetically repressed in virtually all normal cells. Overall design: CAGE-, ChIP-, and WGB-sequencing of NCI-H1299 EGFP-NEO reporter cells after treatment with DMSO, DAC, SB939, or DAC+SB
DNMT and HDAC inhibitors induce cryptic transcription start sites encoded in long terminal repeats.
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View SamplesTo identify cellular and genetic abnormalities involved in interstrand cross link repair-deficient bone marrow failure and its transformation to leukemia, we used an Ercc1 hypomorphic mouse model (Ercc1 -/d).
ICL-induced miR139-3p and miR199a-3p have opposite roles in hematopoietic cell expansion and leukemic transformation.
Age, Specimen part
View SamplesmRNA profiles of 8 weeks old C57BL/6 mice 2 days after infections with 5e7 pfu of various strains of murine norovirus (MNV) or 1e8 pfu of T1L reovirus were evauated Overall design: mRNA profiles of 8 weeks old C57BL/6 mice 2 days after infections with 5e7 pfu of various strains of murine norovirus (MNV) or 1e8 pfu of T1L reovirus were evauated
Murine Norovirus Infection Induces T<sub>H</sub>1 Inflammatory Responses to Dietary Antigens.
Age, Specimen part, Cell line, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide localization of SREBP-2 in hepatic chromatin predicts a role in autophagy.
Sex, Specimen part
View SamplesWe are using genome-wide ChIP-seq with isoform-specific antibodies and chromatin from select tissues of mice challenged with different dietary conditions that enrich for specific SREBPs.
Genome-wide localization of SREBP-2 in hepatic chromatin predicts a role in autophagy.
Sex, Specimen part
View SamplesGlobal expression analysis of neural crest-like skin-derived precursors (SKPs) and Sox2-positive follicle dermal cells that SKPs originate from.
SKPs derive from hair follicle precursors and exhibit properties of adult dermal stem cells.
Specimen part
View SamplesWe overexpressed the spliced form of transcription factor XBP1 in mature F442A adipocytes by adenoviral infection. Control virus expressed GFP alone.
The role of adipocyte XBP1 in metabolic regulation during lactation.
Specimen part, Cell line
View SamplesComparison of gene expression profile of HEK293 cells stably expressing a shRNA control (SilX-CT) or a shRNA against BAHD1 (SilX-BAHD1)
Overexpression of the Heterochromatinization Factor BAHD1 in HEK293 Cells Differentially Reshapes the DNA Methylome on Autosomes and X Chromosome.
Cell line
View SamplesComparison of gene expression profile of HEK293-CT cells and HEK293 cells stably over-expressing the BAHD1 gene (HEK-BAHD1)
Overexpression of the Heterochromatinization Factor BAHD1 in HEK293 Cells Differentially Reshapes the DNA Methylome on Autosomes and X Chromosome.
Cell line, Treatment
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