ChIP-seq for TP63 transcription factor in MEC1 cell line
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB46226 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Identification of TP63 binding profile (cistrome) at a genome-wide scale in MEC1 cell line, an established and well-characterized cellular model of Chronic Lymphocytic Leukemia.
2022-03-07 | E-MTAB-10713 | biostudies-arrayexpress
Project description:ChIP-seq for TP63 transcription factor in primary CLL cells
| PRJEB46228 | ENA
Project description:Identification of TP63 binding profile (cistrome) at a genome-wide scale, in primary cells derived from patient diagnosed with Chronic Lymphocytic Leukemia.
2022-03-07 | E-MTAB-10717 | biostudies-arrayexpress
Project description:Purpose: To identify TP63 expression regulated pathways in HNSCC Methods: A recombinant lentivirus encoding either NS shRNA or TP63 shRNA was introduced into a HNSCC cell line, FaDu. SCCs were gene generated by implanting either FaDu-NS shRNA (n=3) or FaDu-TP63 shRNA into the tongue of athymic nude mice. Tongue SCCs harvested at the end of study were used for transcriptome analysis
2019-03-15 | GSE120689 | GEO
Project description:Upon replication stress, the Mec1ATR kinase triggers the downregulation of transcription, reducing the level of RNA polymerase on chromatin to facilitate replication fork progression. We identify a hydroxyurea-induced phosphorylation site at Mec1-S1991 that contributes to the eviction of RNAPII and RNAPIII during replication stress. The non-phosphorylatable mec1-S1991A mutant reduces replication fork progression genome-wide and compromises survival on hydroxyurea. This defect can be suppressed by destabilizing chromatin-bound RNAPII with a Rpb3-TAP fusion, suggesting that lethality arises from replication-transcription conflicts. Coincident with a failure to repress gene expression, highly transcribed genes like GAL1 persist at nuclear pores in mec1-S1991A cells. Consistently, we find pore proteins and several components controlling RNAPII and RNAPIII transcription are phosphorylated in a Mec1-dependent manner, suggesting that Mec1-S1991 phosphorylation limits conflicts between replication and either RNA polymerase complex. We further show that Mec1 contributes to reduced RNAPII occupancy on chromatin during an unperturbed S phase.
2021-09-08 | GSE180165 | GEO
Project description:In response to genotoxic stress the TP53 tumour suppressor activates target gene expression to induce cell cycle arrest or apoptosis depending on the extent of DNA damage. These canonical activities can be repressed by TP63 in normal stratifying epithelia to maintain proliferative capacity or drive proliferation of squamous cell carcinomas, where TP63 is frequently overexpressed/amplified. Here we use ChIP-sequencing, integrated with microarray analysis, to define the genome wide interplay between TP53 and TP63 in response to genotoxic stress in normal cells. We reveal that TP53 and TP63 bind to overlapping, but distinct cistromes of sites through utilization of distinctive consensus motifs and that TP53 is constitutively bound to a number of sites. We demonstrate that cisplatin and adriamycin elicit distinct effects on TP53 and TP63 binding events, through which TP53 can induce or repress transcription of an extensive network of genes by direct binding and/or modulation of TP63 activity. Collectively, this results in a global TP53 dependent repression of cell cycle progression, mitosis and DNA damage repair concomitant with activation of anti-proliferative and pro-apoptotic canonical target genes. Further analyses reveals that in the absence of genotoxic stress TP63 plays an important role in maintaining expression of DNA repair genes, loss of which results in defective repair Examination of p63 and p53 binding sites in neonatal foreskin keratinocytes in response to adriamycin or cisplatin treatment
2014-04-11 | E-GEOD-56674 | biostudies-arrayexpress
Project description:In a recent study we identified the transcription factor KLF4 as deregulated by DNA methylation in chronic lymphocytic leukemia (CLL) cells in comparison to healthy B-cells. To analyze the function of KLF4 in leukemia cells and to identify downstream targets of the transcription factor we overexpressed KLF4 in 3 different cell lines: the CLL cell lines MEC1 and MEC2 and in the mantel cell lymphoma cell line JeKo-1.
2017-01-23 | GSE66514 | GEO
Project description:This transcriptome study is intended to discover the effects of MYC and TP63 on human keratinocytes differentiation at the genome level. Human keratinocyte cell line, HaCaT cells were transfected by siRNAs with the help of transfection reagent, INTERFERin. 48 hours post-transfection, total RNA was extracted from cells. We used a non-targeting siRNA as a negative control. siRNA targeting MYC or TP63 was obtained from QIAGEN, and RNAs from wild type HaCaT cells were used as reference samples. We did 3 biological replicates and 2 'dye swap' for each sample. Totally we got 12 samples, with 2 dye-swap for each sample, and 48 arrays used for all hybridization.
2010-05-15 | E-GEOD-17394 | biostudies-arrayexpress
Project description:To study the impact of SF3B1 mutations on alternative splicing and the effect of H3B-8800 splicing modulator in wild type and SF3B1-mutant chronic lymphocytic leukemia cells, we established SF3B1 K700E MEC1 CLL isogenic cell line and carried out RNA deep sequencing in SF3B1 wild type and K700E MEC1 cell lines upon H3B-8800 treatment.
2023-08-08 | GSE190087 | GEO
Project description:The aberrant expression of squamous lineage markers in pancreatic ductal adenocarcinoma (PDA) has been correlated with poor clinical outcomes. However, the functional role of this putative trans-differentiation event in PDA pathogenesis remains unclear. Here, we show that expression of the transcription factor TP63 (ΔN isoform) is sufficient to install and sustain the enhancer landscape and transcriptional signature of the squamous lineage in human PDA cells. In addition, we demonstrate that TP63-driven enhancer reprogramming promotes aggressive tumor phenotypes, including enhanced cell motility and invasion and an accelerated growth of primary PDA tumors and metastases in vivo. Conversely, we provide evidence that squamous PDA remains addicted to TP63 to sustain the growth of primary tumors and metastases. Taken together, our study validates the functional significance of squamous trans-differentiation in PDA, and reveals TP63-based reprogramming of PDA cells as an experimental tool for investigating vulnerabilities linked to this cell fate transition.
2018-11-13 | GSE115461 | GEO