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Mucociliary epidermis RNA-seq data from comparison of controls and DN-tp63 morpholino knockdown in Xenopus animal cap explants.

ABSTRACT: Mucociliary epidermis RNA-seq data from comparison of controls and DN-tp63 morpholino knockdown in Xenopus animal cap explants.

PROVIDER: PRJNA540273 | ENA |

REPOSITORIES: ENA

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Mucociliary epidermis RNA-seq data from comparison of controls and DN-tp63 morpholino knockdown in Xenopus animal cap explants.

Project description:This study was conducted to investigate the effects of DN-tp63 loss-of-function on mucociliary basal stem cells in Xenopus laevis. Uninjected control embryos and DN-tp63 morpholino oligonucleotide injected embryos were used to generate animal cap explants at embryonic stage 8. Explants were grown into mucociliary organoids and collected at embryonic stages 10.5, 16-19, and 24-25 for total RNA extraction.

2019-04-30 | GSE130448 | GEO

The Xenopus animal cap transcriptome: building a mucociliary epithelium.

Project description:Here we investigate dynamics of the RNA landscape during formation of the Xenopus tropicalis larval epidermis. To obtain RNA expression data, we used ectodermal explants (Animal Caps), which differentiate autonomously into a ciliated epidermis, highly related to the one in human airways. Animal caps were harvested at the gastrula neurula and tailbud stage.

2018-09-25 | GSE111171 | GEO

Mucociliary epidermis RNA-seq data from controls and after manipulation of cell fates by Notch (suh-dbm, nicd) and cell type controlers (Foxa1MO, dnMCIDAS)

Project description:This study was conducted to investigate the effects of enriching or depleting cell types in mucociliary organoids in Xenopus laevis. (1) Uninjected control embryos were compared to (2) inhibition of Notch signaling (suh-dbm) which enriches ionocytes and multiciliated cells, (3) inhibition of Notch and suppression of MCIDAS (suh-dbm + dnMCIDAS) which enriches ionocytes and depletes multiciliated cells, (4) overactivation of Notch (nicd) which suppresses ionocytes and multiciliated cells and promotes small secretory cells and basal cells, (5) knockdown of foxa1 (foxa1MO) which depletes small secretory cells. Embryos were injected at 2-4 cell stage and were used to generate animal cap explants at embryonic stage 8. Explants were grown into mucociliary organoids and collected at embryonic stages 10.5, 16, 25, and 32 for total RNA extraction.

2022-10-18 | GSE215373 | GEO

The Xenopus animal cap transcriptome: building a mucociliary epithelium.

Project description:The Xenopus animal cap transcriptome: building a mucociliary epithelium.

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Development of Xenopus Mucociliary Epithelium

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Transciptome analysis of TP63 regulated pathways in HNSCC

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

The role of TP63 fusion in mouse lymphomagenesis

Project description:Patients with lymphoma harboring TP63 rearrangements have aggressive clinical course and dismal prognosis with no target therapy available. Thus, there is an urgent need to elucidate the molecular mechanisms and to develop novel therapeutic options for these patients. We then generated a TBL1XR1::TP63 fusion knockin trangenic mouse model and crossed with CD2/iCre mouse. This project is to study the role and function of TP63 fusion in mouse lymphomagenesis.

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Genome wide characterization reveals complex interplay between TP53 and TP63 in response to genotoxic stress [ChIP-Seq]

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

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Genome wide characterization reveals complex interplay between TP53 and TP63 in response to genotoxic stress [Affymetrix]

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 gene expression levels of HFKS siRNA depleted for p53 or p63 in response to adriamycin or cisplatin treatment We analyzed RNA using the Affymetrix Human Exon 1.0 ST platform. Array data was processed using the AltAnalyze.

2014-04-30 | E-GEOD-57187 | biostudies-arrayexpress

Functional studies of TP63-affected ESCC tumor immune microenvironment

Project description:Our preliminary data from unbiased analyses of both ESCC patient samples and cell lines identified interferon-γ (IFN-γ) signaling pathway as the most significantly enriched pathways suppressed by TP63. To validate the activation of IFN pathways and the immune responses upon silencing of TP63, we utilized immune-competent mice to conduct allograft experiments. To analyze the effect of TP63 on ESCC tumor microenvironment, resected tumors were then collected to perform scRNA-seq.

2024-02-29 | GSE221938 | GEO

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