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P53 independent TAF6delta target genes.

ABSTRACT: To elucidate the impact of TAF6d on cell death and gene expression, here we have employed modified antisense oligonucleotides to enforce expression of endogenous TAF6d. The induction of endogenous TAF6d triggered apoptosis in tumor cell lines, including cells devoid of p53. Microarray experiments revealed that TAF6d activates gene expression independently of cellular p53 status. Our data define TAF6d as a pivotal node in a signaling pathway that acts immediately downstream of p53 to control gene expression programmes and apoptosis. Keywords: Treatment with splice site switching antisense oligonucleotides, induction of apoptosis

ORGANISM(S): Homo sapiens

PROVIDER: GSE10795 | GEO | 2008/06/26

SECONDARY ACCESSION(S): PRJNA107493

REPOSITORIES: GEO

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p53 independent TAF6delta target genes.

Project description:To elucidate the impact of TAF6d on cell death and gene expression, here we have employed modified antisense oligonucleotides to enforce expression of endogenous TAF6d. The induction of endogenous TAF6d triggered apoptosis in tumor cell lines, including cells devoid of p53. Microarray experiments revealed that TAF6d activates gene expression independently of cellular p53 status. Our data define TAF6d as a pivotal node in a signaling pathway that acts immediately downstream of p53 to control gene expression programmes and apoptosis. Keywords: Treatment with splice site switching antisense oligonucleotides, induction of apoptosis Biological triplicates, 4 conditions: isogenic p53+/+ and -/- cells; control oligonucleotide, TAF6 AS2 oligonucleotide

2008-06-26 | E-GEOD-10795 | biostudies-arrayexpress

TAF6 orchestrates transcription programs and apoptosis in the absence of p53

Project description:The decision of metazoan cells to live or undergo programmed cell death hinges on the balance between the levels of pro- versus anti-apoptotic gene products. The general RNA polymerase II (Pol II) transcription factor, TFIID, plays a central role in the regulation of gene expression through its core promoter recognition and co-activator functions. The core TFIID subunit TAF6 is a co-activator for the pro-apoptotic p53 tumour suppressor protein. Our previous studies identified a specialized isoform of TAF6, termed TAF6 that can specifically be induced in apoptosis. To elucidate the impact of TAF6 on gene expression and cell death, we employed modified antisense oligonucleotides to enforce expression of endogenous TAF6. The induction of endogenous TAF6 triggered apoptosis in several cancer cell lines. Importantly, TAF6 also induces apoptosis in tumor cell lines devoid of p53, placing TAF6 function downstream of p53. Microarray experiments uncovered a TAF6-induced transcriptome landscape displaying enhanced expression of genes of the Notch, oxidative stress, integrin, p53 and apoptosis pathways. Our data show that the TAF6 pathway is a pivotal signalling nexus that controls pro-apoptotic gene expression programs. Keywords: Treatment with splice site switching antisense oligonucleotides, induction of apoptosis Biological triplicates, 3 conditions: control oligonucleotide, Taf6 oligonucleotide, specificity control Bcl-x oligonucleotide

2010-11-27 | E-GEOD-8752 | biostudies-arrayexpress

TAF6 orchestrates transcription programs and apoptosis in the absence of p53

2010-11-27 | GSE8752 | GEO

Cytoplasmic mRNA level upon 4.5SH KD

Project description:We demonstrate that Myodonta-clade-specific 4.5S RNAH (4.5SH), an abundant nuclear noncoding RNA that is highly homologous to the retrotransposon SINE B1, controls the expression of multiple genes containing the antisense insertion of SINE B1 The depletion of endogenous 4.5SH with antisense oligonucleotides changes the subcellular distribution of these target transcripts containing the antisense SINE B1 insertions.

2015-09-30 | GSE57264 | GEO

Recruiting Endogenous ADARs with Antisense Oligonucleotides to Reprogram the Transcriptome

Project description:Recruiting Endogenous ADARs with Antisense Oligonucleotides to Reprogram the Transcriptome

| PRJNA497809 | ENA

Gene expression profiling of human anaplastic thyroid carcinoma cells by microarray

Project description:In this study, we profiled the change of gene expression by p53 knock-down on anaplastic thyroid carcinoma (ATC) cell line, KAT-18 cells using Applied Biosystem's Microarrays. When compared with the untreated control KAT-18 cells, 2,926 genes were found to have altered expression levels of 2-fold or more in cells treated with antisense p53 oligonucleotide. Microarray analysis revealed that p53 knock-down modified the expression of numerous apoptosis-related genes. Among those genes, 33 apoptosis pathway activators and 20 apoptosis pathway repressors were identified. We analyzed human thyroid carcinoma cell (KAT18) on Applied Biosystem Human 1700 Chip Arrays. There were control and test sample, respectively, KAT18 untreated and treated antisense p53.

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Splicing Correction as a Therapeutic Approach for Acetylation-Defective p53 K120R mutation

Project description:The TP53 c.359A>G mutation severely impairs expression of the major TP53 transcript variant encoding p53 K120R by creating a new splicing donor site. Antisense morpholino oligomer (AMO) targeting the mutation site restored normal splicing and expression of the major variant. Despite the recovery of mutant TP53 mRNA levels, the functional restoration as the tumor suppressor of p53 K120R was unclear. Given that p53 exerts its tumor suppressor function through regulation of target genes that mediate growth arrest or apoptosis, the p53 K120R mutant exhibits impaired transcriptional regulation of CDKN1A, a key target gene in growth arrest, while maintaining normal induction of the pro-apoptotic BBC3 gene. Consequently, the p53 K120R mutant protein demonstrates a phenotype characterized by defective cell growth arrest but retained apoptotic induction capacity, suggesting that the p53 K120R mutant protein may retain some tumor suppressor functionality. In addition, Lysine 120 provides a critical acetylation site linked to p53 activation. Although other studies of the oncogenic effects of p53 K120R highlight the relevance of acetylation for tumor suppression, our findings indicate that targeting mutant TP53 mRNA is a prerequisite for restoration of p53 function. In particular, despite the presence of mutations, it showed sufficient corrective effect to restore p53 functions, including apoptosis induction. In conclusion, this study highlights the potential of AMO-mediated splice correction as a therapeutic approach for TP53 mutations.

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Proteomic analysis of Psmd9 knockdown in the liver

Project description:We have shown that decreasing psmd9 expression effects lipid metabolism in vivo and were interested in investigating the pathways by which psmd9 elicited these changes. To investigate these mechanisms, we performed proteomic analyses on the livers from C57 and DBA mice that had been treated with antisense oligonucleotides targeted to psmd9.

2019-03-14 | PXD010759 | Pride

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