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The effect on lincRNA expression by p53 family members.

ABSTRACT: To evaluate the effect on lincRNA expression by p53 family members, we overexpressed p53 family members in H1299 cells and evaluated the lincRNA expression by microarray analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE52739 | GEO | 2014/02/05

SECONDARY ACCESSION(S): PRJNA229955

REPOSITORIES: GEO

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The effect on lincRNA expression by p53 family members.

Project description:To evaluate the effect on lincRNA expression by p53 family members, we overexpressed p53 family members in H1299 cells and evaluated the lincRNA expression by microarray analysis. lincRNA expression was measured in H1299 cells infected with adenovirus expressing LacZ, p53, p63a, p63g, p73a and p73b.

2014-02-05 | E-GEOD-52739 | biostudies-arrayexpress

The effect on gene expression by p53 family members and the knockdown of AKR1B10

2013-10-31 | GSE47096 | GEO

The effect on gene expression by p53 family members and the knockdown of AKR1B10

Project description:To evaluate the effect on gene expression by p53 family members and AKR1B10, we overexpressed p53 family members in H1299 cells or knocked down AKR1B10 in HCT116 cells and evaluated the gene expression by microarray analysis. Gene expression was measured in H1299 cells infected with adenovirus expressing p53, p63g and p73b, and in HCT116 cells transfected with siRNAs targeting AKR1B10 and then treated with adriamycin.

2013-10-31 | E-GEOD-47096 | biostudies-arrayexpress

p53 family members in myogenic differentiation and rhabdomyosarcoma development

Project description:The p53 family comprises the tumor suppressor p53 and the structural homologs p63 and p73. How the three family members cooperate in tumor suppression remains unclear. Here, we report different but complementary functions of the individual members for regulating retinoblastoma protein (RB) function during myogenic differentiation. Whereas p53 transactivates the retinoblastoma gene, p63 and p73 induce the cyclin-dependent kinase inhibitor p57 to maintain RB in an active, hypophosphorylated state. DeltaNp73 inhibits these functions of the p53 family in differentiation control, prevents myogenic differentiation, and enables cooperating oncogenes to transform myoblasts to tumorigenicity. DeltaNp73 is frequently overexpressed in rhabdomyosarcoma and essential for tumor progression in vivo. These findings establish differentiation control as a key tumor suppressor activity of the p53 family. Keywords: oligonucleotide

2006-10-16 | GSE5447 | GEO

Transcription profiling of DeltaNp73 alpha expressing C2C12 myoblasts examined 6 and 24 hours after shifting the cells to a differentiation medium to study the functions of the individual members of P53 family.

2007-11-22 | E-GEOD-5447 | biostudies-arrayexpress

Human p53 signaling qPCR primer Array

Project description:H1299 cells were overexpressed miR-138 or silenced AGO2. The expression of 92 genes associated with p53 using the “Human p53 Signaling Pathway PCR Array”

2015-06-05 | GSE69562 | GEO

Human p53 signaling qPCR primer Array

Project description:H1299 cells were overexpressed miR-138 or silenced AGO2. The expression of 92 genes associated with p53 using the “Human p53 Signaling Pathway PCR Array” qPCR gene expression profiling. H1299 cells were transfected with NC mimics, AGO2 siRNA or miR-138 for 48h. Equal amount total RNA from each group was pooled prior to gene expression analysis.

2015-06-05 | E-GEOD-69562 | biostudies-arrayexpress

Transcription profiling of human H1299 cellls transformed with different p73/p53 constructs shows C-terminal diversity within the p53 family accounts for differences in DNA binding and transcriptional activity

Project description:The p53 family is known as a family of transcription factors with functions in tumor suppression and development. Whereas the central DNA binding domain is highly conserved among the three family members p53, p63 and p73, the C-terminal domains (CTDs) are diverse and subject to alternative splicing and post-translational modification. Here we demonstrate that the CTDs strongly influence DNA binding and transcriptional activity. While p53 and the p73 isoform p73ï§ have basic CTDs and form weak sequence-specific protein-DNA complexes, the major p73 isoforms ï¡, ï¢ and ï¤ have neutral CTDs and bind DNA strongly. A basic CTD has been previously shown to enable sliding along the DNA backbone and to facilitate the search for binding sites in the complex genome. Our experiments, however, reveal that a basic CTD also reduces protein-DNA complex stability, intranuclear mobility, promoter occupancy in vivo, transgene activation and induction of cell cycle arrest or apoptosis. A basic CTD in p53 and p73ï§ therefore provides both positive and negative regulatory functions presumably to enable rapid switching of protein activity in response to stress. In contrast, most p73 isoforms exhibit constitutive DNA binding activity consistent with a predominant role in developmental control. Experiment Overall Design: Infection of H1299 cell with different p73/p53 constructs by adenoviral system

2008-10-18 | E-GEOD-8660 | biostudies-arrayexpress

The effect on lincRNA expression by p53 family members

| S-ECPF-GEOD-52739 | biostudies-other

PINT lincRNA connects the p53 pathway with epigenetic silencing by the Polycomb Repressive Complex 2 (tissue)

Project description:It has been recently shown that the transcription factor p53 induces the expression of multiple lincRNAs. However, relatively little is known about the role that lincRNAs play in this pathway. Here we characterize a lincRNA named PINT (p53 Induced Noncoding Transcript). We show that PINT is a ubiquitously expressed lincRNA that is finely regulated by p53. In mouse cells, PINT promotes cell proliferation and survival by regulating the expression of genes of TGF-beta, MAPK and p53 pathways. PINT is a nuclear lincRNA that directly interacts with Polycomb Repressive Complex 2 (PRC2), being required for PRC2 targeting of specific genes for repression. Furthermore, PINT functional activity is dependent on PRC2 expression, representing a connection between the p53 pathway and epigenetic regulation by PRC2. We have also identified PINT human ortholog (hPINT), which presents suggestive analogies with the mouse lincRNA. hPINT is similarly regulated by p53, and its expression correlates significantly with the same cellular pathways as the mouse ortholog, including the p53 pathway. Interestingly, hPINT is significantly downregulated in colon cancer, representing a novel tumor suppressor candidate. Our results not only help our understanding of the role of p53 and lincRNAs in cancer, but also contribute to the open debate regarding the utility of mouse models for the study of lincRNAs.

2013-08-09 | GSE46271 | GEO

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