Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Coordinated control of senescence by lncRNA UCA1 and a novel CAPERα/TBX3 co-repressor

ABSTRACT: Coordination of a complex series of transcriptional, structural and signaling events culminates in cellular senescence, a crucial tumor suppressor mechanism. We have discovered a repressor complex composed of TBX3 and CAPERa which functions upstream of the RB and p53 effector pathways and is required to prevent senescence of primary cells and in mouse embryos. TBX3/ CAPERa directly binds and represses transcription and chromatin structure of genes in multiple senescence pathways and the LncRNA UCA1, which we have identified as a novel tumor suppressor. The TBX3/ CAPERa complex is physically disrupted in oncogene induced senescence, providing a new molecular mechanism for derepression of prosenescence pathways in this system. Our results provide new insight into the oncogenic properties of TBX3, and are the first demonstration of CAPERa and UCA1 function in vivo.

ORGANISM(S): Homo sapiens

PROVIDER: GSE76572 | GEO | 2016/01/07

SECONDARY ACCESSION(S): PRJNA308072

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Coordinated control of senescence by lncRNA UCA1 and a novel CAPERÎ±/TBX3 co-repressor

Project description:Coordination of a complex series of transcriptional, structural and signaling events culminates in cellular senescence, a crucial tumor suppressor mechanism. We have discovered a repressor complex composed of TBX3 and CAPERa which functions upstream of the RB and p53 effector pathways and is required to prevent senescence of primary cells and in mouse embryos. TBX3/ CAPERa directly binds and represses transcription and chromatin structure of genes in multiple senescence pathways and the LncRNA UCA1, which we have identified as a novel tumor suppressor. The TBX3/ CAPERa complex is physically disrupted in oncogene induced senescence, providing a new molecular mechanism for derepression of prosenescence pathways in this system. Our results provide new insight into the oncogenic properties of TBX3, and are the first demonstration of CAPERa and UCA1 function in vivo. mRNA Seq based gene differential expression analysis of two sample types (TBX3, Caper) relative to control and two sample types (pCDNA3.1, UCA1) relative to each other.

2016-01-07 | E-GEOD-76572 | biostudies-arrayexpress

TBX3 defines the functional identity of hypothalamic melanocortin neurons

Project description:Purpose: Identify cellular pathways controlled by Tbx3 Methods: RNA sequencing of hypothalamic primary neurons from Tbx3 loxP/loxP mice infected with Ad-Cre or Ad-GFP viruses. Results: Unbiased pathway analysis revealed that Tbx3 deletion in primary neurons significantly affected the expression of genes involved in several pathways responsible for controlling cellular proliferation, differentiation and determination of cellular fate. Conclusions: Tbx3 in primary neurons might be implicated in the development and maintenance of neuronal identity.

2019-01-22 | GSE119883 | GEO

A dynamic role of Tbx3 in the pluripotency circuitry

Project description:Pluripotency represents a cell state comprising a fine-tuned pattern of transcription factor activity required for embryonic stem cell (ESC) self-renewal. TBX3 is the earliest expressed member of the T-box transcription factor family and is involved in maintenance and induction of pluripotency. Hence, TBX3 is believed to be a key member of the pluripotency circuitry, with loss of TBX3 coinciding with loss of pluripotency. We report a dynamic expression of TBX3 in vitro and in vivo using genetic reporter tools tracking TBX3 expression in mouse ESCs (mESCs). Low TBX3 levels are associated with reduced pluripotency, resembling the more mature epiblast. Notably, TBX3-low cells maintain the intrinsic capability to switch to a TBX3-high state and vice versa. Additionally, we show TBX3 to be dispensable for induction and maintenance of naive pluripotency as well as for germ cell development. These data highlight novel facets of TBX3 action in mESCs. 12 samples in total

2015-12-09 | E-GEOD-73862 | biostudies-arrayexpress

A dynamic role of Tbx3 in the pluripotency circuitry

2015-12-09 | GSE73862 | GEO

Homo sapiens

Project description:Coordinated control of senescence by lncRNA UCA1 and a novel CAPERα/TBX3 co-repressor

| PRJNA308072 | ENA

Mouse embryo heart, e10.5 AVC: Control vs. Tbx3 hypomorphic mutant

Project description:Transcriptional profiling of the atrioventricular canal from e10.5 mouse hearts comparing wild-type control with Tbx3 GH/N hypomorphic mutant microdissected tissue. The goal was to identify direct and indirect targets of the transcription factor Tbx3, because Tbx3 is expressed in the AVC and hypomorphs develop embryonic AV conduction block at e12.5. Two-condition experiment, wild-type control and Tbx3 mutant AVC tissue. Tissue from 5 hearts was pooled to make each sample. Biological replicates: 4.

2011-04-01 | E-GEOD-24122 | biostudies-arrayexpress

Mouse embryo heart, e10.5 AVC: Control vs. Tbx3 hypomorphic mutant

2011-04-01 | GSE24122 | GEO

Genome-wide maps of Tbx3 binding sites in mouse ESCs

Project description:Induced pluripotent stem (iPS) cells can be obtained through the introduction of defined factors into somatic cells. The combination of Oct4, Sox2 and Klf4 (OSK) constitutes the minimal requirement for generating iPS cells from mouse embryonic fibroblasts (MEFs). Through the genomic analyses of ESC genes that have roles in pluripotency and fusion-mediated somatic cell reprogramming, we identified Tbx3 as a transcription factor that significantly improves the quality of iPS cells. Induced-PS cells generated with OSK + Tbx3 (OSKT) are superior in both germ cell contribution to the gonads and germ-line transmission frequency. However, global gene expression profiling could not distinguish between OSK and OSKT iPS cells. Genome-wide ChIP-sequencing analysis of Tbx3 binding sites in ESCs suggests that Tbx3 regulates pluripotency-associated and reprogramming factors, in addition to sharing many common downstream regulatory targets with Oct4, Sox2, Nanog and Smad1. ChIP-seq of Tbx3 binding in mouse ESCs

2009-12-04 | E-GEOD-19219 | biostudies-arrayexpress

Identification of TBX3 and shared HAND2-TBX3 target gene in early mouse limb buds [RNA-seq]

Project description:ChIP-seq is combined with RNA-seq analysis to identify the TBX3 and HAND2 target genes during mouse limb bud development. This analysis identifies the DEGs and direct transcriptional targets of HAND2 and TBX3 during the early determinative period critical to establishment of limb axis polarity and the SHH signaling center in the posterior limb bud mesenchyme. In particular, bioinformatics analysis identifies the target gene networks that are co-regulated by both TBX3 and HAND2 transcription factors in the limb bud mesenchyme. A significant fraction of the target genes identified are required for normal limb bud development and their spatio-temporal expression patterns are changed in mutant limb buds at early stages. This project was supported by SNSF Grant 310030_184734 to Rolf Zeller (project partner: Aimée Zuniga).

2023-12-31 | GSE192485 | GEO

Identification of TBX3 and shared HAND2-TBX3 target genes in early mouse limb buds [ChIP-seq]

2023-12-31 | GSE192484 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data