Mus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA390577 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5684980.fastq.gz | Fastqsanger.gz | |||
| SRR5684981.fastq.gz | Fastqsanger.gz | |||
| SRR5684982.fastq.gz | Fastqsanger.gz | |||
| SRR5684983.fastq.gz | Fastqsanger.gz | |||
| SRR5684984.fastq.gz | Fastqsanger.gz |
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Project description:Prep1 prevents premature adipogenesis of mesenchymal progenitors [ChIP-seq]
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Project description:Prep1 prevents premature adipogenesis of mesenchymal progenitors
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Project description:Prep1 is a tumor-suppressor, whereas Meis1 is an oncogene. We show that to perform these activities in MEFs both proteins competitively hetero-dimerize with Pbx1. Meis1 alone transforms Prep1-deficient fibroblasts while Prep1 overexpression inhibits Meis1 tumorigenicity. Pbx1 can therefore alternatively act as oncogene or tumor-suppressor. Prep1 post-translationally controls the level of Meis1 decreasing its stability by sequestering Pbx1. The different levels of Meis1 and the presence of Prep1 are followed at the transcriptional level by the induction of specific transcriptional signatures. The decrease of Meis1 prevents Meis1 interaction with Ddx3x and Ddx5, which are essential for Meis1 tumorigenesis, and modifies the growth promoting DNA binding landscape of Meis1 to the growth controlling landscape of Prep1. Hence the key feature of Prep1 tumor inhibiting activity is the control of Meis1 stability. Examination of Prep1 and Meis1 in three cell type
2014-03-05 | E-GEOD-54221 | biostudies-arrayexpress
Project description:Prep1 is a tumor-suppressor, whereas Meis1 is an oncogene. We show that to perform these activities in MEFs both proteins competitively hetero-dimerize with Pbx1. Meis1 alone transforms Prep1-deficient fibroblasts while Prep1 overexpression inhibits Meis1 tumorigenicity. Pbx1 can therefore alternatively act as oncogene or tumor-suppressor. Prep1 post-translationally controls the level of Meis1 decreasing its stability by sequestering Pbx1. The different levels of Meis1 and the presence of Prep1 are followed at the transcriptional level by the induction of specific transcriptional signatures. The decrease of Meis1 prevents Meis1 interaction with Ddx3x and Ddx5, which are essential for Meis1 tumorigenesis, and modifies the growth promoting DNA binding landscape of Meis1 to the growth controlling landscape of Prep1. Hence the key feature of Prep1 tumor inhibiting activity is the control of Meis1 stability. Examination of Prep1 and Meis1 in two cell types
2016-06-01 | E-GEOD-58802 | biostudies-arrayexpress
Project description:Prep1 is a tumor-suppressor, whereas Meis1 is an oncogene. We show that to perform these activities in MEFs both proteins competitively hetero-dimerize with Pbx1. Meis1 alone transforms Prep1-deficient fibroblasts while Prep1 overexpression inhibits Meis1 tumorigenicity. Pbx1 can therefore alternatively act as oncogene or tumor-suppressor. Prep1 post-translationally controls the level of Meis1 decreasing its stability by sequestering Pbx1. The different levels of Meis1 and the presence of Prep1 are followed at the transcriptional level by the induction of specific transcriptional signatures. The decrease of Meis1 prevents Meis1 interaction with Ddx3x and Ddx5, which are essential for Meis1 tumorigenesis, and modifies the growth promoting DNA binding landscape of Meis1 to the growth controlling landscape of Prep1. Hence the key feature of Prep1 tumor inhibiting activity is the control of Meis1 stability.
2016-06-01 | GSE58802 | GEO
Project description:Prep1 is a tumor-suppressor, whereas Meis1 is an oncogene. We show that to perform these activities in MEFs both proteins competitively hetero-dimerize with Pbx1. Meis1 alone transforms Prep1-deficient fibroblasts while Prep1 overexpression inhibits Meis1 tumorigenicity. Pbx1 can therefore alternatively act as oncogene or tumor-suppressor. Prep1 post-translationally controls the level of Meis1 decreasing its stability by sequestering Pbx1. The different levels of Meis1 and the presence of Prep1 are followed at the transcriptional level by the induction of specific transcriptional signatures. The decrease of Meis1 prevents Meis1 interaction with Ddx3x and Ddx5, which are essential for Meis1 tumorigenesis, and modifies the growth promoting DNA binding landscape of Meis1 to the growth controlling landscape of Prep1. Hence the key feature of Prep1 tumor inhibiting activity is the control of Meis1 stability.
2014-03-05 | GSE54221 | GEO
Project description:We have defined the tumor and tumor suppressor signature for Meis1 and Prep1 (pKnox1), respectively, using ChIP-seq and RNA-seq in a cell system in which tumor suppressor Prep1 and oncogene Meis1 compete for tumorigenesis [GSE54221; GSE58802]. In this paper we report that the number of Meis1 or Prep1 DNA binding sites increases linearly with the level of expression of the two transcription factors. Overexpression of Meis1 induces tumors. At the molecular level it modifies the DNA target specificity by increasing the number of low-affinity binding sites, which results in a different choice of consensus sequences with predominance of sites normally bound by the AP1 transcription factor family. Upon concomitant overexpression of Prep1 and Meis1 tumorigenesis is inhibited. Prep1 dominates over Meis1 not only because it partially decreases Meis1 protein level but also because it prevents the binding to a substantial fraction of the low affinity binding sites. Overall, overexpression of Prep1 reverses the nature of the bound and regulated genes from stimulatory to inhibitory of signal transduction and transcription, which suppresses tumorigenesis. By identifying the Meis1 tumor signature, specific relevant signaling pathways are identified. In line with these results, tumorigenic Meis1-overexpressing cells are uniquely hypersensitive to inhibitors of the MAPK/Akt pathways. Examination of Prep1 and Meis1 in five cell type
2016-06-25 | E-GEOD-58818 | biostudies-arrayexpress
Project description:The Prep1 (Pknox1) homeodomain transcription factor is essential at multiple stages of embryo development. In the E11.5 embryo trunk, we previously estimated that Prep1 binds about 3,300 genomic sites at a highly specific decameric consensus sequence, mainly governing basal cellular functions. We now show that in embryonic stem (ES) cells Prep1 binding pattern only partly overlaps that of the embryo trunk, with about 2,000 novel sites, highlighting a change of targets between embryonic differentiated v. embryonic stem cells. RNA-seq identifies about 1800 genes down-regulated in Prep1- /- ES cells which belong to gene ontology categories not enriched in the E11.5 Prep1i/i differentiated embryo, including in particular the Wnt and Fgf pathways. Indeed, we find aberrant Wnt and Fgf expression levels in the Prep1-/- ES cells which agrees with a deficient embryoid bodies (EBs) differentiation. Re-establishment of the Prep1 level rescues the phenotype. [ChIP-Seq] Examination of genome-wide Prep1 binding in mouse ES cells using ChIP-seq and Illumina GAII sequencing. [RNA-Seq] Examination of gene expression in wild type and Prep1-/- mouse ES cells using RNA-seq and Illumina GAII sequencing.
2015-04-01 | E-GEOD-63282 | biostudies-arrayexpress
Project description:Singular olfactory receptor (OR) expression is critical for vertebrate olfaction because the sequence of the chosen OR protein determines both the receptive field and axon guidance properties of each olfactory sensory neuron (OSN). However, numerous single cell RNA-seq studies reveal that OSN progenitors co-transcribe seemingly random combinations of OR genes before a gradual transition to transcriptional singularity. Here, we show that MEX3A, a RING and KH domain protein expressed during polygenic OR transcription, prevents efficient OR protein expression before the emergence of a prevalent, transcriptionally dominant OR allele. Consequently, MEX3A deletion enhances OR mRNA and OR protein abundance in OSN progenitors, resulting in premature induction of Perk signaling, biased OR gene choice, and OSN axon mistargeting. Our experiments uncover a novel, post-transcriptional mechanism of OR gene regulation that assures that the identity of the expressed OR can influence the identity of the OSN only at the onset of singular OR choice.
2024-06-12 | MSV000095005 | MassIVE
Project description:An equivalent dosage of human umbilical cord-derived mesenchymal stem cell (HucMSC), adipose tissue-derived mesenchymal stem cell (ADSC), and SVF was orthotopically administered into a cyclophosphamide (CTX)-induced premature ovarian insufficiency (POI) mouse model. The therapeutic impacts were meticulously evaluated employing a suite of assays. The underlying mechanisms were investigated through RNA sequencing (RNA-seq) and mass spectrometry, offering insights into the cellular and molecular responses.
2025-05-31 | PXD064540 |