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Trip12 deficiency effect on embryonic stem cell line

ABSTRACT: Analysis of E14 embryonic stem cells lacking Trip12 ubiquitin ligase activity. We used microarrays to detail the global gene expression profiles affected by Trip12 ubiquitin ligase activity in mouse embryonic stem cell.

ORGANISM(S): Mus musculus

PROVIDER: GSE27527 | GEO | 2014/01/01

SECONDARY ACCESSION(S): PRJNA138535

REPOSITORIES: GEO

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Trip12 deficiency effect on embryonic stem cell line

Project description:Analysis of E14 embryonic stem cells lacking Trip12 ubiquitin ligase activity. We used microarrays to detail the global gene expression profiles affected by Trip12 ubiquitin ligase activity in mouse embryonic stem cell. Total RNA was extracted from wild-type and Trip12 mutant mouse embryonic stem cells and hybridized on Affymetrix microarrays.

2014-01-01 | E-GEOD-27527 | biostudies-arrayexpress

The intrinsically disordered region of the E3 ubiquitin ligaseTRIP12 induces the formation of chromatin condensates and interferes withDNA damage response.

Project description:Chromatin compaction is crucial for the expression and the integrity of the genome. We previously showed that the nuclear HECT-type E3 ubiquitin ligase TRIP12 (Thyroid hormone Receptor Interacting Protein 12) is tightly associated to chromatin. Overexpressed in several types of cancers, we explored herein the consequences of TRIP12 overexpression on chromatin homeostasis. First, we established the proxisome of TRIP12 by BioID and unveiled its pleiotropic role in chromatin regulation. Second, we demonstrated that an overexpression of TRIP12, via its intrinsically disordered region, leads to the formation of chromatin condensates enriched in heterochromatin epigenetic marks. We further discovered that the formation of TRIP12 mediated-chromatin condensates is highly dynamic and driven by a mechanism of polymer-polymer phase separation (PPPS). Chromatin condensates formation is dependent not only on the concentration, the length of TRIP12-IDR but also electrostatic interactions. Chromatin compaction is a determinant parameter in several biological processes. Indeed, we measured that the formation of TRIP12 mediated-chromatin condensates alters cell cycle progression, genome accessibility, transcription as well as DNA damage response (DDR) by inhibiting the accumulation of Mediator DNA Damage Checkpoint (MDC1). Altogether, this study reveals a novel dynamic role for TRIP12 in chromatin compaction independently of its ubiquitin ligase activity with important consequences on cellular processes.

2023-11-11 | GSE247490 | GEO

Transcriptomic profiling of human pancreatic cancer-derived cell lines PANC-1 depleted of TRIP12 mRNA compared to control cells

Project description:TRIP12 (Thyroid hormone Receptor Interacting Protein) is an E3 ubiquitin ligase involved in numerous cellular processes. TRIP12 controls the stability of the PTF1A transcription factor that is implicated in pancreatic cancer initiation. To elucidate the role of TRIP12 on the expression of pancreatic cancer-derived cell lines, Trip12 mRNA expression was inhibited using a shRNA strategy. Transcriptomic profiling of shTrip12-PANC-1 cell s was perfomed and compared to ShScramble control cells.

2024-04-19 | GSE147717 | GEO

Transcriptomic profiling of human pancreatic cancer-derived cell lines MiaPACA-2 depleted of TRIP12 mRNA compared to control cells

Project description:TRIP12 (Thyroid hormone Receptor Interacting Protein) is an E3 ubiquitin ligase involved in numerous cellular processes. TRIP12 controls the stability of the PTF1A transcription factor that is implicated in pancreatic cancer initiation. To elucidate the role of TRIP12 on the expression of pancreatic cancer-derived cell lines, Trip12 mRNA expression was inhibited using a shRNA strategy. Transcriptomic profiling of shTrip12-MiaPACA-2 cell s was perfomed and compared to ShScramble control cells.

2024-04-19 | GSE147549 | GEO

Effect of depletion of TRIP12 on gene expression in adult murine pancreatic acinar cells and murine pancreatic cancer cell lines

Project description:To investigate the role of the E3 ubiquitin ligase Thyroid Receptor Interacting Protein 12 (TRIP12) in pancreatic acinar cell identity and pancreatic carcinogenesis, we used genetically engineered mouse models of pancreas-selective Trip12 deletion, mutant Kras (G12D) and mutant P53 (R172H). We performed gene expression analysis using RNA-seq data from adult acinar cells. We established cell lines from murine pancreatic tumors.

2024-04-19 | GSE221587 | GEO

Mus musculus

Project description:Trip12 deficiency effect on embryonic stem cell line

| PRJNA138535 | ENA

The ubiquitin ligase HUWE1 regulates hematopoietic stem cell maintenance and lymphoid commitment [microarray]

Project description:We identified the ubiquitin ligase Huwe1 as a crucial regulator of hematopoietic stem cell (HSC) functions. We generated Huwe1 conditional knock-out mice and discovered that the loss of this ligase causes an increased proliferation and stem cell exhaustion, together with a decreased lymphoid specification in vivo. We observed that the ubiquitin ligase Huwe1 is controlling the expression of N-myc at the level of the most immature stem and progenitor hematopoietic populations, mediating the described effects. Hematopoietic stem cells (HSC) from the bone marrow of transgenic animals carrying a N-myc/mCherry fusion gene were sorted according to N-myc expression (defined by mCherry) into N-myc high and low subpopulations. Each of these 2 populations was subjected to microarray gene expression profiling.

2016-08-20 | E-GEOD-85832 | biostudies-arrayexpress

The ubiquitin ligase HUWE1 regulates hematopoietic stem cell maintenance and lymphoid commitment [microarray]

2016-08-20 | GSE85832 | GEO

The ubiquitin ligase HUWE1 regulates hematopoietic stem cell maintenance and lymphoid commitment [high-throughput sequencing]

2016-08-17 | GSE85723 | GEO

Hematopoietic Stem Cell Differentiation Regulated by a Single Ubiquitin Ligase: Substrate Complex

Project description:Hematopoietic stem cell (HSC) differentiation is regulated by cell-intrinsic and extrinsic cues. In addition to transcriptional regulation, post-translational regulation may also control HSC differentiation. To test this hypothesis, we visualized ubiquitin-regulated protein stability of a single transcription factor, c-Myc. The stability of c-Myc protein was instructive of HSC quiescence and c-Myc protein abundance was controlled by the ubiquitin ligase Fbw7. Fine changes in stability of c-Myc protein regulated the HSC “gene expression signature”. Using whole genome genomic approaches, we identified specific regulators of HSC function that are directly controlled by c-Myc binding, however adult HSCs and embryonic stem cells sense and interpret distinctly c-Myc regulated gene expression. These studies show a ubiquitin ligase–substrate pair can orchestrate the molecular program of HSC differentiation.

2010-03-01 | GSE19502 | GEO

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