Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ACGH analysis of liver tumors generated in C57BL/6J mice with a liver specific loss of Trp53-/-

ABSTRACT: aCGH analysis of liver tumors generated in C57BL/6J mice with a liver specific loss of Trp53-/-

PROVIDER: PRJNA657237 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

aCGH analysis of liver tumors generated in C57BL/6J mice with a liver specific loss of Trp53-/- [Agilent-024427]

Project description:aCGH analysis of liver tumors generated in C57BL/6J mice with a liver specific loss of Trp53-/- [Agilent-024427]

| PRJNA657193 | ENA

aCGH analysis of liver tumors generated in C57BL/6J mice with a liver specific loss of Trp53-/- [Agilent-027411]

Project description:aCGH analysis of liver tumors generated in C57BL/6J mice with a liver specific loss of Trp53-/- [Agilent-027411]

| PRJNA657191 | ENA

aCGH analysis of liver tumors generated in C57BL/6J mice with a liver specific loss of Trp53-/- [Agilent-024427]

Project description:Background and aims: P53 limits the self-renewal of stem cells from various tissue. A Loss of p53 in combination with other oncogenic events results in aberrant self-renewal and transformation of progenitor cells. Here, we investigated whether a loss of p53 as a single genetic lesion is sufficient to induce liver tumor formation. Methods: AlfpCre mice were crossed with Trp53 conditional knockout mice to achieve a liver-specific loss of Trp53. Results: The liver-specific loss of Trp53 results in liver tumor formation. A high percentage of the tumors showed a mixed differentiation of hepatocellular carcinoma and intrahepatic cholangiocarcinoma. Conclusion: The liver-specific deletion of Trp53 is sufficient to induce liver tumor formation.

2021-01-22 | GSE156253 | GEO

aCGH analysis of liver tumors generated in C57BL/6J mice with a liver specific loss of Trp53-/- [Agilent-027411]

2021-01-22 | GSE156252 | GEO

aCGH analysis of liver tumors generated in FAH-/- Trp53-/- mice, a mouse model of metabolic liver injury

Project description:aCGH analysis of liver tumors generated in FAH-/- Trp53-/- mice, a mouse model of metabolic liver injury

| PRJNA657190 | ENA

aCGH analysis of liver tumors generated in FAH-/- Trp53-/- and FAH-/- mice, a mouse model of metabolic liver injury

Project description:aCGH analysis of liver tumors generated in FAH-/- Trp53-/- and FAH-/- mice, a mouse model of metabolic liver injury

| PRJNA659719 | ENA

aCGH analysis of liver tumors generated in FAH-/- mice, a mouse model of metabolic liver injury

Project description:aCGH analysis of liver tumors generated in FAH-/- mice, a mouse model of metabolic liver injury

| PRJNA659723 | ENA

aCGH analysis of liver tumors generated in C57BL/6J mice with a liver specific loss of Trp53-/-

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-01-22 | GSE156263 | GEO

aCGH analysis of liver tumors generated in FAH-/- Trp53-/- mice, a mouse model of metabolic liver injury

Project description:Background and aims: A coordinated stress and regenerative response is important following hepatocyte damage. Here, we investigate the phenotypes that result from genetic abrogation of individual components of the CHK2/ p53/ p21 pathway in a murine model of metabolic liver injury. Methods: NTBC was reduced or withdrawn in Fah / mice lacking Chk2, p53 or p21, and survival, tumor development, liver injury and regeneration were analyzed. Partial hepatectomies were performed and mice were challenged with the Fas-antibody Jo2. Results: In a model of metabolic liver injury, loss of p53, but not of Chk2, impairs the oxidative stress re-sponse and aggravates liver damage, indicative of a direct p53-dependent protective effect on hepatocytes. Cell cycle control during chronic liver injury critically depends on the presence of both p53 and its downstream effector p21. In p53-deficient hepatocytes, unchecked proliferation occurs despite a strong induction of p21, revealing a complex interdependency between p21 and p53. The increased regenerative potential in the absence of p53 cannot fully compensate the surplus injury and is not sufficient to promote survival. Despite the different phenotypes as-sociated with the loss of individual components of the DNA damage response, gene expression patterns are dominated by the severity of liver injury, but reflect distinct effects of p53 on prolif-eration and the anti-oxidative stress response. Conclusion: Characteristic phenotypes result from the genetic abrogation of individual components of the DNA damage response cascade in a liver injury model. The extent to which loss of gene function can be compensated, or affects injury and proliferation, depends on the level at which the cas-cade is interrupted.

2021-04-02 | GSE156251 | GEO

RNAseq of E14.5 fetal liver isolated from wild-type control, Rps19R67∆/R67∆, Rps19R67∆/R67∆ Trp53−/− and Trp53−/− mutant embryos.

Project description:This RNA sequencing experiment is part of the study \\"Preclinical animal model of Diamond-Blackfan anemia with single amino acid mutation of ribosomal protein Rps19\\". A mouse model with conserved arginine 67 deletion of ribosomal protein Rps19 mutation develops features characteristic of human Diamond-Blackfan anemia, a rare bone marrow failure syndrome, including hematologic dysfunctions, early onset growth delay, intrinsic anemia, severe craniofacial, skeletal, urogenital, cardiovascular, and cerebral abnormalities leading to premature lethality during the adolescence of the mouse. This DBA mouse model exhibits cell intrinsic activation of the Trp53 signaling pathway in hematopoietic stem cells (HSCs) leading to reduced erythroid lineage development that may be rescued after inactivation of the tumor suppressor Trp53. The E14.5 fetal liver transcriptome analysis study confirms the involvement of non-canonical components of the p53 signaling pathway in the etiopathogenesis of DBA, manifested already during fetal development, consistent with the early onset of DBA-like phenotypes in mouse embryos as well as development of the disease in neonatal human patients. These results confirm our previous findings in adult hematopoietic progenitors as well as indicate that the development of DBA occurs well into the fetal development in both humans and our mouse model.

2023-05-31 | E-MTAB-12448 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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