Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Zhang2020 - Draft metabolic reconstruction model of Atlantic cod liver generated from gadMor1 and iHepatocyte2322

ABSTRACT: This is an auto-generated model with COBRA Matlab toolbox.

SUBMITTER: Xiaokang Zhang

PROVIDER: MODEL2010090003 | biostudies-other |

SECONDARY ACCESSION(S): 10.3389/fmolb.2020.591406

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Similar Datasets

Zhang2020 - Draft metabolic reconstruction model of Atlantic cod liver generated from gadMor3 and iHepatocyte2322

Project description: Not available

| MODEL2010090001 | biostudies-other

Zhang2020 - Draft metabolic reconstruction model of Atlantic cod liver generated from gadMorTrinity and iHepatocyte2322

Project description: Not available

| MODEL2010090002 | biostudies-other

aCGH analysis of liver tumors generated in FAH-/- 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 Methods: NTBC was reduced or withdrawn in FAH-/- mice lacking Chk2, p53 or p21, and survival, tumor development, liver injury and regeneration were analyzed.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 | GSE156981 | 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

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

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

2021-04-02 | GSE156983 | GEO

3D deuterium metabolic imaging (DMI) of the human liver at 7 T using low-rank and subspace model-based reconstruction.

Project description: Not available

| S-EPMC11893041 | biostudies-literature

iMM1865: A New Reconstruction of Mouse Genome-Scale Metabolic Model.

Project description: Not available

| S-EPMC7148337 | biostudies-literature

Addressing uncertainty in genome-scale metabolic model reconstruction and analysis.

Project description: Not available

| S-EPMC7890832 | biostudies-literature

Reconstruction of Danio rerio metabolic model accounting for subcellular compartmentalisation.

Project description: Not available

| S-EPMC3498201 | biostudies-literature

Reconstruction and analysis genome-scale metabolic model of thermophilic fungus Myceliophthora thermophila

Project description:Myceliophthora thermophila is a thermophilic fungus with great biotechnological characteristics for industrial applications, which can degrade and utilize all major polysaccharides in plant biomass. Nowadays, it has been developing into a platform for production of enzyme, commodity chemicals and biofuels. Therefore, an accurate genome-scale metabolic model would be an accelerator for this fungus becoming a universal chassis for biomanufacturing. Here we present a genome-scale metabolic model for M. thermophila constructed using an auto-generating pipeline with consequent thorough manual curation. Temperature plays a basic and critical role for the microbe growth. we are particularly interested in the genome wide response at metabolic layer of M. thermophilia as it is a thermophlic fungus. To study the effects of temperature on metabolic characteristics of M. thermophila growth, the fungus was cultivated under different temperature. The metabolic rearrangement predicted using context-specific GEMs integrating transcriptome data.The developed model provides new insights into thermophilic fungi metabolism and highlights model-driven strain design to improve biotechnological applications of this thermophilic lignocellulosic fungus.

2022-09-14 | GSE184074 | GEO

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