Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile of WT and TAK1 KO livers.

ABSTRACT: The effect of ablation of Tak1 gene in the liver was characterized.

ORGANISM(S): Mus musculus

PROVIDER: GSE51962 | GEO | 2014/12/22

SECONDARY ACCESSION(S): PRJNA225938

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profile of WT and TAK1 KO livers.

Project description:The effect of ablation of Tak1 gene in the liver was characterized. RNA was extracted from 1-month-old WT and hepatocyte specific TAK1-deleted mice

2014-12-22 | E-GEOD-51962 | biostudies-arrayexpress

Chromosomal aberrations in Tak1-/- mice

Project description:Characterization of chromosomal aberrations in liver tumors of Tak1-/- mice of different ages The aim of the project is to dissect signaling mechanisms which could be of importance during the process of liver carcinogenesis. Keywords: Array comparative genomic hybridization analysis (aCGH).

2010-03-31 | GSE19105 | GEO

TAK1 deficient liver parenchymal cells with Rip3 double knockout TAK1LPC

Project description:Genomic copy number profiling of TAK1 deficient liver parenchymal cells with Rip3 double knockout

2013-05-01 | GSE45206 | GEO

Hepatocyte-Specific TAK1 Deficiency Drives RIPK1 Kinase-dependent Inflammation to Promote Liver Fibrosis and Hepatocellular Carcinoma

Project description:Transforming growth factor beta-activated kinase1 (TAK1) encoded by the gene MAP3K7 regulates multiple important downstream effectors involved in immune response, cell death and carcinogenesis. Hepatocyte-specific deletion of TAK1 in Tak1_Hep mice promotes liver fibrosis and hepatocellular carcinoma (HCC) formation. Here, we report that genetic inactivation of RIPK1 kinase using kinase dead knock-in D138N mutation in Tak1_Hep mice inhibits the expression of liver tumor biomarkers, liver fibrosis and HCC formation. Inhibition of RIPK1, however, has no or minimum effect on hepatocyte loss and compensatory proliferation, which are the recognized factors important for liver fibrosis and HCC development. Using single cell RNA-seq, we discover that inhibition of RIPK1 strongly suppresses inflammation induced by hepatocyte-specific loss of TAK1. Activation of RIPK1 promotes the transcription of key proinflammatory cytokines, such as CCL2, and CCR2+ macrophage infiltration. Our study demonstrates the role and mechanism of RIPK1 kinase in promoting inflammation, both cell-autonomously and cell-non-autonomously, in the development of liver fibrosis and HCC, independent of cell death and compensatory proliferation. We suggest the possibility of inhibiting RIPK1 kinase as a therapeutic strategy for reducing liver fibrosis and HCC development by inhibiting inflammation.

2020-07-08 | GSE148859 | GEO

TAK1 deficient liver parenchymal cells with Rip3 double knockout TAK1LPC

Project description:Genomic copy number profiling of TAK1 deficient liver parenchymal cells with Rip3 double knockout Sample vs. Reference (pool of 4 normal liver tissues)

2013-05-01 | E-GEOD-45206 | biostudies-arrayexpress

Nuclear orphan receptor TAK1/TR4-deficient mice are protected against obesity-linked inflammation, hepatic steatosis, and insulin resistance

Project description:The nuclear receptor TAK1/TR4/NR2C2 is expressed in several tissues that are important in the control of energy homeostasis. TAK1-deficient (TAK1-/-) mice are resistant to the development of age- and high fat diet (HFD)-induced metabolic syndrome. Biochemical analysis showed significantly lower hepatic triglyceride levels and reduced lipid accumulation in adipose tissue in TAK1-/- mice compared to wild type (WT) mice. Gene expression profiling analysis revealed that the expression of several genes encoding proteins involved in lipid uptake and triglyceride synthesis and storage, including Cidea, Cidec, Mogat1, and CD36, was greatly decreased in the liver of TAK1-/- mice. Moreover, TAK1-/- mice exhibit reduced infiltration of inflammatory cells and expression of inflammatory genes in adipose tissue and were resistant to the development of glucose intolerance and insulin resistance. TAK1-/- mice consume more oxygen and produce more carbon dioxide than WT mice suggesting a higher rate of energy expenditure. Together, these results indicate that TAK1 plays a critical role in the regulation of energy and lipid homeostasis and potentiates the development of metabolic syndrome. Our study suggests that TAK1 might provide a novel therapeutic target in the management of metabolic syndrome. For microarray liver total RNAs were purified from WT and TAK1 KO mice and applied on Agilent mouse genome chip. Liver from 1 year old- WT and TAK1 KO mice.

2010-09-30 | E-GEOD-21903 | biostudies-arrayexpress

RNA-seq analysis of whole liver derived from endothelial specific TAK1 conditional knockout mice.

Project description:In this study we show that TGFβ-activated kinase 1 (TAK1), is crucial for ensuring EC survival on TNFα stimulation. EC-specific TAK1-knockout in adult mice resulted in rapid death of the animal due to destruction of intestinal and liver blood vessels. TNFα from myeloid cells responding to intestinal microbiota was responsible for EC death in the intestine and liver. Our results illuminate mechanisms ensuring survival of intestinal and liver EC under physiological conditions

2019-01-11 | GSE115190 | GEO

Nuclear orphan receptor TAK1/TR4-deficient mice are protected against obesity-linked inflammation, hepatic steatosis, and insulin resistance

2010-10-01 | GSE21903 | GEO

Expression data from livers from Sco1 liver-specific KO and WT adult mice

Project description:Sco1 is a gene required for cytochrome c oxidase biogenesis and the regulation of copper homeostasis. We characterized the transcriptional changes that occur as a result of liver-specific deletion of Sco1 in mice at 27 days of age In this dataset, we include the expression data obtained from dissected wild-type mouse livers and mouse livers in which Sco1 has been specifically deleted. 8 samples: 4 Sco1 liver knockouts (Alb-Cre Sco1fl/fl), 4 wild-type (Sco1fl/fl)

2014-07-02 | E-GEOD-58997 | biostudies-arrayexpress

Pharmacological Inhibition of TAK1 Prevents and Induces Regression of fibrosis

Project description:To evaluate the effects of TAK1 inhibition on TGF-beta regulated fibrosis using a novel small molecule inhibitor of TAK1.

2023-05-17 | GSE232435 | GEO