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Comparison of gene expression pattern between Wild-type and Trib1-deficient mice (Gene chip data for JEM 20070183)

ABSTRACT: The purpose of this experiment was to compare the gene expression pattern between wild-type and Trib1-deficient macrophages in response to LPS. Keywords: Comparison of gene expression pattern between Wild-type and Trib1-deficient mice

ORGANISM(S): Mus musculus

PROVIDER: GSE8788 | GEO | 2007/08/17

SECONDARY ACCESSION(S): PRJNA102087

REPOSITORIES: GEO

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Transcription profiling of mouse Trib1-deficient animals vs controls

Project description:The purpose of this experiment was to compare the gene expression pattern between wild-type and Trib1-deficient macrophages in response to LPS. Experiment Overall Design: Two samples to define LPS-inducible gene and 4 samples (2 for wild-type and the rests for Trib1-deficient mice) for comparison.

2008-11-06 | E-GEOD-8788 | biostudies-arrayexpress

Expression data of GMP and MDP from wild-type and Trib1-/- mice

2013-01-18 | GSE43563 | GEO

Expression data of GMP and MDP from wild-type and Trib1-/- mice

Project description:Trib1 is critical for some myeloid cell differentiation. Therefore we used microarrays to investigate gene expression profiles in wild-type and Trib1-/- progenitor of myeloid cells. Progenitor cells, such as GMP and MDP, obtained from wild-type and Trib1-/- mice were sorted, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.

2013-01-18 | E-GEOD-43563 | biostudies-arrayexpress

Trib1 promotes the development of acute myeloid leukemia in the Ts1Cje Down syndrome model mouse

Project description:Down syndrome (DS) is caused by trisomy of chromosome 21 and it predisposes to hematological disorders such as transient myeloproliferative disorder and acute megakaryocytic leukemia. Our previous study identified a gain-of-function mutation of TRIB1 encoding a pseudokinase that suppresses C/EBP and enhances MEK/ERK signaling. In this study, we aimed to examine whether Trib1 expression cooperates with trisomy 21 in the development of leukemia. The wild type or R107L mutant Trib1 was retrovirally introduced into bone marrow cells derived from the Ts1Cje Down syndrome model mice or C57Bl6/J mice. Trib1 expression in hematopoietic cells of Ts1Cje mice accelerated the onset of AML development compared with that in wild type mice. Gene expression analysis showed up-regulation of Hox downstream genes and down-regulation of genes for the myeloid differentiation program and C/EBP targets. These results suggest that Trib1-mediated signaling plays an important role in promoting leukemogenesis in Down syndrome. We used microarrays to detail the global program of gene expression in mouse AML

2022-03-29 | GSE168531 | GEO

Liver gene expression profiles of Tribbles-homolog1 (Trib1)/Ldl-receptor (Ldlr) double-knockout mice against Ldlr-knockout mice

Project description:Genetic variants at the TRIB1 (Tribbles-homolog 1) gene locus are strongly associated with plasma lipid traits and the risk of coronary artery disease in humans. In this study, we analyzed the consequences of Trib1-deficiency (Trib1-/-) on hepatic gene expression in mice on the atherosclerosis-susceptible LDL-receptor deficient (Ldlr-/-) background. Therefore, Trib1-/- mice were crossed onto the Ldlr-/- background to generate double knockout mice (Trib1-/-Ldlr-/-) and fed a semisynthetic, modified AIN76 diet (0.02% cholesterol, 4.3% fat). At 20 weeks of age, Trib1-/-Ldlr-/- mice and Trib1+/+Ldlr-/- control mice were sacrificed and liver tissue was snap frozen in liquid nitrogen and stored at -80°C until further processing. Total RNA was isolated from liver tissue (n=8 mice per genotype) and subjected to microarray gene expression analysis.

2023-03-15 | E-MTAB-12669 | biostudies-arrayexpress

Trib1 regulates mouse LDL metabolism through Cebpa-mediated regulation of the LDL receptor in hepatocytes.

Project description:The Tribbles homolog 1 protein (TRIB1), encoded by the gene TRIB1, has been identified by genome-wide association studies (GWAS) as likely to be causal of a remarkable number of cardiometabolic traits, including plasma lipids, hepatic steatosis, adiponectin levels, and coronary artery disease. In its best-known function, Tribbles 1 interacts with the ubiquitin ligate COP1 protein to target the transcription factors CCAAT/enhancer-binding protein alpha and beta (CEBP a/b) for proteasomal degradation. We have previously published that specific Trib1 deletion in mice increased de novo lipogenesis, hepatic steatosis, and plasma triglycerides, attributable at least in part to increased protein levels of hepatic Cebpa. However, the mechanism by which Trib1 regulates plasma lipids and specifically LDL-C metabolism remained unknown. In this experiment our aim was to identify possible molecular interactions by which hepatic Trib1 regulates specifically LDL-C metabolism dependently of Cebpa expression. To do this, we compared total gene expression in livers of wild type mice, Trib1, Cebpa and Trib1;Cebpa hepatic deleted mice. Gene expression data was then used in Ingenuity Pathway analysis to identify upstream transcription factors that might be responsible for the gene expression changes observed.

2023-09-29 | GSE158815 | GEO

Mus musculus

Project description:Comparison of gene expression pattern between Wild-type and Trib1-deficient mice (Gene chip data for JEM 20070183)

| PRJNA102087 | ENA

TRIB1 suppression on human hepatocytes transcriptome

Project description:The TRIB1 locus has been associated with lipid dysfunction. The underlying mechanisms were investigated by examining the transcription landscape in response to TRIB1 suppression in human primary hepatocytes.

2015-04-13 | GSE61473 | GEO

Trib1 promotes acute myeloid leukemia progression by modulating transcriptional programs of Hoxa9 [array]

Project description:The pseudokinase Trib1 functions as a myeloid oncogene that recruits E3 ubiquitin ligase COP1 to C/EBPa, and interacts with MEK1 to enhance ERK phosphorylation. Close genetic interaction between Trib1 and Hoxa9 has been observed in myeloid leukemogenesis as Trib1 overexpression significantly accelerates Hoxa9-induced leukemia onset. Yet the mechanism how Trib1 functionally modulates Hoxa9 transcription activity is unclear. Here we provide evidence that Trib1 modulates Hoxa9-associated super-enhancers. ChIP-seq analyses identified increased Histone H3K27Ac signals at the super-enhancers such as Erg, Aff3, Spns2 and Coro2 loci, as well as increased mRNA expression of these genes. The modification of super-enhancer activities is mostly achieved by degradation of C/EBPa by Trib1 and the MEK/ERK pathway only slightly contributes to the activities. Silencing of Erg abrogates the growth advantage acquired by Trib1 overexpression, indicating that Erg is a critical downstream target of the Trib1/Hoxa9 axis. Moreover, treatment of AML cells with the BRD4 inhibitor JQ1 showed growth inhibition in the Trib1/Erg-dependent manner. Upregulation of ERG by TRIB1 was also observed in human AML cell lines, suggesting that Trib1 is a potential target of Hoxa9-associated AML. We used microarrays to detail the global program of gene expression in mouse AML

2020-10-21 | GSE139641 | GEO

Analysis of 3D- and TRIB1-dependent gene expression in prostate cancer cells

Project description:A capability to proliferate under the three-dimensional (3D) conditions is a characteristic property of cancer. Therefore, factors that regulate the 3D growth are considered rational targets for cancer therapy. We analyzed gene expression profile of human prostate cancer PC3 cells which were cultured in normal 2D conditions or in spheroid culture conditions (3D). The analysis suggested that the sheroid conditions would mimic a part of tumor-like 3D conditions. In addition, we analyzed genes regulated by TRIB1, a candidate oncogene in PC3 cells by comparing the gene expression profiles between control (shGFP)-treated and TRIB1 shRNA- (shTRIB1-1 and shTRIB1-2) treated cells. Our analysis identified a subset of genes that are downstream of TRIB1 in prostate cancer cells.

2014-12-01 | GSE53245 | GEO

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