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. Keywords: Comparison of gene expression pattern between Wild-type and Trib1-deficient mice
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.
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.
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
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.
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.
