Gene expression profiles of ASK1-deficient adipose tissues
ABSTRACT: To elucidate the potential function of ASK1 in adipose tissues, microarray analysis was performed using iBAT and eWAT. Tissue samples were collected from 10-week-old male mice, and RNA samples derived from three individuals were pooled to analyze. These data provide novel insights into the physiological functions of ASK1. To elucidate the potential function of ASK1 in adipose tissues, microarray analysis was performed using iBAT and eWAT.
Project description:To investigate the effect of CEBPA on the expression of mRNAs and long non-coding RNAs ( lncRNAs), we utilized the K562 AML cell line carrying a stable and Tet-on inducible CEBPA allele. K562 cells lack endogenous CEBPA and restoration of its expression induces proliferation arrest and granulocytic differentiation . Based on the expression of known CEBPA transcriptional targets, we selected RNA extracted from 48 hours of induction (CEBPA) together with RNA extracted from control-induced cells (CTR). 4 biological replicates for each sample have been utilized.
Project description:To identify the gene signature induced by MCMV that modulates innate immune function Microarray comparison of gene expression in the lungs of 4 individual naive and 4 eMCMV infected mice two weeks after infection.
Project description:NQO1 silencing by a specific shRNA against NQO1 increased migration and hormone-independent survival in hormone-dependent human prostate cancer cells LNCaP. Genome wide array revealed that NQO1 blockade significantly upregulated pro-inflammatory mediators (e.g., IL-32, CCL2, IL-8, IL-17C, IL-10RA, CXCR2, CXCR7, NOS3) associated with prostate tumorigenesis. Two-condition experiment, control vs. NQO1 knockdown LNCaP cells. Biological replicates: 3 control replicates, 3 NQO1 knockdown replicates.
Project description:Elucidating the molecular mechanisms controlling dendrite development is key to understanding the pivotal role these structures play in influencing synaptic integration and neural function. Despite significant advances in this field, genetic pleiotropy remains a significant impediment to investigating such complex developmental processes. To circumvent this problem, we have applied class specific neuron transcriptional expression profiling coupled to an in vivo RNAi functional validation screen in order to dissect the molecular bases of Drosophila class IV dendritic arborization (da) neuron dendritogenesis. Microarray analyses reveal transcriptional regulation as one highly enriched biological and functional category with 420 transcription factors significantly expressed in class IV neurons. Among these, we identify roles for 268 genes in mediating a broad spectrum of functions including dendritic field coverage, branching, routing, and tiling. Collectively, our analyses provide a more comprehensive framework of the role complex transcriptional networks play in directing distinct aspects of class specific dendrite morphogenesis. Gene expression profiling of class IV da neurons performed at the third instar larval stage of development from two independent cell isolations from 40-50 age-matched third instar larvae expressing mCD8::GFP under the control of the GAL4ppk.1.9 driver
Project description:During hematopoietic differentiation of hESCs, HOXA9 expression parallels hematopoietic development but is restricted to the hemogenic precursors (HEP, CD31+CD34+CD45-), and diminishes as HEPs differentiate into blood cells (CD45+). Enforced expression of Hoxa9 in hESCs robustly promoted differentiation into primitive (CD34+CD45+) and total (CD45+) blood cells with higher clonogenic (CFU) potential. To identify patterns of gene expression that could explain at the molecular level the developmental impact of HOXA9 in hematopoietic commitment of hESCs, we performed gene expression profile in FACS-purified EV- and HOXA9-HEPs. 10^5 HoxA9 over expressing and EV control HEPs purified by FACS from H9 and AND1 hEBs at day 15 of hematopoietic differentiation were used for gene expression analysis using Whole Human Genome Oligo Microarray chips (Agilent Technologies).
Project description:The immune system can recognize and respond to tumors. However there are some conditions in which the genetic instability and heterogeneity of tumor cells leads to the development of variants that can escape the immune system. T cells have infiltrated inside many tumors (Tumor Infiltrating Lymphocytes or TILs), but generally these TILs have lost their functional capacity and are unable to eliminate tumor cells. We developed a model of autochthonous melanoma in mice that recapitulates some aspects of inflammatory melanoma in humans. These include a systemic Th2/Th17-oriented chronic inflammation, recruitment of immunosuppressive myeloid cells and acquisition by TILs of an “exhausted” phenotype characterized by expression of receptors for multiple inhibitory molecules. To address the molecular bases for the “exhausted” TILs phenotype, we performed transcriptomic analyses on sorted CD8 or T cells from the induced melanomas. These transcriptomes were compared to those of naïve CD8 T cells and of CD8 T cells immunized with a virus. 10 samples, 3 replicates for controls (untreated and infected with AdP1A), 4 replicates for TILs CD8 from melanoma
Project description:In hESCs, expression of the Notch ligand DLL4 parallels the emergence of bipotent hematoendothelial progenitors (HEPs) and promotes their hematopoietic differentiation. During differentiation, DLL4 is only expressed in a subpopulation of HEPs. To study the developmental fate of the two subpopulations of HEPs identified by DLL4 expression, we FACS-isolated DLL4high and DLL4low/- HEPs at day 15 of differentiation and performed gene expression analysis using microarrays 10^5 DLL4high and DLL4low/- HEPs purified by FACS from H9 and AND1 hEBs at day 15 of hematopoietic differentiation were used for gene expression analysis using Whole Human Genome Oligo Microarray chips (Agilent Technologies).
Project description:To deepen the understanding of the molecular mechanisms that regulate megakaryocytic differentiation mediated by SCL, We performed gene expression profiling (GEP) using oligonucleotide microarrays of control (EV) and SCL-overexpressing cells that were undifferentiated or at day 14 of EB differentiation. We studied the SCL-overexpression-associated transcriptomic changes during megakaryocytic differentiation from hESCs at 14 days. Two independent experiments were performed.
Project description:In vivo antigen (Ag)-induced differentiation of B lymphocytes into plasma cells (PCs) takes place in extra-follicular foci and germinal centers of the secondary lymphoid organs (SLOs). Most of these SLO PCs are short-living and only relatively few PCs, characterized by secreting high-affinity antibodies (Ab), travel through the circulation and finally home in specialized survival niches of the bone marrow (BM) and, at a lesser extent, in the SLOs, where they become long-living Ab-secreting PCs. We have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish between human circulating Ag-induced PCs in comparison with tonsil and BM PCs distinctively regulate genes involved in cell proliferation. Gene expressions in human plasma cells isolated from tonsil (7 samples), blood (6 samples) and bone marrow (7samples) were measured. Each sample was isolated from a different donor.
Project description:Transcriptional profiling of murine bone marrow c-kit+, Sca-1+ lineage neative (KSL) cells from p21CDKN1a-/- and p21+/+ overexpressing Flt3/ITD. The goal was to determine the effect on global gene expression by loss of p21 in Flt3/ITD transformed KSL cells Internal tandem duplication (ITD) mutations in the Flt3 gene (Flt3-ITD) are associated with poor prognosis in patients with acute myeloid leukemia (AML). Few inhibitors of Flt3-ITD are effective against Flt3-ITD+ AML due to the development of drug-resistance. In this study, we demonstrate that Flt3-ITD activates a novel pathway involving p21Cdkn1a (p21) and pre-B cell leukemia transcription factor 1 (Pbx1) that attenuates Flt3-ITD cell proliferation and is involved in the development drug resistance. Flt3-ITD up-regulated p21 expression in mouse bone marrow c-kit+-Sca-1+-Lin- (KSL) cells and in Ba/F3 cells. Loss of p21 expression enhanced growth factor-independent proliferation and sensitivity to cytarabine as a consequence of enriching the S+G2/M phase population concomitant with a significant increase in the expression of Pbx1, but not Evi-1, in Flt3-ITD+ cells. This enhancement of cell proliferation by loss of p21 was partially abrogated when Pbx1 expression was silenced in Flt3-ITD+ primary bone marrow colony-forming cells (CFCs) and Ba/F3 cells. Antagonizing Flt3-ITD using AC220, a selective inhibitor of Flt3-ITD, decreased the expression of p21, coincident with the up-regulation of Pbx1 mRNA and a rapid decline in the number of viable Flt3-ITD+ Ba/F3 cells, however the cells eventually became refractory to AC220. Overexpressing p21 in Flt3-ITD+ Ba/F3 cells delayed the emergence of cells refractory to AC220, whereas silencing p21 accelerated their development. These data demonstrate that Flt3-ITD is capable of inhibiting the proliferation of Flt3-ITD+ cells through the p21/Pbx1 axis and that antagonizing Flt3-ITD contributes to the subsequent development of cells refractory to Flt3-ITD inhibitor by disrupting p21 expression. biological replicates: 3 KSL cell replicates overexpressing ITD-Flt3 from p21+/+ and p21-/- cells, 1 KSL cell replicate from p21+/+ and p21-/- cells