Transcription profiling of left ventricular myocardium after sham or TAC surgery in BL/6N and BL/6J mice
ABSTRACT: The most commonly used inbred mouse strain, C57BL/6J, lacks a functional nicotinamide nucleotide transhydrogenase (Nnt) and thus, is protected from pressure-overload-induced oxidative stress and heart failure. We screened for differential gene expression in left ventricular myocardium after sham/transverse aortic constriction (TAC) surgery in 10-12 weeks old mice from BL/6N (functional Nnt) and BL/6J (non-functional Nnt, missense of exons 7-11) strains.
Project description:The most commonly used inbred mouse strain, C57BL/6J, lacks a functional nicotinamide nucleotide transhydrogenase (Nnt) and thus, is protected from pressure-overload-induced oxidative stress and heart failure. We screened for differential gene expression in left ventricular myocardium after sham/transverse aortic constriction (TAC) surgery in 10-12 weeks old mice from BL/6N (functional Nnt) and BL/6J (non-functional Nnt, missense of exons 7-11) strains.
Project description:Comparison of gene expression profiling between DLEU1 downregulated Raji BL cell and wild type Raji BL cell Transcription Activator-Like Effector Nucleases (TALENs) mediated DLEU1 downregulated Raji burkitt lymphoma (BL) cell clone and wild type (control) Raji cell clone were analyzed in duplicate. Four samples were hybridized to HGU133_plus_2 Genechip(Affymetrix) and scanned with the Scanner 3000 7G.
Project description:Background: Adenosine deaminases that act on RNA (ADARs) bind to double-stranded and structured RNAs and deaminate adenosines to inosines. This A to I editing is widespread and required for normal life and development. Besides mRNAs and repetitive elements, ADARs can target miRNA precursors. Editing of miRNA precursors can affect processing efficiency and alter target specificity. Interestingly, ADARs can also influence miRNA abundance independent of RNA-editing. In mouse embryos where editing levels are low, ADAR2 was found to be the major ADAR protein that affects miRNA abundance. Here we extend our analysis to adult mouse brains where high editing levels are observed. Results: Using Illumina deep sequencing we compare the abundances of mature miRNAs and editing events within them, between wild-type and ADAR2 knockout mice in the adult mouse brain. Reproducible changes in abundance of specific miRNAs are observed in ADAR2 deficient mice. Most of these quantitative changes seem unrelated to A to I editing events. However, many A to G transitions in cDNAs prepared from mature miRNA sequences, reflecting A to I editing events in the RNA, are observed with frequencies reaching up to 80%. About half of these editing events are primarily caused by ADAR2 while a few miRNAs show increased editing in the absence of ADAR2, suggesting preferential editing by ADAR1. Moreover, novel, previously unknown editing events were identified in several miRNAs. In general 64% of all editing events are located within the seed region of mature miRNAs. In one of these cases retargeting of the edited miRNA could be verified in reporter assays. Also, altered processing efficiency upon editing near a processing site could be experimentally verified. Conclusions: ADAR2 can significantly influence the abundance of certain miRNAs in the brain. Only in a few cases changes in miRNA abundance can be explained by miRNA editing. Thus, ADAR2 binding to miRNA precursors, without editing them, may influence their processing and thereby abundance. ADAR1 and ADAR2 have both overlapping and distinct specificities for editing of miRNA editing sites. Over 60% of editing occurs in the seed region possibly changing target specificities for many edited miRNAs. Examination of the effect of ADAR2 on gene expression in mature mouse wildtype and ADAR2 knockout brain using Affymetrix® GeneChip® Whole Transcript (WT) Expression Arrays (Analysis by KFB Regensburg, Germany)
Project description:We performed genomic and transcriptomic analysis of seven cases of molecular Burkitt lymphoma (mBL) developed in immunosuppressed patients who underwent solid organ transplantation. Interestingly, three cases (43%) were MYC-translocation-negative and revealed the 11q-gain/loss aberration recently identified in 3% of mBL developed in immunocompetent hosts.1 Based on array CGH data, minimal gain and loss regions of 11q (MGR/~4Mb and MLR/~13.5Mb, respectively) were defined and integrative genomic and transcriptomic analysis identified 35 differentially expressed genes, when compared with classic BL. All 16 MGR-dysregulated genes were upregulated, including cancer related USP2, CBL and PAFAH1B2. As expected, all 19 MGL-dysregulated genes were downregulated and two of them, TBRG1 and EI24, are potential tumor suppressor genes. Interestingly, the vast majority of dysregulated 11q23-q25 genes are involved in the MYC and TP53 networks. We hypothesize that the 11q-gain/loss aberration represents a “molecular variant” of t(8q24/MYC) and affects the same pathological pathways as the MYC oncogene. Seven cases of PTLD with BL features were selected from a cohort of 174 posttransplant patients diagnosed with PTLD between 1989 and 2012 at the University Hospitals of KU Leuven (Leuven, Belgium). In addition, five classic BL cases were selected as immunocompetent controls (IC-BL). Morphologic, immunophenotypic, clinical and cytogenetic characteristics of the selected cases were reviewed.
Project description:8 weeks old Chickens (White leghorn (LSL), 4 per group), were i.v. injected every three hours with 1x10^7 Units recombinant chicken interferon alpha to obtain a plasma concentration similar to the amount of type I IFN produced during natural infection. Three (1 IFN injection), six (2 injections) and nine (three injections) hours after the first injection spleen and lung of the birds were sampled and subjected to microarray analysis using Agilent 4x44k chicken arrays customized with a multitude of immune genes (e.g. chemokines and chemokine receptors, cytokines and cytokine receptors). Birds receiving buffer only served as control.
Project description:Our aim is to analyze how does the lack of each of the Ca2+ channels, involved in excitation-contraction coupling in skeletal muscle - RYR1 and Cav1.1, affect gene expression in embryonic mouse limb skeletal muscle during secondary myogenesis. We extracted total RNA from the limb skeletal muscle of WT, heterozygous RYR1-/+ and Cav1.1+/-, and homozygous RYR1-/- and Cav1.1-/- mutants from 3 litters (n = 3 for each group) at days E14.5 and E18.5 and subjected it to microarray analyses.
Project description:This SuperSeries is composed of the following subset Series: GSE12997: Comparative transcriptomic analysis of BA- or BL- associated murine colonic epithelium GSE12998: Comparative transcriptomic analysis of BA- or BL- associated murine colonic epithelium after O157 infection Refer to individual Series