RIp-chip experiments with proteins that do not contain RNA-binding domains
Ontology highlight
ABSTRACT: In order to assess the prevalence of cotranslational assembly of protein complexes we performed RIp-chip experiments with many proteins that do not conatin RNA-binding motifs
Project description:To investigate the contribution of RNA-binding proteins to the regulation of RNA decay we used an in vivo labelling system (Cleary et al. 2005 Nat Biotechnol. 23, 232-7) to estimate the decay rates of RBP mutants and wild type S. pombe cells
Project description:The Upf1 protein is a major factor in nonsense-mediated decay. We used an in vivo labelling system (Cleary et al. 2005 Nat Biotechnol. 23, 232-7) to estimate the decay rates of upf1delta and wild type cells over-expressing the transcription factor Mei4.
Project description:Ribonucleoprotein immunoprecipitation microarray (RIp-chip) study using the RNA-binding protein Meu5 from the fission Schizosaccaromyces pombe
Project description:The Upf1, Upf2 and Upf3 proteins cooperate to implement nonsense-mediated decay. We used DNA microarrays for profiling RNA expression levels of upf2 and upf3 mutants
Project description:To study the contribution of RNA-binding proteins (RBPs) to the regulation of RNA turnover, we used DNA microarrays to examine the transcriptome of S. pombe strains containing deletions in non-essential genes encoding RBPs
Project description:The Meu5 RNA-binding protein stabilises its targets during meiosis. We compared wild type and meu5delta cells transcriptome under different conditions: pat1-induced meiosis in diploid cells, wild type meiosis in diploid cells and cells overexpressing the Mei4 transcription factor.
Project description:We applied in parallel RNA-Seq and Ribosome-profiling to S. pombe pat1 diploids undergoing meiosis and sporulation in a synchronous manner
Project description:To investigate the contribution of RNA-binding proteins to the regulation of RNA decay we used an in vivo labelling system (Cleary et al. 2005 Nat Biotechnol. 23, 232-7) to estimate the decay rates of RBP mutants and wild type S. pombe cells
Project description:CHX is an inhibitor of translation elongation often used in ribosome profiling experiments. There is evidence that CHX treatment of cells may cause artefacts in the distribution of ribosomes on mRNAs. We investigate this possibility in S. pombe by performing ribosome profiling in the presence and absence of this drug.
Project description:The regulation of complex cellular activities in palmitate treated HepG2 cells, and the ensuing cytotoxic phenotype, involves cooperative interactions between genes. While previous approaches have largely focused on identifying individual target genes, elucidating interacting genes has thus far remained elusive. We applied the concept of information synergy to reconstruct a ?gene-cooperativity? network for palmititate-induced cytotoxicity in liver cells. Our approach integrated gene expression data with metabolic profiles to select a subset of genes for network reconstruction. Subsequent analysis of the network revealed insulin signaling as the most significantly enriched pathway, and desmoplakin (DSP) as its top neighbor. We determined that palmitate significantly reduces DSP expression, and treatment with insulin restores the lost expression of DSP. Insulin resistance is a common pathological feature of fatty liver and related ailments, whereas loss of DSP has been noted in liver carcinoma. Reduced DSP expression can lead to loss of cell-cell adhesion via desmosomes, and disrupt the keratin intermediate filament network. Our findings suggest that DSP expression may be perturbed by palmitate and, along with insulin resistance, may play a role in palmitate induced cytotoxicity, and serve as potential targets for further studies on non-alcoholic fatty liver disease (NAFLD). free fatty acids(palmitate, oleate, linoleate) 0.7mM and tnf-alpha (0 20,100 ng/ml) were subjected to HepG2 cell line to study the cytotoxicity induced by these two factors. control(Hepg2 medium and BSA medium) treatment(combinations of TNFa+FFAs) two biological replicates for each condition, color swap for each sample