Global RNA stability profiling in human NBDY knockout using TimeLapse-seq
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA607951 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We previously identified a conserved human microprotein NoBody/NBDY that can interact with the mRNA decapping complex through EDC4 and affects the expression of an NMD (nonsense-mediated decay) substrate. However, it remains unclear the exact mechanism of NBDY-regulated RNA stability change and whether this is the direct cause/consequence of its modulation of P-body structure/numbers. Here we present a global profile of RNA stability in human NBDY knockout cells via TimeLapse-seq. By comparing this dataset to our previous work done in DCP2 KO cells, we demonstrate that NBDY is a specificity factor of the 5'-3' RNA decay. In addition, these data indicate a role of NBDY in cell cycle and other signaling transduction processes as well.
2020-12-16 | GSE145682 | GEO
Project description:Global RNA stability profiling in HEK293T cells under EGF treatment using TimeLapse-seq
| PRJNA609717 | ENA
Project description:Multiple RNA decapping enzymes coexist in mammalian cells to regulate decay of partially overlapping sets of cellular transcripts, but a comprehensive understanding of cellular substrate selectivity of each enzyme is yet to be achieved. Previously we demonstrate the utility of TimeLapse-seq in global profiling of RNA stability changes in human Dcp2 knockout cells. However, secondary transcriptional changes and upregulation of alternative decay pathways have obscured complete mapping of Dcp2 substrates. Here, we present the discovery and first application of a cell-permeable, highly selective Dcp2 ligand in the chemical genetic study of its RNA substrates.
2020-12-16 | GSE153258 | GEO
Project description:We discovered through LC-MS/MS followed by biochemical assays and immunofluorescence that human microprotein NoBody/NBDY can be phosphorylated during EGF signaling transduction, and that this single post-translational modification of the smallest decapping complex component known to date is necessary to the observed disappearance of P-bodies under EGF treatment. RNA stability measurement of a known hDcp2 substrate, RRP41, showed decreased RNA life-time under EGF treatment. We hence wish to investigate the effect of this phospho-NBDY mediated P-body disassembly on global RNA turnover. Here we present a global profile of RNA stability in human HEK293 cells under EGF treatment via TimeLapse-seq. By comparing this dataset to our previous and current work done in DCP2 KO and in NBDY KO cells, respectively, we demonstrate that P-body dissociation observed during EGF signaling does not cause RNA stability change globally except for a few known EGF regulated transcripts.
2021-12-31 | GSE146213 | GEO
Project description:Global RNA stability profiling during selective chemical inhibition of human Dcp2
| PRJNA641880 | ENA
Project description:Interventions: experimental group :PD-1 Knockout Engineered T Cells
Primary outcome(s): Number of participants with Adverse Events and/or Dose Limiting Toxicities as a Measure of Safety and tolerability of dose of PD-1 Knockout T cells using Common Terminology Criteria for Adverse Events (CTCAE v4.0) in patients
Study Design: historical control
| 2662961 | ecrin-mdr-crc
Project description:Multiple RNA decapping enzymes coexist in mammalian cells to regulate decay of distinct subsets of cellular transcripts, but their specificity remains incompletely defined to date. Here we present a global profile of RNA stability changes in human Dcp2 knockout cells via TimeLapse-seq. We demonstrate that P-body enrichment is the strongest correlate of Dcp2-dependent RNA decay, and that post-transcriptional modifications such as m6A present additive effect for Dcp2 targeting. Importantly, our data support a model in which P-bodies are sites that sort translationally repressed transcripts for cytoplasmic decay through additional molecular marks.
2020-05-06 | GSE143662 | GEO
Project description:We have developed QUAD (Quantification of Azidohomoalanine Degradation), a technique to quantitate global protein degradation using mass spectrometry. Azidohomoalanine (AHA) is pulsed into mouse tissues through their diet. The mice are then returned to a normal diet and the decrease of AHA abundance can be quantitated in the proteome. QUAD analysis reveals that protein stability varied within tissues, but discernible trends in the data suggest that cellular environment is a major factor dictating stability. Within a tissue, different organelles, post-translation modifications, and protein functions were enriched with different stability patterns. Surprisingly, subunits of the TRIC molecular chaperonin possessed markedly distinct stability trajectories in the brain. Further investigation revealed that these subunits also possessed different subcellular localization indicating a potential non-canonical chaperonin. Finally, QUAD analysis demonstrated that protein stability is enhanced with age in the brain but not in the liver. Overall, QUAD allows the first global quantitation of protein stability rates in tissues, which may lead to new insights and hypotheses in basic and translational research.
| MSV000084376 | MassIVE
Project description:To evaluate the effect of SETD2 and METTL14 on mRNA stability, we conducted RNA-seq in SETD2 or METTL14 knockdown HepG2 cells as well as control cells with or without actinomycin D treatment. Our RNA stability profiling revealed that depletion of SETD2 and METTL14 resulted in global reduction of RNA stability, and the changes were correlated between SETD2 and METTL14 knockdown cells.
2019-02-21 | GSE121949 | GEO
Project description:Fibrosis is defined as an abnormal matrix remodeling and loss of tissue homeostasis due to excessive synthesis and accumulation of extracellular matrix proteins in tissues. At present, there is no effective therapy for organ fibrosis. Previous studies demonstrated that aged plasminogen activator inhibitor-1(PAI-1) knockout mice develop spontaneously cardiac-selective fibrosis without affecting any other organs including kidney. Therefore, the PAI-1 knockout model of cardiac fibrosis provides an excellent opportunity to find the igniter(s) of cardiac fibrosis and its status in unaffected organs. We hypothesized that differential expressions of profibrotic and antifibrotic genes in PAI-1 knockout hearts and unaffected organs lead to cardiac selective fibrosis. In order to address this prediction, we have used a genome-wide gene expression profiling of transcripts derived from aged PAI-1 knockout hearts and kidneys. The variations of global gene expression profiling were compared within four groups: wildtype heart vs. knockout heart; wildtype kidney vs. knockout kidney; knockout heart vs. knockout kidney and wildtype heart vs. wildtype kidney. Analysis of illumina-based microarray data revealed that several genes involved in different biological processes such as immune system processing, response to stress, cytokine signaling, cell proliferation, adhesion, migration, matrix organization and transcriptional regulation were affected in hearts and kidneys by the absence of PAI-1, a potent inhibitor of urokinase- and tissue-type plasminogen activator. Importantly, the expressions of a number of genes, involved in profibrotic pathways were upregulated or downregulated in PAI-1 knockout hearts compared to wildtype hearts and PAI-1 knockout kidneys. To our knowledge, this is the first comprehensive report on the influence of PAI-1 on global gene expression profiling in the heart and kidney and its implication in several biological processes including fibrogenesis. Total RNA was extracted from hearts and kidneys derived from three PAI-1 knockout (12- month old) and three wild-type mice (12-month old) using RNeasy Fibrous Tissue Mini Kit (Qiagen, Valencia, CA) following the manufacturer’s instructions. The quality of RNA (RNA Integrity, RIN) in all 12 samples (3 wildtype hearts; 3 PAI-1 KO hearts; 3 wildtype kidneys; and 3 PAI-1 KO kidneys) was checked using the bioanalyzer. We have used a genome-wide gene expression profiling of transcripts derived from aged PAI-1 knockout hearts and kidneys. The variations of global gene expression profiling were compared within four groups: wildtype heart vs. knockout heart; wildtype kidney vs. knockout kidney; knockout heart vs. knockout kidney and wildtype heart vs. wildtype kidney.
2014-04-23 | E-GEOD-46320 | biostudies-arrayexpress