Age-dependent changes in protein incorporation into collagen-rich tissues of mice by in vivo pulsed SILAC labelling
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Orbitrap Fusion Lumos, Q Exactive HF
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): Cartilage, Blood Plasma, Skin, Bone
SUBMITTER: 
Roman Fischer
LAB HEAD: Roman Fischer
PROVIDER: PXD023180 | Pride | 2021-09-23
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| FL0433_MSQ870_Yoanna_1.raw | Raw | |||
| FL0433_MSQ870_Yoanna_11_170303161046.raw | Raw | |||
| FL0433_MSQ870_Yoanna_12.raw | Raw | |||
| FL0433_MSQ870_Yoanna_14.raw | Raw | |||
| FL0433_MSQ870_Yoanna_15.raw | Raw |
Items per page: 5 1 - 5 of 71 |
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE21735: Sinorhizobium meliloti cells: untreated 1021 strain vs. 1021 treated with 2,4-dichlorophenoxyacetic acid (2,4-D) GSE21737: Sinorhizobium meliloti cells: untreated 1021 strain vs. 1021 treated with indole-3-acetic acid (IAA) GSE21740: Sinorhizobium meliloti cells: untreated 1021 strain vs. 1021 treated with indole-3-carboxylic acid (ICA) GSE21742: Sinorhizobium meliloti cells: untreated 1021 strain vs. 1021 treated with indole (IND) GSE21743: Sinorhizobium meliloti cells: untreated 1021 strain vs. 1021 treated with tryptophan (Trp) GSE21744: Sinorhizobium meliloti cells: untreated 1021 wild type strain vs. RD64 strain Refer to individual Series
2010-05-20 | E-GEOD-21745 | biostudies-arrayexpress
Project description:An important question for the use of the mouse as a model for studying human disease is the degree of functional conservation of genetic control pathways from human to mouse. The human and mouse placenta show structural similarities but there have been no systematic attempt to assess their molecular similarities or differences. We built a comprehensive database of protein and microarray data for the highly vascular exchange region micro-dissected from the human and mouse placenta near-term. Abnormalities in this region are associated with two of the most common and serious complications of human pregnancy, maternal preeclampsia (PE) and fetal intrauterine growth restriction (IUGR), each disorder affecting ~5% of all pregnancies. Over 7,000 orthologs were detected with 70% co-expressed and over 80% of genes known to cause placental phenotypes in mouse were co-expressed. These genes form a tight protein-protein interaction network with novel candidate genes likely to be important in placental structure and/or function. The entire data is available as a web-accessible database to guide the informed development of mouse models to study human disease This experiment is now fully represented in NCBI Peptidome database with accession PSE115; http://www.ncbi.nlm.nih.gov/peptidome/search/index.shtml?acc=PSE115 Microdissection of human villous trees and mouse placental labyrinth. Tissues were split for microarray and protein analysis. For protein analysis samples were first fractionated by differential sucrose gradients into mitochrondria, cytosol, microsomes and nuclei. Mitochrondira and neuclei were each extracted by two different methods for soluble and insoluble material. Each subcellular fraction for each tissue was analysed in quintuplet by 9 step 2 dimensional LC/MSMS. This generated a total of 270 mzXML files for each tissue.
2009-06-29 | E-GEOD-13299 | biostudies-arrayexpress
Project description:Congenital hydrocephalus (CH), occurring in approximately 1/1000 live births, represents an important clinical challenge due to the limited knowledge of underlying molecular mechanisms. The discovery of novel CH-genes is thus essential to shed light on the intricate processes responsible for ventricular dilatation in CH Here we identify FLVCR1 (Feline Leukemia Virus Subgroup C Receptor 1) as a novel gene responsible for a severe form of CH in humans and mice. Mechanistically, our data reveal that the heme exporter FLVCR1a interacts with IP3R3-VDAC, a complex located on mitochondrial-associated membranes (MAMs) that controls mitochondrial calcium handling. Loss of Flvcr1 in mouse neural stem cells (NSCs) affects mitochondrial calcium levels and energy metabolism, leading to defective cortical neurogenesis and brain ventricle enlargement. These data point to defective NSC calcium handling and metabolic activity as one of the pathogenetic mechanisms driving CH.
2024-08-09 | PXD047897 | Pride
Project description:Transcriptional regulation by chromatin is a highly dynamic process directed through the recruitment and coordinated action of epigenetic modifiers and readers of these modifications. Using an unbiased proteomic approach to find interactors of H3K36me3, a modification enriched on active chromatin, we identify PWWP2A and HDAC2 among the top interactors. PWWP2A and its paralog PWWP2B form a stable complex with NuRD subunits MTA1/2/3:HDAC1/2:RBBP4/7, but not with MBD2/3, p66α/β, and CHD3/4. PWWP2A competes with MBD3 for binding to MTA1, thus defining a new variant NuRD complex that is mutually exclusive with the MBD2/3-containing NuRD. In mESCs, PWWP2A/B is most enriched at highly transcribed genes. Loss of PWWP2A/B leads to increases in histone acetylation predominantly at highly expressed genes, accompanied by decreases in Pol II elongation. Collectively, these findings suggest a role for PWWP2A/B in regulating transcription through the fine-tuning of histone acetylation dynamics at actively transcribed genes.
2018-07-19 | PXD010445 | Pride
Project description:CarD is an essential mycobacterial protein that we had previously shown to bind the RNA polymerase (RNAP) and affect the transcriptional profile of M. smegmatis and Mycobacterium tuberculosis. For this reason, we suspected that CarD was directly regulating transcriptional complexes but we did not know at what stage of CarD was functioning and at which genes CarD interacted with the RNAP. To determine in which stage of the transcription cycle (initiation, elongation, or termination) CarD acts, we used Chromatin Immunoprecipitation sequencing (ChIP-seq) to survey the distribution of CarD throughout the M. smegmatis chromosome. Specific antibodies targeting core RNAPb, RNAPσ, or a hemagglutinin (HA) epitope fused to CarD (CarD-HA) were used to co-immunoprecipitate associated DNA. CarD-HA was immunoprecipitated from the M. smegmatis Mc2155 ΔcarD attB::tetcarD-HA strain and unfused HA was immunoprecipitated from the Mc2155 attB::pmsg431 strain with monoclonal antibodies specific for HA (Sigma). RNAP β and σ were immunoprecipitated from M. smegmatis ΔcarD attB::tetcarD-HA with monoclonal antibodies specific for these subunits (Neoclone, Madison, WI; 8RB13 for β, 2G10 for σ). Co-precipitated DNA was sequenced using a SOLiD sequencer (Life Technologies), which provided sufficient reads for 100-fold coverage of the genome. The number of sequence reads per base pair was normalized to the total number of reads and expressed as a log2 value. The reads per base pair from the HA-alone sample served as the background and was subtracted from the other datasets. We found that CarD was never present on the genome in the absence of RNAP. However, whereas RNAP core enzyme was found throughout transcribed regions of the genome, CarD was primarily associated with promoter regions and highly correlated with RNAPσ. The colocalization of σA and CarD led us to propose that in vivo, CarD associates with RNAP initiation complexes at most promoters and is therefore a global regulator of transcription initiation. The genome sequences associated with M. smegmatis CarD, RNAPb, and RNAPs were determined by ChIP-seq analysis. Samples were done in duplicate, except for RNAPs. And sequencing was performed using a SOLiD sequencer (Life Technologies).
2013-08-01 | E-GEOD-48164 | biostudies-arrayexpress
Project description:microRNAs (miRNAs) are small noncoding RNAs that mediate post-transcriptional gene regulation and have emerged as essential regulators of many developmental events. The transcriptional network during early embryogenesis of the purple sea urchin, Strongylocentrotus purpuratus, is well described and would serve as an excellent model to test functional contributions of miRNAs in embryogenesis. We examined the loss of function phenotypes of the major components of the miRNA biogenesis pathway. Inhibition of de novo synthesis of Drosha and Dicer in the embryo led to consistent developmental defects, a failure to gastrulate, and embryonic lethality, including changes in the steady state levels of transcription factors and signaling molecules involved in germ layer specification. We annotated and profiled small RNA expression from the ovary and several early embryonic stages by deep sequencing followed by computational analysis. All miRNAs have dynamic accumulation profiles through early development as do a large population of putative piRNAs (piwi-interacting RNAs). Defects in morphogenesis caused by loss of Drosha can be rescued with four miRNAs which permits a strong miRNA functional assay. Taken together our results indicate that post-transcriptional gene regulation directed by miRNAs is functionally important for early embryogenesis and is an integral part of the early embryonic gene regulatory network in S. purpuratus. Small RNA expression profiling in early sea urchin development
2012-02-17 | E-GEOD-35876 | biostudies-arrayexpress
Project description:Huntington’s disease is a fatal autosomal dominant neurodegenerative disorder, characterized by neuronal cell loss, primarily in the striatum, cortex, and hippocampus, causing motor, cognitive, and psychiatric impairments. Unfortunately, no treatments are yet available to modify the progression of the disease. Recent evidence from Huntington’s disease mouse models suggests that protein phosphorylation (catalysed by kinases and hydrolysed by phosphatases) might be dysregulated, making this major posttranslational modification a potential area of interest to find novel therapeutic targets. Furthermore, environmental enrichment (EE), used to model an active lifestyle in preclinical models, has been shown to alleviate Huntington’s disease-related motor and cognitive symptoms. However, the molecular mechanisms leading to these therapeutic effects are still largely unknown. In this study, we applied a phosphoproteomics approach combined with proteomic analyses on brain samples from pre-motor symptomatic R6/1 Huntington’s disease male mice (HD mice) and their wild-type (WT) littermates, after being housed either in EE conditions, or in standard housing (SH) conditions from 4 to 8 weeks of age (n=6 per group). We hypothesised that protein phosphorylation dysregulations occur prior to motor onset in this mouse model, in two highly affected brain regions, the striatum and hippocampus. Furthermore, we hypothesised that these phosphoproteome alterations are rescued by EE. When comparing 8-week-old HD mice and WT mice in SH conditions, our analysis revealed 229 differentially phosphorylated peptides in the striatum, compared to only 15 differentially phosphorylated peptides in the hippocampus (statistical thresholds FDR0.05, FC1.5). At the same disease stage, minor differences were found in protein expression, with 24 and 22 proteins dysregulated in the striatum and hippocampus, respectively. Notably, we found no differences in striatal protein phosphorylation and protein expression when comparing HD mice and their WT littermates in EE conditions. In the hippocampus, only four peptides were differentially phosphorylated between the two genotypes under EE conditions, and 22 proteins were differentially expressed. Together, our data indicates that protein phosphorylation dysregulations occur in the striatum of HD mice, prior to motor symptoms, and that the kinases and phosphatases leading to these changes in protein phosphorylation might be viable drug targets to consider for this disorder. Furthermore, we show that an early environmental intervention was able to rescue the changes observed in protein expression and phosphorylation in the striatum of HD mice and might underlie the beneficial effects of EE, thus identifying novel therapeutic targets.
2023-03-11 | PXD032205 | Pride
Project description:In mammals, double-stranded RNA (dsRNA) plays roles in sequence-specific RNA interference, sequence-independent interferon response, and RNA editing by adenosine deaminases. We have previously shown that long hairpin dsRNA expression in cultured cells does not activate the interferon response, it is poorly processed into siRNAs, and it is partially edited. Here, we demonstrate that dsRNA expressed from transiently transfected plasmids strongly inhibits expression of co-transfected reporter plasmids but not expression of endogenous genes or reporters stably integrated in the genome. The inhibition is concentration-dependent and independent of a cell type, transfection method, or dsRNA sequence. The inhibition occurs at the level of translation and is mediated by protein kinase R (PKR). PKR binds the expressed dsRNA, becomes phosphorylated and changes its distribution along polysome fractions. In conclusion, we demonstrate that expression from plasmids is selectively repressed if one of co transfected plasmids produces dsRNA. Our results highlight the importance of proper controls and careful interpretation of co-transfection experiments. HEK293 cells (human origin) were transiently transfected with hairpin dsRNA-expressing (MosIR) and control (pCag) plasmids.
2013-12-27 | E-GEOD-46959 | biostudies-arrayexpress
Project description:The mechanisms by which RNA-binding proteins control the translation of subsets of mRNAs are not yet clear. Slf1p is an atypical La motif containing protein (LARP). LARPs are members of a superfamily of RNA-binding proteins conserved across eukaryotes. We performed transcriptomics and RIP-Seq analysis in order to explore the effect of Slf1 on the amount of mRNA of genes involved in the response to oxidative stress.
2015-05-01 | E-MTAB-2567 | biostudies-arrayexpress
Project description:The availability of human genome sequence has transformed biomedical research over the past decade. However, an equivalent map for the human proteome with direct measurements of proteins and peptides was lacking. To this end, Akhilesh Pandey's lab reported a draft map of the human proteome based on high resolution Fourier transform mass spectrometry-based proteomics technology, which included an in-depth proteomic profiling of 30 histologically normal human samples including 17 adult tissues, 7 fetal tissues and 6 purified primary hematopoietic cells ( http://dx.doi.org/10.1038/nature13302 ). The profiling resulted in identification of proteins encoded by greater than 17,000 genes accounting for ~84% of the total annotated protein-coding genes in humans. This large human proteome catalog (available as an interactive web-based resource at http://www.humanproteomemap.org) complements available human genome and transcriptome data to accelerate biomedical research in health and disease. Pandey's lab and collaborators request that those considering use of this primary dataset for commercial purposes contact pandey@jhmi.edu. The full details of this study can be found in the PRIDE database: www.ebi.ac.uk/pride/archive/projects/PXD000561/. This ArrayExpress entry represents a top level summary of the metadata only which formed the basis of the reanalysis performed by Joyti Choudhary's team ( jc4@sanger.ac.uk ), results of which are presented in the Expression Atlas at EMBL-EBI : http://www.ebi.ac.uk/gxa/experiments/E-PROT-1.
2015-03-10 | E-PROT-1 | biostudies-arrayexpress