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Choroid plexus proteome with and without LPS

ABSTRACT: Choroid plexus was isolated and pooled from the 5 mice after the perfusion with bromo phenol blue from 0 h and 6 h LPS treated mice. Proteins were isolated and trypsin digested and labelled with the NHS-porp (0h –LPS and 6h +LPS). Pre-fractionated using RP-HPLC and analysed on the Qexactive.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cerebrospinal Fluid

SUBMITTER: Sriram Balusu

LAB HEAD: Kris Gevaert

PROVIDER: PXD001347 | Pride | 2016-09-27

REPOSITORIES: Pride

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			Action	DRS
	E05119_1d_3943_sriram_CPE-1-1_140707121334.raw	Raw
	E05120_1d_3943_sriram_CPE-1-2_140707130816.raw	Raw
	E05121_1d_3943_sriram_CPE-1-3_140707140259.raw	Raw
	E05122_1d_3943_sriram_CPE-1-4_140707145741.raw	Raw
	E05123_1d_3943_sriram_CPE-1-5_140707155223.raw	Raw

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1 - 5 of 140

Publications

Identification of a novel mechanism of blood-brain communication during peripheral inflammation via choroid plexus-derived extracellular vesicles.

Balusu Sriram S Van Wonterghem Elien E De Rycke Riet R Raemdonck Koen K Stremersch Stephan S Gevaert Kris K Brkic Marjana M Demeestere Delphine D Vanhooren Valerie V Hendrix An A Libert Claude C Vandenbroucke Roosmarijn E RE

EMBO molecular medicine 20161004 10

Here, we identified release of extracellular vesicles (EVs) by the choroid plexus epithelium (CPE) as a new mechanism of blood-brain communication. Systemic inflammation induced an increase in EVs and associated pro-inflammatory miRNAs, including miR-146a and miR-155, in the CSF Interestingly, this was associated with an increase in amount of multivesicular bodies (MVBs) and exosomes per MVB in the CPE cells. Additionally, we could mimic this using LPS-stimulated primary CPE cells and choroid pl ...[more]

PMID: 27596437

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Exosomal proteome from mouse CSF

Project description:Exosomes were isolated from the mouse CSF using total exosome isolation kit (Life Technologies) from 0h and 6h LPS treated mice. These exosomes were separated on the RP-HPLC in to 20 fractions and analysed on the Qexactive.

2016-09-27 | PXD001346 | Pride

Cell-intrinsic regulation of interneuron migration controls cortical neurogenesis

Project description:Interneurons navigate along multiple tangential paths to settle into appropriate cortical layer. They undergo saltatory migration, which is paced by intermittent nuclear jumps whose regulation relies on interplay between extracellular cues and genetic-encoded information. However, it remains unclear how cycles of pause and movement are coordinated at the molecular level. Post-translational modification of proteins contributes to cell migration regulation. The present study uncovers that carboxypeptidase 1, which promotes deglutamylation, is a pivotal regulator of pausing of cortical interneurons. Moreover, we show that pausing during migration controls the flow of interneurons invading the cortex by generating heterogeinity in movement at the population level. Interfering with the regulation of pausing not only affects the size of the cortical interneuron cohort but also secondarily impairs the generation of age-matched upper layer projection neurons.

2018-02-14 | PXD006397 | Pride

Quantitative Proteomic Analysis of C57BL/6J mice after optic nerve crush Using iTRAQ Labeling

Project description:We used two groups of C57BL/6J mice, one with optic nerve crush on one eye, and another with no crush as control. Three mice were subjected to optic nerve crush, with sample names 121, 113, 114 and two were used as control with sample names 118 and 119. For the optic nerve crush, a surgical peritomy was made behind and above the eyeball and the eye muscles were gently retracted to expose the optic nerve. Dumont #5 forceps (FST) were used to crush the optic nerve approximately 0.5-1 mm behind the globe without damaging retinal vessels or affecting the blood supply.

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The dynamics of protein-bound methionine oxidation events in Arabidopsis thaliana during oxidative stress

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N-Acetylation of secreted proteins is widespread in Apicomplexa and independent of acetyl-CoA transporter AT1

Project description:Acetyl-CoA critically participates in post-translational modification of proteins, central carbon and lipid metabolism in several compartments of eukaryotic cells. In mammals, the acetyl-CoA transporter 1 (AT1) facilitates the flux of cytosolic acetyl-CoA into the endoplasmic reticulum (ER) enabling the acetylation of proteins of the secretory pathway in concert with dedicated acetyltransferases including Nat8. Homologues of AT1 and Nat8 were identified in the apicomplexan parasites Toxoplasma gondii and Plasmodium berghei. However, the implication of acetyl-CoA pool influx into the ER in acetylation of ER-transiting proteins and their relevance throughout the parasites’ life cycle is unknown. Here, we report proteome-wide analyses, which revealed unprecedented widespread N-terminal acetylation marks of secreted proteins in both parasites. Deletion of the gene coding for AT1 in both parasites, resulted in global loss of fitness and in addition to retardation in erythrocytic development, malaria parasites are blocked in transmission to mosquitoes. However, in absence of AT1 proteome wide lysine and N-terminal acetylation modifications remain unaltered. This highlights a role of AT1 in parasite development uncoupled to acetylation capacity, indicative of an unusually active acetylation machinery occurring in the ER of Apicomplexa.

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Human PBMNCs: Control vs. Patients with Kawasaki disease

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Targeting the lineage-specific long non-coding RNA LINC01212 as an effective anti-melanoma therapeutic strategy

Project description:Focal amplifications of 3p13-3p14 occur in about 10% of melanoma and are associated with poor prognosis. The melanoma-specific oncogene MITF resides at the epicenter of this amplicon1 . However, whether other loci present in this amplicon also contribute to melanomagenesis is unknown. Here we show that the recently annotated long non-coding RNA gene LINC01212 is consistently cogained with MITF. In addition to being amplified, LINC01212 is a target of the lineage-specific transcription factor SOX10 and, consequently, it is expressed in more than 90% of human melanomas, but not in normal adult tissues. Whereas exogenous LINC01212 functions in trans to increase melanoma clonogenic potential, LINC01212 knock-down drastically decreases the viability of melanoma cells irrespective of their transcriptional cell state, BRAF, NRAS or TP53 status and increases their sensitivity to MAPK-targeting therapeutics both in vitro and in Patient-Derived Xenograft (PDX) models. Mechanistically, LINC01212 interacts with p32, a master regulator of mitochondrial homeostasis and metabolism, to increase its mitochondrial targeting and pro-oncogenic function. Our results indicate that targeting the lineage addiction oncogene LINC01212, especially in combination with BRAFV600Einhibitors, disrupts vital mitochondrial functions in a cancer-cell specific manner and is therefore expected to deliver highly effective and tissuerestricted anti-melanoma therapeutic responses.

2016-01-13 | PXD002565 | Pride

Novel surface functionalized superparamagnetic nanoparticles with engineered cellular uptake as a means for intracellular omics

Project description:Superparamagnetic nanoparticles (SPMNPs) are appealing for use in organelle isolation strategies. Yet, this potential remains largely unexplored because thus far research has focused on either physicochemical design or on their application in micron-sized beads. For their use in life sciences, the biocompatibility of SPMNPs goes beyond their chemical composition and shape, and features like their size and more importantly their surface properties are becoming more important to exploit extra- and intracellular interactions. Here we introduce thermal decomposition to manufacture iron oxide based SPMNPs (Ø10nm) and demonstrate how different surface functionalizations can lead to different types of cellular interactions. Cationic aminolipid-coated SPMNPs reside surprisingly strong at the outer cell surface. In contrast, anionic dimercaptosuccinic acid-coated SPMNPs are efficiently internalized and accumulate in a time-dependent manner in endosomal and lysosomal populations. These features allowed us to establish a standardized magnetic isolation procedure to selectively isolate plasma membranes and intracellular late endosomes/lysosomes with high yields and purities as consolidated by biochemical and ultrastructural analyses. Subsequent quantitative and qualitative proteome analysis underpins the overall high enrichment for hydrophobic (membrane) proteins as well as plasma membrane and lysosomal constituents in the respective purified fractions. This nano based technology provides therefore a breakthrough in the field of subcellular ‘omics’ as it allows the identification of subtle alterations in the biomolecular composition of different SPMNP-isolated compartments that would be otherwise not detected in total cell or tissue analysis.

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The Nuclear-retained non-coding RNA MALAT1 regulates alternative splicing by modulating SR splicing factor phosphorylation

Project description:Alternative splicing (AS) of pre-mRNA is utilized by higher eukaryotes to achieve increased transcriptome and proteomic complexity. The serine/arginine (SR) splicing factors regulate tissue- or cell type-specific AS in a concentration and phosphorylation dependent manner. However, the mechanisms that modulate the cellular levels of active SR proteins remain to be elucidated. In the present study, we provide evidence for a role for the long nuclear-retained regulatory RNA (nrRNA), MALAT1 in AS regulation. MALAT1 interacts with SR proteins and influences the distribution of these and other splicing factors in nuclear speckle domains. Depletion of MALAT1 changes AS of endogenous pre-mRNAs, similar to what was observed upon overexpression of SR proteins. Furthermore, MALAT1 regulates cellular levels of phosphorylated forms of SR proteins. Taken together, our results suggest that MALAT1 regulates AS by modulating the levels of active SR proteins. Our results further highlight a novel role for a nrRNA in the regulation of gene expression. Malat1 Antisense and control knockdowns evaluated on a microarray platform to profile alternative splicing levels for 5782 cassette-type alternative exons.

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