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1.
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Highlights
  • •TOP: robust, bio-friendly FFPE proteome extraction method with less fixation bias.
  • •Proteome of MSI-H colorectal cancer identifies immunobiology key elements.
  • •MSI-H tumor displays an “INFg-STAT1 centric signature”.
  • •Long-term IFNg induction In-vitro mimicks MSI-H signature.
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2.
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Highlights
  • •Sufficient tumor tissues are often unavailable large HLA peptidome discovery.
  • •Using patient derived xenograft (PDX) tumors can overcome this limitation.
  • •The large PDX HLA peptidomes expand significantly those of the original biopsies.
  • •The HLA peptidomes of the PDX tumors included many tumor antigens.
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3.
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Highlights
  • •In depth performance assessment of leading tools for differential protein abundance.
  • •Novel fast modular framework MSqRobSum for robust protein summarization and inference.
  • •MsqRobSum outperforms leading protein summarization-based tools.
  • •MSqRobSum is on par with top-performing peptide based tool MSqRob.
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4.
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Highlights
  • •Organelle profiling maps capture localizations of 1000s of proteins in one experiment.
  • •Comparing maps +/− perturbation reveals disease mechanisms & cellular responses.
  • •A conceptual guide to planning and interpreting organellar profiling experiments.
  • •A cross-study consensus set of human organellar marker proteins.
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5.
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Highlights
  • •Monocytes are isolated from single donors after apheresis.
  • •Monocytes process CD16a and CD32a N-glycosylation differently by site and donor.
  • •CD16a with hybrid and oligomannose type N-glycans bind IgG1 Fc with stronger affinity than complex type.
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6.
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Highlights
  • •Proteomics uncovers the flow-induced remodeling of the endothelial basement membrane.
  • •Flow alters the composition and localization of the laminin-integrin network.
  • •Flow induces proteolytic processing of LAMA4, resulting in shedding of LG4–5 region.
  • •TNFα- and flow-exposure induce a distinct proteomic signature with limited interplay.
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7.
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Highlights
  • •Brain membrane protein extraction.
  • •Protein prenylation.
  • •Prenyl peptide capture and characterization by LC-MS/MS.
  • •HCD and EThcD peptide fragmentation.
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8.
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Highlights
  • •Label-free and dimethyl labeling MS analysis of 6 RBPs from Drosophila ovaries.
  • •Functionally related RBPs show overlapping proteomes.
  • •Selective co-purification of splicing factors and translational regulators.
  • •Validation of 26 novel interactions by co-immunoprecipitation.
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9.
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Highlights
  • •Two molecular groups in anal squamous carcinoma according proteomic profile.
  • •Differences in possible targeted processes such as metabolism or immune response.
  • •Different percentage of tumor lymphocyte infiltration.
  • •Difference in the frequency of ATM variants, related to PPAR inhibitors.
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10.
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Highlights
  • •Summarize the development of functional protein microarray.
  • •Application of functional proteome microarray in basic research.
  • •Application of functional proteome microarray in translational research.
  • •Fabrication of functional membrane protein array using virion display method.
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11.
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Highlights
  • •Highly parallelizable 4D feature detection in ion mobility enhanced shotgun proteomics.
  • •Multidimensional non-linear mass, retention time and ion mobility recalibration.
  • •Collision cross section aware matching between runs.
  • •Label-free quantification of ion mobility MS data.
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12.
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Highlights
  • •EGFR-TKI molecular response profiling covering 10138 proteins and 13486 mRNAs.
  • •EGFR-TKI combination therapy screen using a library of 528 compounds.
  • •Several new candidate EGFR-TKI escape mechanisms and combination therapy targets.
  • •Combined targeting of the oncogene BCL6 and EGFR results in synergy in NSCLC cells.
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13.
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Highlights
  • •Quantitative proteomics and machine learning to study plasma biomarkers in HCM.
  • •Six peptides are increased in plasma of LVH+ HCM compared to controls.
  • •Peptide biomarkers correlate with imaging markers of phenotype severity.
  • •Peptide biomarkers correlate with the estimated sudden cardiac death risk.
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14.
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Highlights
  • •Comprehensive molecular profiling of cutaneous and cerebellar metastasis variants.
  • •Identification of differentially regulated metastasis-associated molecules.
  • •Evidence for individually distinct patterns of metastasis-associated molecules.
  • •Highlighting the evident need for establishing meta-analyses strategies.
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15.
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Highlights
  • •Cecal Ligation Puncture (CLP) mouse model to study sepsis-induced kidney disease.
  • •Quantitative global proteome and phosphoproteome profiling of mouse kidneys.
  • •Highly significant candidate markers for onset and progression of AKI to CKD.
  • •Mechanistic insights into sepsis-associated kidney injuries.
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16.
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Highlights
  • •Signaling networks can be highly heterogeneous across cells in a tissue.
  • •Various technologies allow analyzing signaling networks at single-cell resolution.
  • •The advantages and limitations of each single-cell approach are summarized.
  • •Confounding factors in single-cell signaling network analysis are discussed.
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17.
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Highlights
  • •PRMT5 glutathionylation is increased in aged mice or under oxidative stress.
  • •Deglutathionylation of PRMT5 is catalyzed by glutaredoxin-1.
  • •PRMT5 glutathionylation decreases its methyltransferase activity.
  • •PRMT5 glutathionylation results in G2/M arrest and inhibits cell proliferation.
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18.
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Highlights
  • •Co-elution stands out as a global interactome mapping method.
  • •Benefits include all-to-all protein analysis and measurement of interactome perturbations.
  • •Different separation, quantification and bioinformatic strategies are available.
  • •Design considerations depend largely on system under study.
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19.
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Highlights
  • •Quantitative proteomics of isolated lysosomes, autophagosomes and proteasomes.
  • •Pharmacological inhibition of proteasomes leads to their accumulation within lysosomes.
  • •Inhibition of classical autophagy pathways cannot completely block this process.
  • •Known autophagy adaptor proteins are not involved.
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20.
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Highlights
  • •cGAS acetylations and phosphorylations under basal and immune-stimulated states.
  • •K384 and K414 acetylations and S305 phosphorylation inhibit cGAS-mediated apoptosis.
  • •Acetylation at K198 stimulates cGAS-dependent interferon signaling.
  • •K198 acetylation is decreased upon herpesvirus infection.
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