Jeroen Krijgsveld

R2T2P integrates transcriptomics and proteomics data to study FSHD, revealing novel RNAs and their impact on translation and protein levels.

The paper shows EWSR1::FLI1 fusion drives the production of cancer-specific neoproteins in Ewing sarcoma, revealing a reversible dark proteome with therapeutic potential.

This study identifies MAGEL2-driven defects in human corticogenesis shared between Prader-Willi and Schaaf-Yang syndromes using multi-omics profiling of induced neurons.

The paper uses CRISPR screens to identify regulators of immunosuppressive surface molecules in cancer cells, finding DNAJC13 as a key regulator that enhances T-cell sensitivity and tumor survival.

The paper shows that inflammatory injury leads to polyploid pancreatic acinar cells with CIN and STING loss, contributing to tissue repair and cancer risk.

The paper identifies semaphorin 3A as a secreted factor from revitalized MSCs that regulates HSPC proliferation in steady state and stress conditions.

This study identifies PTPRK as a gene modulated by TMPRSS2::ERG fusion and a regulatory SNP, showing its role in prostate cancer progression and potential as a biomarker.

The paper uses a patient-derived rectal cancer organoid platform to identify MEK and PARP inhibitors that synergize with radiation to enhance treatment response in locally advanced rectal cancer.

This study shows MEK1/2 inhibitors reduce AXIN1 levels in CRC by mTOR-dependent translational repression, not by affecting protein stability.

This study shows that p53 deficiency causes hypertranscription and nucleotide insufficiency, leading to replication stress and genomic instability, including chromothripsis.

The paper identifies CACNA2D2 as a super-enhancer-driven target of EWSR1::WT1 and demonstrates its utility as a diagnostic biomarker for DSRCT.

The paper introduces iPOC, a method to isolate DNA-bound proteins, and applies it to study changes in the DNA-bound proteome upon perturbation of the PI3K/AKT/mTOR pathway.

The paper introduces a method to identify direct protein substrates of small-molecule degraders using degradome analysis and mass spectrometry.

The paper shows that oxytocin-induced astrocyte process retraction in the amygdala modulates freezing behavior during stress by enhancing neuronal sensitivity to potassium.

The paper identifies essential RNA modifications in cancer using CRISPR screens and finds that mitochondrial metabolic plasticity influences drug resistance through specific RNA modifications.

The paper introduces a single-sample workflow, MTBE-SP3, for simultaneous proteomic and metabolomic analysis, showing it reduces technical variation and enables consistent results across biological matrices.

This paper introduces a deep learning model called Proformer for classifying bulk and single-cell proteomic samples, showing improved performance over existing methods.

The paper introduces DIA-ME, a method for single-cell proteomics that improves sensitivity and data completeness, revealing co-existing cell states in response to IFN-gamma.

This paper develops a workflow called QuaNPA for analyzing newly synthesized proteins, showing its application in studying the cellular response to interferon-gamma.

IceR improves proteome coverage and data completeness in global and single-cell proteomics by combining DDA's identification rates with DIA's low missing value rates.

The paper analyzes 3'UTR changes during neuronal differentiation and in ASD, finding longer 3UTRs in ASD patients and a role for CPEB4 and APLP1 in APA regulation.

The paper introduces autoSP3, an automated proteomics workflow for low-input clinical samples, demonstrating reproducible quantification of 500-1000 proteins from 100-1000 cells and application to FFPE lung cancer samples.

The paper introduces XRNAX, a method to purify protein-RNA complexes, and shows it captures all RNA biotypes and reveals dynamic changes in the RNA-bound proteome during arsenite-induced stress.

The paper quantifies host proteome dynamics during Salmonella infection, revealing cathepsin-dependent cell death mechanisms.