Jeroen Demmers

This study shows that tubulin overexpression causes proteostasis defects and replication stress by disrupting mitochondrial translation and cell cycle regulation.

This study uses proteomics to show that USP7's deubiquitylation effects are substrate-specific, revealing its role in neurodevelopment and tumor suppression.

The paper shows that the SHANK3-CAMSAP2 interaction links synapses to dendritic microtubule organisation in parvalbumin neurons, with the SHANK3L68P mutation enhancing this interaction and altering microtubule dynamics.

The paper shows that X-chromosome upregulation occurs gene-by-gene at both RNA and protein levels in mouse pluripotent stem cells.

This study identifies HCFC1 and YY1 as factors that recruit COMPASS and Integrator complexes to initiate X chromosome inactivation by regulating Xist and its cis-regulatory elements.

This study identifies KIF2A's role in maintaining cytokinesis in mouse embryonic stem cells by stabilizing intercellular bridge microtubules, which prolongs cytokinesis to support pluripotency.

This study examines how saliva from different mosquito species affects human endothelial cell permeability and West Nile virus pathogenesis in mice, finding that certain salivary proteases enhance virus transmission.

This study identifies the ADNP-KDM1A-GTF2I complex as critical for neural differentiation balance in HVDAS by repressing transposable elements and regulating gene transcription.

The paper identifies USP7's role in neuronal differentiation by regulating BCOR-ncPRC1.1, revealing a shared epigenetic network in neurodevelopmental disorders.

This study characterizes cytotrophoblast dynamics during pregnancy using single-cell RNA sequencing, identifying distinct subsets and their functional roles.

This study identifies bi-allelic XPNPEP3 variants causing mitochondrial disease with pediatric cardiomyopathy, revealing impaired mitochondrial protein processing as the underlying mechanism.

This study identifies USP53 and USP54 as active deubiquitinases specific for K63-linked polyubiquitin, revealing their role in regulating tricellular junctions and correcting previous annotations of them as pseudo-enzymes.

The paper identifies novel endogenous CAMK2 substrates by analyzing phosphoproteomic data from double knockout mice.

This study identifies ROPN1 as a target for TCR-engineered T-cells effective against TNBC in preclinical models and demonstrates their safety and efficacy.

This study identifies STK19 as a critical factor in transcription-coupled nucleotide excision repair by stabilizing the repair complex and promoting Pol II ubiquitylation and TFIIH recruitment.

This study identifies PCID2 as a novel HIV-1 latency-promoting factor that represses transcription and dysregulates viral RNA processing through its role in the TREX2 complex.

This study identifies LRP10 interactors and pathways, showing its role in autophagy and NDFIP1-mediated alpha-synuclein secretion, with differences between LRP10-WT and LRP10-Splice variants.

Catchet-MS identifies thalidomide analogues targeting IKZF1 as novel HIV-1 latency reversal agents by reversing latency in CD4+ T-cells.

This study shows that GTF-2H5 is essential for DNA repair in C. elegans but not for viability, highlighting its role in transcription and repair processes.

The paper shows ATP hydrolysis enables chromatin remodeler release, allowing continuous genome probing by limiting BRM chromatin binding.

This study identifies RPH3A as a novel UBE3A ubiquitination target and shows that UBE3A mono-ubiquitination of RPH3A does not mediate degradation.

The paper shows that synaptic ER stabilization depends on calmodulin and caldendrin regulating myosin V activity to control spine apparatus formation in active dendritic spines.

This study shows XAB2 interacts with ERCC1-XPF and XPG to process RNA-loops during mammalian development, linking splicing and DNA repair.

This study identifies myosin V as essential for synaptopodin clustering at post-synaptic sites, showing that the spine apparatus is assembled locally rather than transported.

This study identifies HSF2BP as a regulator of homologous recombination in ICL repair by interacting with BRCA2, showing its role in genomic instability and cancer.