Birgit Schilling

This study identifies a proteomic signature of aging in female skeletal muscle linked to physical function decline using proteomic profiling and clinical measurements.

This study identifies that plasma proteins selectively reflect tissue-specific aging processes in muscle and ovary, revealing context-dependent age-related changes.

This study identifies age-related molecular changes in postmenopausal ovaries using proteomics, revealing dynamic remodeling and new biological insights.

This study shows that acute LINE-1 overexpression in human fibroblasts causes widespread changes in transcriptome, proteome, and secretome, affecting cell cycle and interferon pathways, beyond retrotransposition.

This study identifies RECS1 as a structural component of the exosomal trafficking machinery and shows it modulates extracellular vesicle biogenesis through a channel-independent mechanism.

This study shows that oral DBM treatment prevents cognitive decline in a C9ORF72 FTD mouse model without altering protein inclusions but corrects gene expression changes related to cytoskeleton, ALS, and metabolism.

This study identifies PCSK5A and GDF9 as key regulators of cumulus-oocyte-complex matrix integrity and cumulus cell migration during late ovulation, with implications for fertility therapeutics.

The paper identifies distinct fibroblast and perivascular senescence subtypes in fibrosis using single-cell and spatial transcriptomics, showing their spatial organization and roles in fibrosis progression.

This paper develops a proteomic workflow to confidently identify and quantify lysine methylmalonylation in mouse brain tissue, revealing its regulation by SIRT5 and its role in myelin stability.

The paper uses single-nucleus profiling to show age-related changes in the postmenopausal ovary, which are counteracted by parity.

This study shows that γδ17 T cells influence fibrosis by altering ECM composition and vascularity through interactions with stromal cells.

This study shows APOE4 affects female bone quality more than male bone, without structural changes, by disrupting osteocyte function.

This study shows that human brain aging involves asymmetric remodeling of the insoluble proteome, with intermediate-stability aggregates accumulating and being linked to neurodegenerative disease.

The paper uses spatial proteomics to show age-related delays in fracture healing by analyzing extracellular matrix composition in young and aged mice.

This study uses PAMAF mode HRIM-MS to quantify succinylation sites in mouse kidney, showing Sirt5 regulates succinylation of mitochondrial proteins involved in metabolism.

The paper identifies a distinct p16INK4a-associated senescence signature in human ovarian tissue through proteogenomic profiling and spatial analysis.

The paper identifies age-associated Th2-like CD8 memory T cells in human blood and links their accumulation to health conditions like asthma and diabetes.

This study uses spatial mass spectrometry imaging to identify ECM peptide markers distinguishing OA-affected subchondral bone from healthy tissue and less affected regions.

This study shows that tau oligomers cause progressive synapse dysfunction by initially weakening both presynaptic and postsynaptic components, followed by synaptic loss.

This study shows that overexpressing an Alu transposon in human fibroblasts causes widespread disruptions in aging-related pathways across transcriptome, proteome, and secretome.

The paper identifies and maps senescent cells in postmenopausal ovaries using p16 expression and spatial transcriptomics, revealing a fibro-inflammatory signature associated with aging.

This paper shows that altering the gut microbiome changes bone matrix proteomics and reduces fracture toughness, with micropillar splitting as a precise method to measure these effects.

This study shows that feeding mice odd-chain dicarboxylic acids reproduces the biochemical features of glutaric aciduria type-1.

This paper develops a proteomic workflow using data-independent acquisitions to analyze APOE3-derived neurons and microglia, identifying cell type-specific markers and pathways.

This study uses single-cell RNA sequencing to identify immune changes in the colon of Alzheimer's disease mice, finding reduced antibody-secreting cells and altered immune trafficking.

This study identifies functionally distinct senescent cell subpopulations based on cell cycle status, showing G2-arrested cells secrete more IL-6 and are more sensitive to senolytic treatment.

This study identifies aging-associated proteomic and lipid signatures in exosomes from senescent cells and human plasma, revealing shared biomarkers and pathways linked to senescence and tissue damage.

The paper identifies a fibroblast state called STIF that drives YAP-dependent regenerative programs and (pre)malignancy through mechanotransduction in response to tissue injury.

This study identifies age-related dysregulation of the splicing machinery in older AML patients through proteomic analysis, highlighting potential targets for age-specific therapies.