Georg Fuellen

This study shows that fertilization can reverse the negative effects of maternal age on oocyte quality in mice, provided the fertilization environment is not aged.

This study shows that ZP2, a zona pellucida protein, is re-synthesized and functionally required in mouse embryos, playing an active role in blastocyst formation and cell lineage development.

This paper performs a harmonised meta-analysis of rapamycin's effects on the mouse gut microbiome, identifying reproducible taxonomic shifts and dose-dependent responses.

The paper identifies natural compounds that mimic dasatinib's senotherapeutic effects using gene expression data, highlighting potential alternatives for senolytic therapy.

The paper shows that the orientation of the first cleavage in mouse oocytes follows the shorter diameter of the unfertilized oocyte, leading to segregation of animal and vegetal hemispheres and explaining differences in monozygotic twins.

This study identifies a novel intracellular function of zona pellucida proteins in mice, showing they are critical for embryonic cell survival during the oocyte-to-embryo transition.

The paper identifies conserved healthspan-related gene modules across species using co-expression network analysis and meta-analysis of transcriptomic data.

The paper compiles healthspan-related gene pathways in C. elegans and humans using literature review and molecular interaction data, identifying common themes like transcription and lipids.

The paper integrates multi-omics data to analyze gene expression dynamics in mouse embryos, revealing discrepancies between transcript and protein levels during early development.

This study shows that a mutation in mt-Nd2, a mitochondrial complex I gene, reduces lifespan and increases glucose intolerance in mice by affecting tryptophan levels and aging pathways.

The paper describes a method using pathway maps to analyze omics data, focusing on cellular senescence and its role in disease.

This study shows that high mitochondrial heteroplasmy in mice reduces lifespan and impairs glucose metabolism.

The paper shows that combining mitochondrial tRNA and OXPHOS mutations in mice leads to reduced lifespan and physical condition with age, but not with single mutations.