G. F. Spaeth

This study shows that inhibiting LSD1 in macrophages reduces Leishmania parasite load and reverses infection-induced transcriptomic changes.

This study shows Leishmania amazonensis suppresses macrophage-regulated cell death pathways to promote chronic infection in vitro and in vivo.

This study identifies IGF2BP2 as an m6A reader that stabilizes glycolytic transcripts in Leishmania-infected macrophages, promoting HIF-1-independent glycolysis and immune-metabolic reprogramming.

This study identifies oxidative DNA damage signatures in Leishmania donovani during sand fly infection, linking them to allelic and haplotype selection through genomic analysis.

SILAkin identifies kinase substrates using a combination of phosphatase treatment, pulse heating, IVKA, and SILAC-based MS, revealing 225 host substrates phosphorylated by pathogen-excreted kinases.

This study shows that post-transcriptional regulation, not just genome instability, drives fitness gain in Leishmania parasites during in vitro adaptation.

This study identifies low complexity regions in the C-terminus of Leishmania CK1.2 as essential for its subcellular localization but not activity, revealing new insights into its role in parasite biology.

This study shows that Leishmania-infected macrophages undergo pyroptosis, exposing amastigotes to the extracellular environment, which may aid parasite spread.

This study shows Leishmania amazonensis modulates macrophage epigenetics to suppress NF-κB and NLRP3 inflammasome activation, aiding parasite survival.