Sara Anna Dochnal

This study shows that TLR-4 enhances TRPV1-mediated calcium influx in DRG neurons through PKA signaling, contributing to pain hypersensitivity.

The paper develops a human-derived in vitro model of nociceptive signaling using HD10.6 cells to study pain mechanisms and drug responses.

This study identifies SEMA4D and OSM as mediators of neutrophil-neuron communication in arthritis-induced pain, showing their role in neuronal sprouting and hypersensitivity.

This study shows that H2AK119ub1, deposited by PRC1, is critical for HSV-1 reactivation from latency, while H3K27me3 is not.

This study evaluates the analgesic effects of intrathecal NaV 1.7 antisense oligonucleotides in rats, showing reduced channel binding and pain behaviors with concentration-dependent knock-down of Scn9a mRNA.

This study shows HSV-1 UL12.5 promotes reactivation by inducing mitochondrial nucleic acid sensing, which activates innate immune pathways and supports lytic gene expression during latency exit.

This study shows that culturing primary neurons at physiological oxygen levels (5%) improves neuronal health and reduces HSV-1 reactivation without affecting latency establishment.

This study investigates the association of HSV-1 genomes with H3K27me2 and PHF20L1 in fibroblasts, finding that H3K27me2 is linked to genome silencing and that this association is influenced by demethylase activity and transcriptional state.

This study shows c-Jun signaling during HSV-1 initial infection promotes latency and enhances later reactivation by facilitating the transition from Phase I to Phase II reactivation.