Jing Zhao

The paper identifies analgesic targets in mouse sensory neurons by analyzing translatomes in somata and terminals under different pain conditions.

The paper compares genetic and pharmacological loss-of-function mechanisms of Nav1.7 analgesia, highlighting distinct opioid-dependent and -independent pathways in embryonic and adult stages.

This study identifies 261 proteins interacting with human Nav1.7, revealing shared and distinct interactions with mouse Nav1.7 and their functional roles in pain signal regulation.

The paper profiles transcriptomic and proteomic data from NaV1.8-expressing mouse nociceptors, identifying 353 transcripts and 78 proteins, and finds moderate correlation between proteome and transcriptome datasets.

This study identifies opioid-dependent inhibition of neurotransmitter release as the primary mechanism of analgesia in NaV1.7 null mutants in mice and humans.

This study shows that Nav1.7 from sensory neurons affects dorsal horn neuron excitability, with functional effects not predicted by mRNA levels.

The paper identifies 267 NaV1.7-associated proteins in mice using epitope-tagged gene targeting and mass spectrometry, including novel interactors validated by co-immunoprecipitation and functional assays.

This study shows that BDNF from peripheral sensory neurons is critical for transitioning acute to chronic pain.

The paper shows that increased intracellular sodium inhibits fentanyl's effect on Nav1.8 currents in sensory neurons.