An intracellular domain fragment of the p75 neurotrophin receptor (p75 NTR) enhances tropomyosin receptor kinase A(TrkA) receptor function

Abstract

Background: The mechanism by which the p75 neurotrophin receptor (p75 NTR) and TrkA interact to enhance neurotrophin signaling is unknown. Results: The p75NTR intracellular domain fragment, p75ICD, but not full-length p75NTR enhanced NGF binding to TrkA and neurite outgrowth. Conclusion: The results suggest that p75ICD causes a conformational change within the extracellular domain of TrkA. Significance: The findings challenge our current understanding of how p75NTR enhances neurotrophic activity. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.