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Updated: Mar 25, 2026

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Molecular determinants and interaction data of cyclic peptide inhibitor with the extracellular domain of TrkB

Nitin Chitranshi1, Vivek Gupta1, Yogita Dheer1

  • 1Faculty of Medicine and Health Sciences, Macquarie University, F10A, 2 Technology Place, North Ryde, NSW 2109, Australia.

Data in Brief
|February 25, 2016
PubMed

Insights

Cyclotraxin B (CTXB) inhibits brain-derived neurotrophic factor (BDNF) signaling by binding to the TrkB receptor. This study reveals CTXB

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Brain-derived neurotrophic factor (BDNF) is crucial for neuronal growth, differentiation, and maintenance via its high-affinity receptor, TrkB.
  • Understanding TrkB receptor activators and inhibitors, including their binding mechanisms, is vital for elucidating biochemical pathways and protein crystallization studies.

Purpose of the Study:

  • To investigate the binding mechanism and interaction parameters of Cyclotraxin B (CTXB) with the TrkB receptor.
  • To determine the critical residues involved in CTXB-TrkB interaction using molecular modeling and docking.

Main Methods:

  • Generation of a molecular model for CTXB.
  • Docking of the CTXB molecular model with the TrkB receptor domain.

Main Results:

  • CTXB, a cyclic peptide, interacts with the TrkB receptor.
  • CTXB inhibits downstream signaling pathways activated by BDNF/TrkB.
  • Identification of critical residues mediating CTXB-TrkB interaction.

Conclusions:

  • This study provides the first report on the binding mechanism and interaction parameters of CTXB with the TrkB receptor.
  • The findings contribute to understanding the pharmacological regulation of BDNF/TrkB signaling and offer insights for drug development targeting neurotrophic pathways.
Keywords:
Cyclotraxin BDockingGSK3βTrkB

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