Reactome: A Curated Pathway Database

p75NTR regulates axonogenesis (R-HSA-193697)

Species Homo sapiens


p75NTR modulates axonal growth by regulating the activity of small GTPases like RHOA and RHOB, that control the state of actin polymerization. The best studied is RHOA. In its active, GTP-bound form, RHOA rigidifies the actin cytoskeleton, thereby inhibiting axonal elongation and causing growth cone collapse. Depending on the ligand that binds to it, p75NTR can either promote or inhibit axonal growth, Neurotrophin binding leads to inhibition of RHOA activity and axonal growth. Axonal growth inhibition is caused by myelin molecules named MDGIs (myelin-derived growth inhibitors), such as NOGO, MAG, OMGP. MDGIs bind to a complex made up of p75NTR and the NOGO receptor, causing RHOA activation and axonal growth inhibition.

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Additional Information
GO Biological Process regulation of axonogenesis (0050770)
Literature References
pubMedId Title Journal Year
17335080 Roles of glial p75NTR in axonal regeneration J Neurosci Res 2007