Complete ablation of the neurotrophin receptor p75NTR causes defects both in the nervous and the vascular system.

Abstract

We identified a protein isoform of the common neurotrophin receptor p75NTR that arises from alternative splicing of exon III in the p75NTR locus. Because this protein is left intact in the previously described p75NTR mutant mouse line1, we generated a new p75NTR mutant allele. Mice homozygous for this mutation lack both protein isoforms, display severe nervous system defects and reveal a previously unknown role of p75NTR in the formation of blood vessels.