Complete ablation of the neurotrophin receptor p75 super(NTR) causes defects both in the nervous and the vascular system

We identified a protein isoform of the common neurotrophin receptor p75 super(NTR) that arises from alternative splicing of exon III in the p75 super(NTR) locus. Because this protein is left intact in the previously described p75 super(NTR) mutant mouse line, we generated a new p75 super(NTR) mutant allele. Mice homozygous for this mutation lack both protein isoforms, display severe nervous system defects and reveal a previously unknown role of p75 super(NTR) in the formation of blood vessels.