Kallmann syndrome: adhesion, afferents, and anosmia

Neuron. 2002 May 30;34(5):675-8. doi: 10.1016/s0896-6273(02)00720-1.

Abstract

Three new studies into the function of human anosmin-1 and related proteins in C. elegans and rodents show that these influence axon branching and axon targeting. The rodent anosmin appears to work at two stages of development, initially promoting axon outgrowth from the olfactory bulb and then stimulating branching from axons into the olfactory cortex. CeKal-1 further influences morphogenesis, and, as the human and nematode anosmins are functionally conserved, these studies provide insights into the pathogenesis of Kallmann syndrome (KS).

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Adhesion / genetics
  • Cell Adhesion Molecules / deficiency
  • Cell Adhesion Molecules / genetics
  • Cell Differentiation / genetics*
  • Cell Movement / genetics*
  • Extracellular Matrix Proteins*
  • Humans
  • Kallmann Syndrome / genetics*
  • Kallmann Syndrome / metabolism
  • Kallmann Syndrome / physiopathology
  • Nerve Tissue Proteins / deficiency
  • Nerve Tissue Proteins / genetics
  • Olfaction Disorders / genetics*
  • Olfactory Pathways / abnormalities*
  • Olfactory Pathways / metabolism
  • Olfactory Pathways / physiopathology

Substances

  • ANOS1 protein, human
  • Cell Adhesion Molecules
  • Extracellular Matrix Proteins
  • Nerve Tissue Proteins