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Keywords:

  • ADAM33;
  • asthma;
  • disease mapping;
  • linkage disequilibrium;
  • positional cloning;
  • SNP

Background:  ADAM33 has been described to be the first positional cloned asthma gene. Consecutive association studies have found inconsistent results. At present no functional relevant variation is being known.

Objective:  Aim of the study was to test if genes in close physical distance could also be responsible for the observed linkage signal.

Method:  We downloaded three public single-nucleotide polymorphism (SNP) data sets and tested if linkage disequilibrium extends beyond ADAM33.

Results:  Linkage disequilibrium extends upstream to a region including GDNF family receptor alpha (GFRA4), attractin (ATRN) and downstream to sialoadhesin (SN) with a peak recombinatory rate at ADAM33 exon S to V.

Conclusion:  Resequencing of the ADAM33 region including GFRA4, ATRN and SN is expedient.