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.