© 2005 BMJ Publishing Group Ltd & British Thoracic Society
Editorial
ADAM33 and asthma
Is big beautiful? The continuing story of ADAM33 and asthma
1 Allergy and Inflammation Research, Division of Infection, Inflammation and Repair, School of Medicine, Southampton General Hospital, Southampton SO16 6YD, UK
2 Division of Human Genetics, School of Medicine, Southampton General Hospital, Southampton SO16 6YD, UK
Correspondence to:
Correspondence to:
Professor S T Holgate
Allergy and Inflammation Research, MP810, Level D, Centre Block, Southampton General Hospital, Southampton SO16 6YD, UK; sth@soton.ac.uk
Role of ADAM33 in the development and progression of asthma
Keywords: asthma; genetics; ADAM33
| The first 150 words of the full text of this article appear below. |
The gene encoding A Disintegrin And Metalloprotease (ADAM) 33 was the first asthma susceptibility gene to be discovered by positional cloning.1 In 460 families enriched with asthma, linkage analysis using microsatellite markers spaced 
9 cM apart revealed a region on chromosome 20p13 that carried one or more asthma genes, achieving a Maximum Lod Score (MLS) of 2.24 at 9.99 cM. The addition of further markers at 1.2 cM increased the MLS to 2.94 at 12.1 cM which further rose to 3.93 when bronchial hyperresponsiveness was included in the definition of asthma despite halving the sample size, thereby exceeding the threshold for genome wide significance. Physical mapping, direct cDNA selection, and sequencing of DNA cloned into bacterial artificial chromosomes (BACs) identified 25 candidate genes. Linkage disequilibrium mapping of single nucleotide polymorphisms (SNPs) on 23 genes spanning the peak of linkage together with case-control and family
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