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© 1994 Oxford University Press

OTHER

Characterization of a new member of the human /-adaptin gene family from chromosome 22q12, a candidate meningioma gene

Myriam Peyrard1, Ingegerd Fransson1, Ya-Gang Xie1, Fei-Yu Han1, Martin H.Ruttledge1,2, Sofie Swahn1, John E. Colllns3, Ian Dunham3, V.Peter Collins2,4 and Jan P.Dumanski1,*

1Department of Molecular Medicine, Clinical Genetics Unit, Karolinska Hospital L-6 Building, S-171 76 Stockholm 2Ludwig Institute for Cancer Research, Stockholm Branch, Clinical Unit, Karolinska Hospital S-171 76 Stockholm, Sweden 3Sanger Centre, Hinxton Hall Hinxton, Cambridge CB10 1RQ, UK 4Department of Pathology, Karolinska Hospital S-171 76 Stockholm, Sweden

*To whom correspondence should be addressed

Received April 29, 1994; Accepted June 13, 1994

A 140 kb homozygous deletion from 22q12 In one menlngioma directed us towards the cloning and characterization of a new member of the human ß-adaptln gene family (named BAM22). Adaptins are essential for the formation of clathrin coated vesicles in the course of intracellular transport of receptor-ligand complexes. The BAM22 gene is totally inactivated In the tumor with homozygous deletion. Northern blot analysis of 70 sporadic meningiomas showed specific loss of expression in 8 tumors, suggesting inactivation of BAM22. Based on this, we propose BAM22 as a second chromosome 22 locus Important in meningioma development, after the neuroflbromatosis type 2 gene.


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