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Nature Medicine 15, 249 - 250 (2009)
doi:10.1038/nm0309-249
When integrins fail to integrate
Andrés Hidalgo1 & Paul S Frenette1
- Andrés Hidalgo and Paul S. Frenette are at Mount Sinai School of Medicine, Departments of Medicine and Gene and Cell Medicine, Black Family Stem Cell Institute, Immunology Institute, 1 Gustave Levy Place, Box 1079, New York, New York 10029, USA. e-mail: paul.frenette@mssm.edu
Abstract
Three studies implicate Kindlin-3, a molecule that mediates signaling through integrins, in a rare disorder characterized by spontaneous bleeding and susceptibility to infection (pages 300–305, 306–312 and 313–318).
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RESEARCH
Kindlin-3 is required for β 2 integrin?mediated leukocyte adhesion to endothelial cellsNature Medicine Letter (01 Mar 2009)
Leukocyte adhesion deficiency-III is caused by mutations in KINDLIN3 affecting integrin activationNature Medicine Letter (01 Mar 2009)
A point mutation in KINDLIN3 ablates activation of three integrin subfamilies in humansNature Medicine Letter (01 Mar 2009)
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