A new mutation in theKINDLIN-3gene ablates integrin-dependent leukocyte, platelet, and osteoclast function in a patient with leukocyte adhesion deficiency-III

Kindlin-3–mediated signaling from multiple integrin classes is required for osteoclast-mediated bone resorption

(2011) Sarah Schmidt et al.   JOURNAL OF CELL BIOLOGY

Two mutations in the KINDLIN3 gene of a new leukocyte adhesion deficiency III patient reveal distinct effects on leukocyte function in vitro

(2010) A. McDowall et al.   BLOOD

Novel integrin-dependent platelet malfunction in siblings with leukocyte adhesion deficiency-III (LAD-III) caused by a point mutation in FERMT3

(2010) Kerstin Jurk et al.   THROMBOSIS AND HAEMOSTASIS

Prompt recovery of recipient hematopoiesis after two consecutive haploidentical peripheral blood SCTs in a child with leukocyte adhesion defect III syndrome

(2009) R Elhasid et al.   BONE MARROW TRANSPLANTATION

A point mutation in KINDLIN3 ablates activation of three integrin subfamilies in humans

(2009) Nikolay L Malinin et al.   NATURE MEDICINE

Leukocyte adhesion deficiency-III is caused by mutations in KINDLIN3 affecting integrin activation

(2009) Lena Svensson et al.   NATURE MEDICINE

LAD-1/variant syndrome is caused by mutations inFERMT3

(2008) Taco W. Kuijpers et al.   BLOOD

The Clinical Spectrum of Leukocyte Adhesion Deficiency (LAD) III due to Defective CalDAG-GEF1

(2008) Sara S. Kilic et al.   JOURNAL OF CLINICAL IMMUNOLOGY