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1 ult in a serious bleeding disorder, known as Glanzmann thrombasthenia.
2 nonexpression and a bleeding tendency termed Glanzmann thrombasthenia.
3 nding domains of alphaIIb in 2 patients with Glanzmann thrombasthenia.
4 chain or SLP-76 and in patients with type I Glanzmann thrombasthenia.
5 n 3 ethnically distinct families affected by Glanzmann thrombasthenia.
6 3 complexes on the platelet surface produces Glanzmann thrombasthenia.
7 5-year-old white man was diagnosed as having Glanzmann thrombasthenia.
8 defective alphaIIbbeta3 from a patient with Glanzmann thrombasthenia.
9 beta(3) integrin cause the bleeding disorder Glanzmann thrombasthenia.
12 nique patient with clinical features of both Glanzmann thrombasthenia and leukocyte adhesion deficien
13 ch presents with bleeding similar to that in Glanzmann thrombasthenia and platelet dysfunction in add
14 demonstrate ex vivo phenotypic correction of Glanzmann thrombasthenia and support the potential use o
15 aturally occurring mutations responsible for Glanzmann thrombasthenia and to point mutations that aff
16 ing of new mechanisms of mutagenesis causing Glanzmann thrombasthenia, and our findings will be valua
17 l, with basic insights resulting in improved Glanzmann thrombasthenia carrier detection and prenatal
20 previously reported as being associated with Glanzmann thrombasthenia (GT), 20 associated with alloim
22 ated in iPSCs derived from two patients with Glanzmann thrombasthenia (GT), an inherited platelet dis
23 One rare example of a platelet disorder, Glanzmann thrombasthenia (GT), is characterized by life-
24 in forms of the inherited platelet disorder, Glanzmann thrombasthenia (GT), mutant alpha(IIb)beta(3)
25 his is exemplified by the bleeding disorder, Glanzmann thrombasthenia (GT), where abnormalities of th
27 During studies of the molecular basis of Glanzmann thrombasthenia in a child of mixed Caucasian b
29 rction and other thrombotic diseases whereas Glanzmann thrombasthenia, in which platelet aggregation
30 so observed on platelets from a patient with Glanzmann thrombasthenia, indicating that alphaII(b)beta
34 yndrome and kindlin-3 deficiency, but not in Glanzmann thrombasthenia lacking the platelet pool of fi
35 sruption of the ligand binding domain by the Glanzmann thrombasthenia mutation beta3-D119Y constituti
37 752Pro) responsible for the genetic disorder Glanzmann thrombasthenia Paris I did not inhibit cell ad
38 IIa, which we confirmed using platelets from Glanzmann thrombasthenia patients and transgenic mouse l
39 he Leu214Pro mutation appears to produce the Glanzmann thrombasthenia phenotype by both qualitative a
41 telets from a patient with a variant form of Glanzmann thrombasthenia that expressed normal levels of