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1 Glanzmann thrombasthenia (GT), an autosomal recessive bl
2 Glanzmann thrombasthenia is an inherited bleeding disord
3 Glanzmann thrombasthenia is an inherited bleeding disord
4 Glanzmann thrombasthenia is an inherited bleeding disord
5 Glanzmann thrombasthenia, an inherited bleeding disorder
6 Glanzmann's thrombasthenia is a qualitative platelet dis
8 was not observed in platelets derived from a Glanzmann's patient, who lacked functional integrin alph
11 ovel flow cytometry-based aggregation assay, Glanzmann platelets were still capable of forming small
12 nique patient with clinical features of both Glanzmann thrombasthenia and leukocyte adhesion deficien
14 90 years ago with a clinical description by Glanzmann of a bleeding disorder associated with a defec
15 ing of new mechanisms of mutagenesis causing Glanzmann thrombasthenia, and our findings will be valua
16 ents with severe combined immune deficiency, Glanzmann's thrombasthenia, Hermansky-Pudlak syndrome, M
19 erizes a form of the human bleeding disorder Glanzmann's thrombasthenia, fails to rescue beta 3(-/-)
20 752Pro) responsible for the genetic disorder Glanzmann thrombasthenia Paris I did not inhibit cell ad
21 his is exemplified by the bleeding disorder, Glanzmann thrombasthenia (GT), where abnormalities of th
22 One rare example of a platelet disorder, Glanzmann thrombasthenia (GT), is characterized by life-
23 in forms of the inherited platelet disorder, Glanzmann thrombasthenia (GT), mutant alpha(IIb)beta(3)
24 aturally occurring mutations responsible for Glanzmann thrombasthenia and to point mutations that aff
27 's Republic of China was diagnosed as having Glanzmann's thrombasthenia based on (1) nearly a lifelon
28 ment option in a noncompliant patient having Glanzmann's thrombasthenia and briefly discusses other h
30 l, with basic insights resulting in improved Glanzmann thrombasthenia carrier detection and prenatal
31 alphaIIbbeta3 expression and/or function in Glanzmann's thrombasthenia patients, platelet dysfunctio
32 yndrome and kindlin-3 deficiency, but not in Glanzmann thrombasthenia lacking the platelet pool of fi
36 ch presents with bleeding similar to that in Glanzmann thrombasthenia and platelet dysfunction in add
37 During studies of the molecular basis of Glanzmann thrombasthenia in a child of mixed Caucasian b
39 demonstrate ex vivo phenotypic correction of Glanzmann thrombasthenia and support the potential use o
40 telets from a patient with a variant form of Glanzmann thrombasthenia that expressed normal levels of
43 tients, classic aggregometry or perfusion of Glanzmann or LAD-III platelets over collagen-coated slid
45 roline mutation, known to cause a variant of Glanzmann's thrombasthenia, inhibits the ability of the
46 and genestein], and with Bernard-Soulier or Glanzmann's platelets, we demonstrated that TR1-41-induc
51 sruption of the ligand binding domain by the Glanzmann thrombasthenia mutation beta3-D119Y constituti
53 he Leu214Pro mutation appears to produce the Glanzmann thrombasthenia phenotype by both qualitative a
54 rction and other thrombotic diseases whereas Glanzmann thrombasthenia, in which platelet aggregation
55 previously reported as being associated with Glanzmann thrombasthenia (GT), 20 associated with alloim
57 so observed on platelets from a patient with Glanzmann thrombasthenia, indicating that alphaII(b)beta
60 ated in iPSCs derived from two patients with Glanzmann thrombasthenia (GT), an inherited platelet dis
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