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Mimic chronic immune thrombocytopaenia using murine platelet induced model through immunized CD41-knockout mice.
alphaIIb beta3 antagonist TMV-7/trimucrin prevents thrombosis with causing Fc receptor gamma-chain IIa-mediated thrombocytopenia.
Kindlin supports platelet GPIIB IIIA activation by interacting with paxillin.
Platelets from Dok-1-/- mice displayed normal aggregation, activation of integrin alphaIIbbeta3, P-selectin surface expression, and soluble fibrinogen binding. These findings indicate that Dok-1 does not affect "inside-out" platelet signalling.
platelets clearly support early steps in pulmonary metastasis via GPIIb-dependent formation of platelet-tumor-aggregates
ITGA2b expression increases in response to immunization, raising the possibility that heterogeneous ITGA2b levels reflect variation in exposure to activation signals.
Thrombopoietin/MPL signaling confers growth and survival capacity to CD41-positive cells in a mouse model of Evi1 leukemia.
Direct binding of kindlin-3 to integrin alphaIIbbeta3 is involved in supporting integrin alphaIIbbeta3 activation and integrin alphaIIbbeta3-dependent responses of platelets and consequently contributes significantly to arterial thrombus formation.
ADAP interacts with talin and kindlin-3 to promote platelet Integrin alphaIIbbeta3 activation and stable fibrinogen binding.
reduction of talin-beta3 integrin binding affinity results in decelerated alphaIIbbeta3 integrin activation and protection from arterial thrombosis without pathological bleeding
deficiency of Dok-2 leads to dysregulated integrin alphaIIbbeta3-dependent cytosolic calcium flux and phosphatidylinositol(3,4)P2 accumulation.
Platelets lacking ERp57 have defective activation of the alphaIIbbeta3 integrin and platelet aggregation. The defect in aggregation was corrected by the addition of exogenous ERp57, implicating surface ERp57 in platelet aggregation.
Data indicate that Pyk2 is a common signaling effector downstream of both G12/13 and integrin alphaIIbbeta3 signaling, which contributes to thromboxane generation.
These results identify a novel pathway of integrin alphaIIbbeta3 outside-in signaling and recognize the tyrosine kinase Pyk2 as a major regulator of platelet adhesion and spreading on fibrinogen.
Here we show that platelet integrin CD41 (alphaIIb), currently thought to only transiently mark fetal hematopoietic stem cells, is expressed on an adult subtype that accumulates with age.
identified Hic-5 as a novel and specific regulatory factor for thrombin-induced alphaIIbbeta3 activation and subsequent platelet aggregation in mice.
These results suggested that platelet associated anti-alphaIIbbeta3 antibodies in primary primary immune thrombocytopenia tended to recognize highly restricted regions of alphaIIb with clonality.
Impaired spreading on fibrinogen and clot retraction with normal levels of alpha(IIb)beta(3) was observed in Lgals1(-/-) platelets, indicating a failure in the "outside-in" signaling through this integrin.
Glycoprotein IIb/IIIa-targeted microbubbles specifically bind to activated platelets in vitro, allowing real-time molecular imaging of acute arterial thrombosis in a mouse model.
Data indicate that the inflammatory cytokines TNF-alpha and IL-1 could be key components of the endothelial cell (EC) response and alphaIIb-beta3 integrin in platelets was required for late-phase thrombus stability.
alphaIIbbeta3 binding to polymeric fibrin can be segregated into two binding regimes, one with weaker rupture forces of 30-60 pN and a second with stronger rupture forces >60 pN that peaked at 70-80 pN.
ERp5 triggers fibrinogen dissociation from aIIbb3 integrin.
Hypoxia impairs agonist-induced CD41/CD61 activation and platelet aggregation.
ApoA-IV is a novel ligand of platelet GPIIB IIIA integrin.
mutations disturbing the alphaIIb R995/beta3 D723 salt bridge can cause an abnormal maturation of alpha-granules
ITGA2B gene mutations associated with Glanzmann thrombasthenia (Review)
Sanger sequencing of ITGA2B and ITGB3 in the index case followed by in silico modeling of all known GT-causing missense mutations extending from the lower part of the beta-propeller, and through the thigh and upper calf-1 domains. The index case, a Belgium type I GT patient, identiffied a homozygous c.1772A>C transversion (NC_000017.11:g.44379795T>G) affecting exon 18 of ITGA2B.
Type I Glanzmann thrombasthenia (GT)was found most common in our patients and with lowered mean CD41 expression in comparison with CD61. Type III GT patients had significantly lower numbers of severe bleeders, but the severity of bleeding did not vary significantly in type I and II GT patients
this study shows that in the Caucasian population the HPA-3 system confers susceptibility to acute cellular rejection after liver transplantation
Case Reports: alterations in the platelet proteome in type I Glanzmann thrombasthenia patients caused by different homozygous delG frameshift mutations in ITGA2B.
No genetic abnormalities identified in alpha2IIb and beta3: phenotype overcomes genotype in Glanzmann thrombasthenia.
study strongly supported the contribution of the genes ITGA2B, GSN and RHOA and the two pathways "regulation of actin cytoskeleton" and "leukocyte transendothelial migration" to osteoporosis risk.
A range of affinities from almost no interaction to the relatively high avidity that characterizes alphaIIbbeta3 is seen between various alpha subunits and beta1 transmembrane and cytosolic domains.
Meta-analysis found that glycoprotein Ia C807T T allele or the TT genotype, the Ser-allele of HPA-3 and B allele of glycoprotein Ibalpha variable number tandem repeat polymorphisms were associated with increased risk for ischemic stroke.
Furthermore, the inside-out activation of GPIIb/IIIa of platelets mediated Streptococcus suis suilysin-induced platelet aggregation.
Data suggest that the extreme C terminus of kindlin-2 is essential for interaction with and activation of integrin alphaIIBbeta3; these studies were conducted in macrophage cell line and erythroleukemia cell line.
Both in cell lines and in mouse model, the extracellular matrix receptors including the integrin ( ITGA3 and ITGA2B), collagen ( COL5A1), and laminin ( LAMA5) were significantly inhibited by curcumin at messenger RNA and protein levels.
Case Report: Reduced binding of mutant FLNa to beta3 and the facilitated recruitment of talin by beta3 on platelet stimulation, explaining the increased alphaIIbbeta3 activation and the ensuing gain-of-platelet functions.
Mechanistic basis for the binding of fibrinogen-derived RGD- and AGDV-peptides to the platelet integrin alphaIIb-beta3 has been described.
ITGA2B encodes integrin alpha chain 2b. Integrins are heterodimeric integral membrane proteins composed of an alpha chain and a beta chain. Alpha chain 2b undergoes post-translational cleavage to yield disulfide-linked light and heavy chains that join with beta 3 to form a fibronectin receptor expressed in platelets that plays a crucial role in coagulation. Mutations that interfere with this role result in thrombasthenia. In addition to adhesion, integrins are known to participate in cell-surface mediated signalling.
, GPalpha IIb
, alpha IIb
, integrin alpha-IIb
, platelet glycoprotein IIb of IIb/II Ia complex
, platelet membrane glycoprotein IIb
, platelet fibrinogen receptor, alpha subunit
, platelet-specific antigen BAK