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Platelet Membrane GlycoproteinsBlood PlateletsPlatelet AggregationPlatelet Glycoprotein GPIb-IX ComplexAntigens, Human PlateletPlatelet AdhesivenessImmunoelectrophoresis, Two-DimensionalGlycoproteinsvon Willebrand FactorCell MembranePlatelet CountBlood Platelet DisordersRistocetinFibrinogenThrombinThrombastheniaAntibodies, MonoclonalAdenosine DiphosphateCrotalid VenomsMembrane ProteinsMolecular WeightPlatelet ActivationAmino Acid SequencePlatelet Glycoprotein GPIIb-IIIa ComplexPlatelet Membrane Glycoprotein IIbPlatelet Factor 4Molecular Sequence DataMembrane GlycoproteinsImmunoglobulin Fab FragmentsPlatelet TransfusionEpitopesElectrophoresis, Polyacrylamide GelPlatelet Activating FactorPlatelet Aggregation InhibitorsMembranesMembrane LipidsPlatelet Function TestsKineticsPeptide FragmentsIntracellular MembranesBinding SitesThrombocytopeniaP-SelectinMembrane PotentialsBernard-Soulier SyndromeBleeding TimeCell LineCollagenMegakaryocytesPlatelet Factor 3Membrane FluidityMembranes, ArtificialViral Envelope ProteinsPurpura, ThrombocytopenicMicroscopy, ElectronProtein BindingErythrocyte MembraneThromboxane A2ThrombosisCalciumGlycosylationLysosome-Associated Membrane GlycoproteinsBase SequenceBlood ProteinsRabbitsReceptors, Cell SurfaceSerotoninFluorescent Antibody TechniqueBasement MembraneRecombinant ProteinsCells, CulturedProstaglandin Endoperoxides, SyntheticThrombospondinsHemostasisbeta 2-Glycoprotein IAntibodiesChromatography, AffinityReceptors, ThromboxaneCytoplasmic GranulesBlood CoagulationAntigens, SurfaceOctoxynolCell Membrane PermeabilityCell AdhesionBlood Coagulation FactorsBinding, CompetitiveAntigens, CDAntigens, CD36Receptors, Thromboxane A2, Prostaglandin H2Edetic AcidCricetinaeSolubilityImmunosorbent TechniquesFlow CytometryGlycopeptidesTime FactorsCloning, MolecularOligopeptidesCell FractionationBlood Coagulation Disorders
IIIaAggregationReceptorReceptorsTransmembrane glycoproteinAdhesion of plateletsFlow cytometryProteinsAntigenAdjacent plateletsFibrinCD41MediatesWillebrandHuman PlateletsMutationActivationCD61IntegrinsEndothelial cellExpressed by megakaryocytesThrombinPrimary platelet plugExtracellularThrombosisThrombocytopeniaProteinMegakaryocytes in the bone maLack of plateletAdditional plateletsCD36InhibitionGranuleNeutrophilsBlood clotsGPIb-IXSites of vascularDisordersGPVIMucous membranesBleeding disorderHemostaticCommon pathwayMacrophagesInteractDefectsClot formationPeripheral smearFunctionalGP1B
IIIa30
  • In consequence, this complex activates GPIIb / IIIa membrane glycoproteins, allowing them to bind fibrinogen. (wikipedia.org)
  • In the absence of fibrinogen, the platelets are joined by vWF due to its ability to bind the activated GPIIb / IIIa complex. (wikipedia.org)
  • The IIb / IIIa complex is a major platelet membrane component. (wikipedia.org)
  • Fibrinogen sites recognized by glycoprotein IIb / IIIa complex: dodecapeptide located in the C-terminal of the fibrinogen γ chain (the most important) RGD sequence of the α chain → the Arginine-Glycine-Aspartate amino acid sequence This complex also binds vWF, fibronectin and vitronectin. (wikipedia.org)
  • Platelet Glycoprotein GPIIb-IIIa Complex" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
  • This graph shows the total number of publications written about "Platelet Glycoprotein GPIIb-IIIa Complex" by people in Harvard Catalyst Profiles by year, and whether "Platelet Glycoprotein GPIIb-IIIa Complex" was a major or minor topic of these publication. (harvard.edu)
  • Below are the most recent publications written about "Platelet Glycoprotein GPIIb-IIIa Complex" by people in Profiles. (harvard.edu)
  • Exploratory Use of Glycoprotein IIb/IIIa Inhibition in Prevention of Blalock-Taussig Shunt Thrombosis. (harvard.edu)
  • The platelet GP IIb/IIIa complex mediates platelet-to-platelet interactions (platelet aggregation). (medscape.com)
  • On resting platelets, GP IIb/IIIa is unable to bind fibrinogen or vWf. (medscape.com)
  • However, not all patients in these trials received glycoprotein (GP) IIb/IIIa inhibitors. (acc.org)
  • Scholars@Duke publication: Randomised trial of coronary intervention with antibody against platelet IIb/IIIa integrin for reduction of clinical restenosis: results at six months. (duke.edu)
  • We tested a monoclonal antibody Fab fragment (c7E3) directed against the platelet glycoprotein IIb/IIIa integrin, the receptor mediating the final common pathway of platelet aggregation, to see whether it reduced the frequency of clinical restenosis. (duke.edu)
  • Biosynthesis and processing of platelet GPIIb-IIIa in human megakaryocytes. (rupress.org)
  • Platelet membrane glycoprotein IIb-IIIa forms a calcium-dependent heterodimer and constitutes the fibrinogen receptor on stimulated platelets. (rupress.org)
  • The mouse monoclonal antibody PAC-1 recognizes an extracellular activation-induced conformational epitope PAC-1 on CD41/CD61 complex (gpIIb/IIIa), also known as integrin alpha IIb beta 3, a receptor which mediates platelet aggregation. (exbio.cz)
  • CD41 (platelet glycoprotein IIb, integrin alpha IIb) is composed of two subunits (120 kDa transmembrane alpha chain and 23 kDa extracellular beta chain) and interacts with CD61 (platelet glycoprotein IIIa, integrin beta 3) in the presence of calcium to form a functional adhesive protein receptor. (exbio.cz)
  • Shattil SJ, Hoxie JA, Cunningham M, Brass LF: Changes in the platelet membrane glycoprotein IIb.IIIa complex during platelet activation. (exbio.cz)
  • Qin R , Zhu H , Wang F , Song M , Lin P , Xing Y , Zhang W , Zhong M , Wang Z , . Platelet activation in diabetic mice models: the role of vascular endothelial cell-derived protein disulfide isomerase-mediated GP IIb/IIIa receptor activation. (aging-us.com)
  • The EMP-PDI content and GP IIb/IIIa expression of mice platelets were determined. (aging-us.com)
  • Compared with the normal diet group, the diabetic group had significantly increased plasma EMP-PDI content and accelerated platelet activation by increased GP IIb/IIIa expression. (aging-us.com)
  • In conclusion, EMP-PDI promotes early platelet activation through glycoprotein (GP) IIb/IIIa receptors present on platelet surface in the diabetic state. (aging-us.com)
  • However, the ultimate common pathway of platelet aggregation is the activation of glycoprotein (GP) IIb/IIIa receptors present on platelet surface [ 7 - 9 ]. (aging-us.com)
  • Results of published studies of the association between the glycoprotein IIIa polymorphism and ischemic stroke. (jamanetwork.com)
  • Background: In patients with ST-elevation myocardial infarction (STEMI), direct intracoronary bolus administration of the glycoprotein (GP) IIb/IIIa receptor antagonist abciximab is associated with a reduction in infarct size, better myocardial salvage, less microvascular obstruction and improved myocardial blush grade as compared to intravenous bolus injection, presumably caused by higher local drug concentrations leading to a more pronounced inhibition of platelet aggregation. (uni-luebeck.de)
  • We investigated whether there are differences in the degree of GP IIb/IIIa receptor occupancy and platelet inhibition in blood drawn from the coronary sinus (CS) shortly after intracoronary versus intravenous abciximab bolus administration. (uni-luebeck.de)
  • At late sampling after 30 min no significant differences were found between groups for both platelet reactivity and GP IIb/IIIa receptor occupancy. (uni-luebeck.de)
  • Conclusions: Acutely, direct intracoronary bolus injection resulted in a more pronounced local inhibition of platelet function and a higher degree of GP IIb/IIIa receptor occupancy as compared to standard intravenous bolus injection. (uni-luebeck.de)
  • Platelet receptors for ADP include the P2Y12 receptor, which sends signals to suppress adenylate cyclase, decreases cyclic adenosine monophosphate (cAMP) levels, and promotes activation of the glycoprotein IIb/IIIa receptor (assembled on the activated platelet surface membrane from glycoproteins IIb and IIIa). (msdmanuals.com)
  • Fibrinogen binds to the glycoprotein IIb/IIIa complexes of adjacent platelets, connecting them into aggregates. (msdmanuals.com)
Aggregation18
Receptor12
  • It is an important collagen receptor involved in collagen-induced platelet activation and adhesion. (wikipedia.org)
  • Glycoprotein Ib functions as a receptor for von Willebrand factor and for thrombin . (online-medical-dictionary.org)
  • Shear-Mediated Platelet Microparticles Demonstrate Phenotypic Heterogeneity as to Morphology, Receptor Distribution, and Hemostatic Function. (harvard.edu)
  • Sex-specific platelet activation through protease-activated receptor-1 in patients undergoing cardiac catheterization. (harvard.edu)
  • The ITGB3 gene provides instructions for making the beta3 subunit of a receptor protein called integrin alphaIIb/beta3 (αIIbβ3), which is found on the surface of small cells called platelets. (medlineplus.gov)
  • DLL-4, in turn, instigated neighbouring platelets to switch to 'activated' phenotype through cleavage of Notch receptor and release of its intracellular domain (NICD), which was averted by inhibition of γ-secretase and phosphatidylinositol-3-kinase (PI3K). (elifesciences.org)
  • An integrin found on fibroblasts, platelets, endothelial and epithelial cells, and lymphocytes where it functions as a receptor for COLLAGEN and LAMININ . (nih.gov)
  • CD42b, also known as GP1Ba (GP1B alpha, Glycoprotein 1Ba) is a single pass transmembrane glycoprotein that functions as the key ligand binding subunit of the GP1B platelet surface receptor. (peprotech.com)
  • The association of CD42b/GP1Ba with GP1Bb (covalently) and platelet glycoproteins IX and V (non‐covalently) forms the von Willebrand factor receptor. (peprotech.com)
  • The binding of von Willebrand factor (VWF) to its platelet receptor initiates the primary mechanism for the adhesion of platelets to a site of vascular injury and subsequent platelet activation. (peprotech.com)
  • In the 1970s, the molecular defect was shown to involve the absence of a platelet membrane glycoprotein (GPIb/IX/V) complex which is the receptor for von Willebrand factor (vWF). (medscape.com)
  • We undertook this study to investigate receptor (IL-2R) accumulation is related to whether the cytokine accumulation in PCs the leukocyte content of the platelet comc obtained from single apheresis donors was ponent and can be reduced by prestorage beyond the acceptable limits of WBC conc leukocyte depletion [ 3 ]. (who.int)
Receptors5
  • Membrane glycoproteins GPIa/IIa, GPVI and probably GPIV as well, function as collagen receptors, engaged in platelet adhesion to collagen. (wikipedia.org)
  • 2 Centre of Membrane Proteins and Receptors, The Universities of Birmingham and Nottingham, The Midlands, United Kingdom. (nih.gov)
  • VWF binds to receptors on the platelet surface membrane (glycoprotein Ib/IX). (msdmanuals.com)
  • Refrigerated storage reduces platelet life-span because it causes glycoprotein-Ib (GPIb) receptors to cluster on specific microdomains of the platelet membrane. (sbir.gov)
  • Recognition of specific glycated/syalylated residues on clustered glycoproteins by macrophage b2 integrins and hepatocyte Ashwell-Morell receptors results in platelet phagocytosis by the host and removal from circulation. (sbir.gov)
Transmembrane glycoprotein3
  • This transmembrane glycoprotein complex is composed of four subunits: GPIbα, GPIbβ, GPV and GPIX. (wikipedia.org)
  • CD62P is a 140 kDa type I transmembrane glycoprotein that is also known as P-Selectin, Platelet activation-dependent granule membrane protein (PADGEM), or Granule membrane protein-140 (GMP-140). (bdbiosciences.com)
  • Integrin alpha 2b (ITGA2b), also known as CD41 and GPIIb, is a transmembrane glycoprotein that is expressed by megakaryocytes and platelets. (rndsystems.com)
Adhesion of platelets3
  • The body's reaction to vessel wall injury is rapid adhesion of platelets to the subendothelium. (medscape.com)
  • VWF mediates the adhesion of platelets to sites of vascular damage by binding to specific platelet membrane glycoproteins and to constituents of exposed connective tissue. (embl.de)
  • Additional reported applications (for the relevant formats) include: immunohistochemical staining of acetone-fixed frozen tissue sections 4 and in vitro blocking of adhesion of platelets 1 . (biolegend.com)
Flow cytometry5
Proteins9
  • Integrin αIIbβ3 can also bind other proteins on platelets and in the blood as well as proteins within the intricate lattice that forms in the space between cells (extracellular matrix) to ensure proper clot formation and promote wound healing. (medlineplus.gov)
  • The overactive integrin αIIbβ3 binds inappropriately to clotting proteins within the cell during the formation of platelets, causing the platelets to become misshapen and large. (medlineplus.gov)
  • Platelet activation allows binding of these proteins, which bridges adjacent platelets. (medscape.com)
  • The alpha granules contain hemostatic proteins such as fibrinogen, vWf, and growth factors (eg, platelet-derived growth factor and transforming growth factors). (medscape.com)
  • Ankyrins link integral membrane proteins to the spectrin-based membrane skeleton. (dana-farber.org)
  • Hereditary defects in membrane skeleton proteins. (dana-farber.org)
  • This indicates that AE1 and probably other integral membrane proteins have a 'lipid-anchoring' function. (dana-farber.org)
  • View our protocol for Staining Membrane-associated Proteins . (rndsystems.com)
  • In Sierra Leone during 2015-2018, we assessed LF patients' day-of-admission plasma samples for levels of proteins necessary for coagulation, fibrinolysis, and platelet function. (cdc.gov)
Antigen1
  • It has been suggested that cytokine acc leukoreduction prevents transmission of cyc cumulation in plasma of platelet concenc tomegalovirus and decreases alloimmunizac trates (PC) during storage may contribute tion to human leukocyte antigen (HLA), it to development of nonchaemolytic febrile does not prevent allergic reactions. (who.int)
Adjacent platelets1
  • Attachment of integrin αIIbβ3 from adjacent platelets to the same fibrinogen protein helps platelets cluster together (platelet cohesion) to form a blood clot. (medlineplus.gov)
Fibrin5
  • The initial hemostatic plug, composed primarily of platelets, is stabilized further by a fibrin mesh generated in secondary hemostasis. (medscape.com)
  • A) Platelets localize to the site of injury, binding to fibrin, and forming a hemostatic plug. (comprehensivephysiology.com)
  • platelets and fibrin combine to form a clot. (msdmanuals.com)
  • Thrombin converts fibrinogen into fibrin monomers, and the fibrin monomers polymerize into fibrin polymers that bind aggregated platelets into platelet-fibrin hemostatic plugs. (msdmanuals.com)
  • Coagulation factors interact on platelet and endothelial cell surfaces to produce thrombin , which converts fibrinogen to fibrin. (msdmanuals.com)
CD411
  • Human peripheral blood platelets were stained with FITC-conjugated Anti-Human Integrin a2b/CD41 Antibody (Clone P2) and either (A) Mouse Anti-Human Integrin a2b/CD41 APC-conjugated Monoclonal Antibody (Catalog # FAB7616A) or (B) Mouse IgG 1 Allophycocyanin Isotype Control (Catalog # IC002A ). (rndsystems.com)
Mediates1
  • The binding between GPIbα and vWF mediates the capture of platelets to the injured vascular wall. (wikipedia.org)
Willebrand4
  • Platelets play a primary role in this process, interacting with subendothelium-bound von Willebrand factor (vWf) via the membrane glycoprotein (GP) Ib complex. (medscape.com)
  • The workup of a patient with a platelet-type bleeding pattern typically includes correlation with platelet count ( thrombocytopenia ), evaluation of platelet morphology on peripheral smear, exclusion of acquired causes of platelet dysfunction, and testing for von Willebrand disease (VWD) . (arupconsult.com)
  • Von Willebrand factor (VWF) is a large, multimeric blood glycoprotein synthesized in endothelial cells and megakaryocytes, that is required for normal hemostasis. (embl.de)
  • Initial platelet adhesion is to long strings of von Willebrand factor (VWF) that have been previously secreted by, and anchored to, stimulated endothelial cells. (msdmanuals.com)
Human Platelets1
  • We demonstrate expression of Notch1, its ligand DLL-4 and their respective transcripts in human platelets. (elifesciences.org)
Mutation3
  • Trpc6 gain-of-function disease mutation enhances phosphatidylserine exposure in murine platelets. (harvard.edu)
  • Because the mutation that causes this disorder affects only one copy of the ITGB3 gene, some normal integrin is formed and normal platelets produced, which accounts for the mild signs and symptoms in affected individuals. (medlineplus.gov)
  • Hermans C, Wittevrongel C, Thys C, Smethurst PA, Van Geet C, Freson K. A compound heterozygous mutation in glycoprotein VI in a patient with a bleeding disorder. (medlineplus.gov)
Activation13
CD611
  • Heterodimers of CD51/CD61 are expressed by melanoma cells, endothelial cells and osteoclasts and at very low levels by platelets. (thermofisher.com)
Integrins1
Endothelial cell2
  • Under physiological circumstances, the resistance of the endothelial cell lining to interactions with platelets and coagulation factors prevents thrombosis. (medscape.com)
  • A) EM image of an inflamed mouse cremaster venule, demonstrating platelet‐neutrophil‐endothelial cell interaction. (comprehensivephysiology.com)
Expressed by megakaryocytes1
Thrombin3
  • This initial interaction (platelet adhesion) sets the stage for other adhesive reactions that allow the platelets to interact with other agonists in the vicinity of vessel injury, such as adenosine 5'-diphosphate (ADP), subendothelial collagen, and thrombin. (medscape.com)
  • Download Citation on ResearchGate \textbar Arachidonate induced fibrinogen binding to thrombin degranulated platelets is independent of released ADP \textbar When human or rabbit platelets are stimulated with ADP, fibrinogen (Fbg) binding sites are revealed, the platelets bind Fbg and aggregate. (mcmaster.ca)
  • Thrombin-activated human peripheral blood platelets were stained with CD62P (P-Selectin) (clone AK4) Brilliant Violet 650™ (filled histogram) or mouse IgG1, κ Brilliant Violet 650™ isotype control (open histogram). (biolegend.com)
Primary platelet plug1
  • The end result is the lack of formation of the primary platelet plug, together with an increased bleeding tendency. (medscape.com)
Extracellular3
  • When the blood vessel wall is damaged, platelet membrane glycoproteins interact with the extracellular matrix. (wikipedia.org)
  • Platelet-derived extracellular vesicles were documented with Nanoparticle Tracking Analyzer. (elifesciences.org)
  • The antibody TR9 reacts with an extracellular epitope of CD36 (GPIIIb), a 85 kDa integral membrane glycoprotein expressed on platelets, macrophages, endothelial cells, early erythroid cells and megakaryocytes. (exbio.cz)
Thrombosis1
Thrombocytopenia6
  • These acquired cases of glycoprotein VI deficiency are associated with autoimmune disorders such as immune thrombocytopenia purpura, Graves' disease , or systemic lupus erythematosus (SLE). (medlineplus.gov)
  • Bernard-Soulier syndrome (BSS) is one of a group of hereditary platelet disorders characterized by thrombocytopenia, giant platelets, and qualitative platelet defects resulting in bleeding tendency. (medscape.com)
  • Bernard-Soulier syndrome (BSS) was first described in 1948 as a congenital bleeding disorder characterized by thrombocytopenia and large platelets. (medscape.com)
  • The cause of the thrombocytopenia is not definitely known but is thought probably to be related to the absence of the GPIb/IX/V complex and its role in the production and shedding of platelets from the marrow megakaryocytes. (medscape.com)
  • The cause of the thrombocytopenia is not definitely known but is probably related to a decrease in platelet life span. (medscape.com)
  • Thrombocytopenia is a common feature of hemorrhagic fevers and vascular permeability disorders ( 8 ), but the decrease in platelet counts in acute LF is not low enough to cause spontaneous hemorrhage. (cdc.gov)
Protein6
  • This abnormally active protein is unable to reach the surface of the platelet where it is needed to bind to other platelets during clot formation. (medlineplus.gov)
  • Species diversity in the structure of zonadhesin, a sperm-specific membrane protein containing multiple cell adhesion molecule-like domains. (embl.de)
  • Glycoprotein VI deficiency can be caused by mutations in the GP6 gene, which provides instructions for making a protein called glycoprotein VI (GPVI). (medlineplus.gov)
  • This protein is embedded in the outer membrane of blood cells called platelets, which are an essential component of blood clots. (medlineplus.gov)
  • As a result, there is a shortage (deficiency) of functional GPVI protein on the surface of platelets, which leads to bleeding problems characteristic of glycoprotein VI deficiency. (medlineplus.gov)
  • The impaired homeostasis and platelet dysfunction implicate alterations in the protein C pathway, which might contribute to the loss of endothelial barrier function in fatal infections. (cdc.gov)
Megakaryocytes in the bone ma2
  • The platelets arise from the fragmentation of the cytoplasm of megakaryocytes in the bone marrow and circulate in blood as disc-shaped anucleate particles for 7-10 days. (medscape.com)
  • GPIb/IX/V complex is located in the platelet cytoskeleton and hence is also essential to the production of platelets from the megakaryocytes in the bone marrow (which explains the large size and decreased numbers of platelets in this syndrome). (medscape.com)
Lack of platelet1
  • A lack of platelet cohesion leads to prolonged or spontaneous bleeding episodes experienced by people with Glanzmann thrombasthenia. (medlineplus.gov)
Additional platelets2
  • Once activated, platelets have two major mechanisms to recruit additional platelets to the growing hemostatic plug. (medscape.com)
  • The binding of GPVI to collagen also signals additional platelets to come together to increase the size of the clot. (medlineplus.gov)
CD362
  • Similarly to glucose transporter GLUT4, CD36 is translocated from intracellular pools to the plasma membrane following cell stimulation by insulin. (exbio.cz)
  • van Oort MM, van Doorn JM, Bonen A, Glatz JF, van der Horst DJ, Rodenburg KW, Luiken JJ: Insulin-induced translocation of CD36 to the plasma membrane is reversible and shows similarity to that of GLUT4. (exbio.cz)
Inhibition1
  • The degree of platelet inhibition was also markedly higher with intracoronary compared to intravenous dosing. (uni-luebeck.de)
Granule1
  • Since stimulation with other aggregating agents (arachidonate, collagen or ionophores) releases platelet granule contents, including ADP. (mcmaster.ca)
Neutrophils2
  • P-Selectin is thought to mediate the initial adhesive interactions of neutrophils and monocytes with endothelium in inflammatory responses, and of activated platelets to neutrophils and monocytes in hemostasis. (bdbiosciences.com)
  • Adhesive interactions between activated platelets and neutrophils. (comprehensivephysiology.com)
Blood clots4
  • Platelets circulate in blood and are an essential component of blood clots. (medlineplus.gov)
  • Glycoprotein VI deficiency is a bleeding disorder associated with a decreased ability to form blood clots. (medlineplus.gov)
  • Because people with glycoprotein VI deficiency cannot form blood clots normally, they have an increased risk of nosebleeds (epistaxis) and may experience abnormally heavy or prolonged bleeding following minor injury or surgery. (medlineplus.gov)
  • In addition to their role in blood clots, increasing evidence reveals significant roles for platelets in inflammation and immunity. (comprehensivephysiology.com)
GPIb-IX2
  • The platelet glycoprotein GPV associates with GPIb-IX and is also absent in Bernard-Soulier syndrome . (online-medical-dictionary.org)
  • The underlying biochemical defect in BSS is the absence or decreased expression of the GPIb/IX/V complex on the surface of the platelets. (medscape.com)
Sites of vascular1
  • Platelet membrane glycoprotein complex essential for normal platelet adhesion and clot formation at sites of vascular injury . (online-medical-dictionary.org)
Disorders13
  • For instance, identification of MYH9 as the gene whose mutations cause the May-Hegglin anomaly led to the recognition that Sebastian platelet syndrome, Epstein syndrome, and Fechtner syndrome derive from mutations of the same gene and describe overlapping disorders. (nih.gov)
  • Platelet disorders lead to defects in primary hemostasis and produce signs and symptoms different from coagulation factor deficiencies (disorders of secondary hemostasis). (medscape.com)
  • His research focuses on red blood cell membrane disorders and anemias. (dana-farber.org)
  • How do functional platelet disorders manifest clinically? (arupconsult.com)
  • The clinical features of functional platelet disorders vary. (arupconsult.com)
  • rarely, it may be observed in functional platelet disorders). (arupconsult.com)
  • Functional platelet disorders are generally associated with immediate bleeding in response to surgery or trauma, whereas factor deficiencies are associated with delayed bleeding. (arupconsult.com)
  • What are some causes of acquired functional platelet disorders? (arupconsult.com)
  • Which functional platelet disorders are inherited? (arupconsult.com)
  • Refer to the table, Laboratory Findings in Selected Inherited Functional Platelet Disorders , for additional information and a more comprehensive list of inherited functional platelet disorders. (arupconsult.com)
  • Laboratory testing for functional platelet disorders is appropriate in individuals with bleeding manifestations that suggest a functional platelet disorder (eg, easy bruising, prolonged bleeding following dental work or surgery, menorrhagia), particularly those with a family history of a bleeding disorder and in whom VWD has been previously excluded. (arupconsult.com)
  • BSS is one of a group of hereditary platelet disorders characterized by macrothrombocytopenia and a tendency toward bleeding. (medscape.com)
  • Other disorders in the category of macrothrombocytopenia are the May-Hegglin anomaly and gray platelet syndrome. (medscape.com)
GPVI3
  • As many of these techniques cannot be applied to platelets to resolve this issue, due to the high density of GPVI and its anucleate nature, we used Förster resonance energy transfer (FRET) to show that endogenous GPVI is at least partially expressed as a dimer on resting and activated platelet membranes. (nih.gov)
  • We propose that GPVI may be expressed as a monomer on the cell surface and it forms dimers in the membrane through diffusion, giving rise to a mixture of monomers and dimers. (nih.gov)
  • Without GPVI binding to collagen, platelets cannot come together efficiently to form a clot, leading to the bleeding problems associated with glycoprotein VI deficiency. (medlineplus.gov)
Mucous membranes2
  • Bleeding at mucous membranes and edema generally are seen in the most severe cases ( 3 , 4 ), but bleeding diathesis reportedly was common during a recent outbreak in Nigeria ( 4 ). (cdc.gov)
  • Ebolaviruses enter a person through mucous membranes, breaks in the skin, or parenterally. (cdc.gov)
Bleeding disorder1
  • Mutations in the ITGB3 gene can also cause another rare bleeding disorder called platelet-type bleeding disorder 16. (medlineplus.gov)
Hemostatic2
  • The hemostatic system consists of platelets, coagulation factors, and the endothelial cells lining the blood vessels. (medscape.com)
  • Thus, the release reaction and prostaglandin synthesis act to consolidate the initial hemostatic plug by promoting the participation of other platelets in the growing hemostatic plug. (medscape.com)
Common pathway1
  • This happens in three main steps referred to as platelet plugging, intrinsic and extrinsic pathways , and the common pathway to ultimately stop bleeding. (differencebetween.net)
Macrophages1
  • This complex is located mainly on endothelial cells but also on smooth muscle cells, macrophages and platelets. (wikipedia.org)
Interact1
  • Platelets interact with leukocytes through both adhesive mechanisms as well as release of cytokines/chemokines. (comprehensivephysiology.com)
Defects2
  • During the past decade our laboratory and others have shown that hereditary spherocytosis is caused by defects in the connections that attach the membrane skeleton to the overlying lipid bilayer. (dana-farber.org)
  • Platelet glycoprotein VI-related clinical defects. (medlineplus.gov)
Clot formation1
  • The abnormally shaped platelets have a shortened lifespan, so platelet numbers are often reduced, which impairs clot formation. (medlineplus.gov)
Peripheral smear2
Functional4
  • It is important to rule out acquired conditions during an evaluation for a functional platelet disorder. (arupconsult.com)
  • Existence of functional Notch signaling in enucleate platelets remains elusive. (elifesciences.org)
  • This article reviews the role of platelets in inflammation and immune responses, and highlights their interactions with other immune cells, including examples of major functional consequences of these interactions. (comprehensivephysiology.com)
  • Selected examples of proinflammatory effects of platelets resulting in functional consequences on leukocytes. (comprehensivephysiology.com)
GP1B1