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Pro-platelet basic protein

beta-Thromboglobulin, beta-TG
The protein encoded by this gene is a platelet-derived growth factor that belongs to the CXC chemokine family. This growth factor is a potent chemoattractant and activator of neutrophils. It has been shown to stimulate various cellular processes including DNA synthesis, mitosis, glycolysis, intracellular cAMP accumulation, prostaglandin E2 secretion, and synthesis of hyaluronic acid and sulfated glycosaminoglycan. It also stimulates the formation and secretion of plasminogen activator by synovial cells. [provided by RefSeq, May 2010] (from NCBI)
Top mentioned proteins: HAD, Plasminogen, platelet factor 4, AGE, CAN
Papers on beta-Thromboglobulin
Thrombin Generation among Sudanese Patients with Hematological Malignancies.
Babiker et al., Al Qurayyāt, Saudi Arabia. In Gulf J Oncolog, Jul 2014
UNLABELLED: Hematological malignancies can change the levels of plasma molecules involved in coagulation and fibrinolysis such as fibrinopeptide A, fibrinogen, plasminogen activator inhibitor-1 (PAI-1) and D-dimer, markers of endothelial cell integrity (soluble E-selectin, van Willebrand factor and soluble thromboembolism) and of platelet function (beta-thromboglobulin).
Influence of training on markers of platelet activation in response to a bout of heavy resistance exercise.
Kraemer et al., United States. In Eur J Appl Physiol, 2013
Blood samples were analyzed for platelet count, von Willebrand factor antigen (vWF:Ag), beta-thromboglobulin (β-TG), and platelet factor 4 (PF4).
Newly diagnosed depression is associated with increased beta-thromboglobulin levels and increased expression of platelet activation markers and platelet derived CD40-CD40L.
Herpertz et al., Bochum, Germany. In J Psychiatr Res, 2013
METHODS: This study used whole blood aggregometry, flow cytometry and ELISA to investigate platelet CD62P (P-selectin) expression and atherosclerotic markers (CD40, CD40L) as well as serum platelet factor 4 (PF-4) and beta-thromboglobulin (β-TG) levels in 46 participants.
Proteomic analysis reveals platelet factor 4 and beta-thromboglobulin as prognostic markers in severe acute respiratory syndrome.
Lo et al., Hong Kong, Hong Kong. In Electrophoresis, 2012
Examined the prognostic values of SARS-associated proteome, and deciphered the identities of those with prognostic values.The associations of decreased serum PF4 and increased serum beta-TG levels with poor prognosis were confirmed by Western blot.
Non-chemotactic influence of CXCL7 on human phagocytes. Modulation of antimicrobial activity against L. pneumophila.
Rivero-Lezcano et al., León, Spain. In Immunobiology, 2012
modulates antimicrobial activity of phagocytes against L. pneumophila
Effect of iodinated low-osmolar contrast media on the hemostatic system after intraarterial and intravenous contrast administration.
Galar et al., Białystok, Poland. In Adv Med Sci, 2011
MATERIAL AND METHODS: Hemostatic parameters: vWF (von Willebrand factor), F1+2 (prothrombin fragments 1+2), TAT (thrombin-antithrombin complexes), D-Dimer, β-TG (beta-thromboglobulin) were measured in a group of 35 patients.
Expressions of CXCR7/ligands may be involved in oral carcinogenesis.
Cheng et al., Guangzhou, China. In J Mol Histol, 2011
positive ratios of CXCR7, CXCL12 and CXCL11 in oral leukoplakia and oral squamous cell carcinoma tissues respectively, were significantly higher than that in normal epithelia
Effect of Acacia nilotica leaves extract on hyperglycaemia, lipid profile and platelet aggregation in streptozotocin induced diabetic rats.
Nadeem et al., In J Ayub Med Coll Abbottabad, 2011
Blood glucose levels were measured by glucometer, platelet aggregation by DiaMed method, beta-thromboglobulin and insulin by ELISA technique, and lipid components were measured by enzymatic calorimetric method.
Experimental thermal lesions induce beta-thromboglobulin release from activated platelets.
Schmelz et al., Mannheim, Germany. In Eur J Pain, 2011
Using microdialysis techniques we detected beta-TG release during an inflammatory response. We conclude that local platelet activation is induced by the heating stimulus.
[Beta2-glycoprotein I polymorphism].
Uchiyama et al., Tokyo, Japan. In Brain Nerve, 2008
The mean values of beta-thromboglobulin and platelet factor 4 in patients with the VL genotype were significantly higher than those with the LL genotype.
Platelet function in cutaneous diseases.
Rogala et al., Poland. In Platelets, 2008
Responding to the variety of stimuli such as cell activation leads to the release of several mediators, including RANTES, platelet factor 4, beta-thromboglobulin, thymus and activation-regulated chemokine (TARC/CCL17), serotonin and arachidonic acid metabolites.
A biochemical study on the effect of proteolysis of beta-thromboglobulin proteins released from activated platelets on fibroblast proliferation.
Krishnan et al., Thiruvananthapuram, India. In Pathophysiol Haemost Thromb, 2006
beta-TG is cleaved after being released from activated platelets, thereby becoming less mitogenic for fibroblasts
The paradox of platelet activation and impaired function: platelet-von Willebrand factor interactions, and the etiology of thrombotic and hemorrhagic manifestations in essential thrombocythemia and polycythemia vera.
van Vliet et al., Antwerp, Belgium. In Semin Thromb Hemost, 2006
Patients with essential thrombocythemia (ET) and polycythemia vera (PV), complicated by microvascular ischemic or thrombotic events, have shortened platelet survival, increased beta-thromboglobulin, platelet factor 4, and thrombomodulin levels, and increased urinary thromboxane B2 excretion.
Clinical and laboratory features, pathobiology of platelet-mediated thrombosis and bleeding complications, and the molecular etiology of essential thrombocythemia and polycythemia vera: therapeutic implications.
Schroyens et al., Antwerp, Belgium. In Semin Thromb Hemost, 2006
ET patients with microvascular disturbances have shortened platelet survival, increased beta-thromboglobulin (beta-TG), platelet factor 4 (PF4), and thrombomodulin (TM) levels, and increased urinary thromboxane B2 (TXB2) excretion, indicating platelet-mediated thrombotic processes.
[Advancement of platelet activation measurement: focusing on platelet-derived microparticle measurement].
Matsuno et al., Sapporo, Japan. In Rinsho Byori, 2006
Various methods (platelet factor 4: PF4, beta-thromboglobulin: beta-TG, CD62P, PAC-1, etc.) are used as markers of platelet activation.
Gamma-interferon transcriptionally regulates an early-response gene containing homology to platelet proteins.
Ravetch et al., In Nature, 1985
This gene encodes a protein of relative molecular mass (Mr) 12,378 which has significant amino-acid homology to platelet factor-4 and beta-thromboglobulin, two chemotatic proteins released by platelets on degranulation.
Prognostic value of beta-thromboglobulin in patients with transient cerebral ischaemia.
Forbes et al., In Lancet, 1983
Plasma levels of beta-thromboglobulin (BTG) and fibrinopeptide A (FPA), markers of platelet alpha-granule release and thrombin generation respectively, were measured in 27 subjects with transient cerebral ischaemic attacks (TIA), 43 age-matched controls, and 32 young controls.
Effect of fish oil on platelet kinetics in patients with ischaemic heart disease.
Saynor et al., In Lancet, 1982
After 5 weeks the fish oil caused a 10% lengthening in platelet survival time, a 15% fall in platelet count, a 75% fall in plasma levels of platelet factor 4, and a 30% fall in plasma-beta-thromboglobulin.
Enhanced in-vivo platelet release reaction, increased thromboxane synthesis, and decreased prostacyclin release after tourniquet ischaemia.
Kakkar et al., In Lancet, 1980
Plasma beta-thromboglobulin (beta-TG), a marker of in-vivo platelet release reaction, was measured in 27 meniscectomy patients, 10 patients who underwent total knee replacements (TKR) (both procedures performed under tourniquet ischaemia), and 10 herniorrhaphy patients.
Prostacyclin to prevent platelet activation during charcoal haemoperfusion in fulminant hepatic failure.
Weston et al., In Lancet, 1980
No platelet losses were observed in the six patients treated with haemoperfusion and PGI2 infusion, and there was significant protection from platelet activation, as assessed by the prevention of release into plasma of the platelet-specific protein beta-thromboglobulin.
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