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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Platelet factor 4

platelet factor 4, PF4
This gene encodes a member of the CXC chemokine family. This chemokine is released from the alpha granules of activated platelets in the form of a homotetramer which has high affinity for heparin and is involved in platelet aggregation. This protein is chemotactic for numerous other cell type and also functions as an inhibitor of hematopoiesis, angiogenesis and T-cell function. [provided by RefSeq, Mar 2012] (from NCBI)
Top mentioned proteins: CAN, HAD, V1a, P-selectin, beta-Thromboglobulin
Papers using platelet factor 4 antibodies
Talin is required for integrin-mediated platelet function in hemostasis and thrombosis
Ginsberg Mark H. et al., In The Journal of Experimental Medicine, 2005
... Pf4-Cre transgenic mice allow the generation ...
Papers on platelet factor 4
Serum Biomarkers of Allergic Contact Dermatitis: A Pilot Study.
Girkontaitė et al., Vilnius, Lithuania. In Int Arch Allergy Immunol, Feb 2016
RESULTS: Serum levels of adiponectin, chemokine (C-C motif) ligand 5 (CCL5), C-reactive protein (CRP), chitinase 3-like 1 (CHI3L1), complement factor D (CFD), endoglin, lipocalin-2, osteopontin, retinol-binding protein 4 (RBP4), and platelet factor 4 (PF4) were significantly higher, whereas levels of trefoil factor 3 (TFF3) were significantly lower, in ACD patients than in healthy controls.
Heparin-Induced Thrombocytopenia in Contemporary Cardiac Surgical Practice and Experience With a Protocol for Early Identification.
Lindsay et al., Washington, D.C., United States. In Am J Cardiol, Feb 2016
Patients with thrombocytopenia were tested for antiplatelet factor 4 (PF4)/heparin antibodies by ELISA and clinical evidence of thrombosis sought.
Diagnostic accuracy of rapid immunoassays for heparin-induced thrombocytopenia. A systematic review and meta-analysis.
Cuker et al., Philadelphia, United States. In Thromb Haemost, Feb 2016
UNASSIGNED: The platelet factor 4/heparin ELISA has limited specificity for heparin-induced thrombocytopenia (HIT) and frequently does not provide same-day results.
Effects of a Foot Pump on the Incidence of Deep Vein Thrombosis After Total Knee Arthroplasty in Patients Given Edoxaban: A Randomized Controlled Study.
Migita et al., Nagasaki, Japan. In Medicine (baltimore), Jan 2016
Immunoglobulin G (IgG)-class anti-PF4/heparin antibodies were measured using an IgG-specific enzyme-linked immunosorbent assay.The incidences of any DVT up to POD28 were 31.0%
Bmi strongly impacts the diagnosis and incidence of hit in the Sicu.
Margulies et al., Los Angeles, United States. In J Trauma Acute Care Surg, Jan 2016
Data collected included Warkentin 4-T scores, anti-platelet factor 4 (anti-PF4OD), Serotonin Release Assay (SRA), and thromboembolic diseases.
Heparin-induced thrombocytopenia.
Warkentin, Hamilton, Canada. In Curr Opin Crit Care, Dec 2015
Most patients who form anti-PF4/heparin antibodies do not develop HIT, contributing to HIT overdiagnosis.
The platelet Fc receptor, FcγRIIa.
Gardiner et al., Melbourne, Australia. In Immunol Rev, Nov 2015
Finally, we present some new data investigating whether levels of the extracellular ligand-binding region of platelet glycoprotein VI which is rapidly shed upon engagement of platelet FcγRIIa by autoantibodies, can report on the presence of pathological anti-heparin/platelet factor 4 immune complexes and thus identify patients with pathological autoantibodies who are at the greatest risk of developing life-threatening thrombosis in the setting of heparin-induced thrombocytopenia.
Platelet granule secretion mechanisms: Are they modified in sepsis?
Sun et al., Zhenjiang, China. In Thromb Res, Nov 2015
In sepsis, platelet factor 4, β-thromboglobulin, and other inflammatory mediators are secreted from platelet granules to participate in the inflammatory response and increase sepsis-related impairments.
Pancreatic cancer and thromboembolic disease, 150 years after Trousseau.
Andrén-Sandberg et al., Lund, Sweden. In Hepatobiliary Surg Nutr, Oct 2015
The exact pathophysiological mechanisms are still partly understood, but it is known that pancreatic cancer induces a prothrombotic and hypercoagulable state and genetic events involved in neoplastic transformation (e.g., KRAS, c-MET, p53), procoagulant factors [e.g., tissue factor (TF), platelet factor 4 (PF4), plasminogen activator inhibitor type 1 (PAI-1)], mucin production (e.g., through activation of P- and L-selectin) and pro-inflammatory factors [e.g., cytokines, cyclooxygenase-2 (COX-2)] may be implicated.
[Heparin-induced thrombocytopenia with pseudo-pulmonary embolism in a patient who was newly introduced to hemodialysis treatment].
Kamata et al., In Nihon Jinzo Gakkai Shi, 2014
Serum analysis was positive for heparin-platelet factor 4 (PF4) antibody.
Megakaryocytes regulate hematopoietic stem cell quiescence through CXCL4 secretion.
Frenette et al., New York City, United States. In Nat Med, 2014
Gene expression analyses revealed that MKs are the source of chemokine C-X-C motif ligand 4 (CXCL4, also named platelet factor 4 or PF4) in the bone marrow, and we found that CXCL4 regulates HSC cell cycle activity.
Platelet factor 4 and Duffy antigen required for platelet killing of Plasmodium falciparum.
Foote et al., Sydney, Australia. In Science, 2013
Here, we show that the platelet molecule platelet factor 4 (PF4 or CXCL4) and the erythrocyte Duffy-antigen receptor (Fy) are necessary for platelet-mediated killing of Plasmodium falciparum parasites.
Dynamic antibody-binding properties in the pathogenesis of HIT.
Cines et al., Philadelphia, United States. In Blood, 2012
Differences in the properties of anti-PF4 antibodies that cause thrombocytopenia not revealed by ELISA that correlate with oligomerization of PF4 and sustained high-avidity interactions that may simulate transient antibody-antigen interactions in vivo.
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.
Identification of the platelet-derived chemokine CXCL4/PF-4 as a broad-spectrum HIV-1 inhibitor.
Lusso et al., Bethesda, United States. In Proc Natl Acad Sci U S A, 2012
blockade of HIV-1 infection occurs at the level of virus attachment and entry via a unique mechanism that involves direct interaction of CXCL4 with the major viral envelope glycoprotein, gp120
VEGF, PF4 and PDGF are elevated in platelets of colorectal cancer patients.
Folkman et al., Rochester, United States. In Angiogenesis, 2012
VEGF, PF4 and PDGF are elevated in platelets of colorectal cancer patients
CXCL4-platelet factor 4, heparin-induced thrombocytopenia and cancer.
Sandset, Oslo, Norway. In Thromb Res, 2012
The present review describes the role of CXCL4-PF4 in cancer, the immunobiology, clinical presentation and diagnosis of HIT, and the specific problems faced in cancer patients.
Disrupting functional interactions between platelet chemokines inhibits atherosclerosis in hyperlipidemic mice.
Weber et al., Aachen, Germany. In Nat Med, 2009
Activated platelets can synergize with chemokines to exacerbate atherogenesis; for example, by deposition of the chemokines platelet factor-4 (PF4, also known as CXCL4) and RANTES (CCL5), triggering monocyte arrest on inflamed endothelium.
Circulating activated platelets exacerbate atherosclerosis in mice deficient in apolipoprotein E.
Ley et al., Charlottesville, United States. In Nat Med, 2003
The interactions of activated platelets with monocytes and atherosclerotic arteries led to delivery of the platelet-derived chemokines CCL5 (regulated on activation, normal T cell expressed and secreted, RANTES) and CXCL4 (platelet factor 4) to the monocyte surface and endothelium of atherosclerotic arteries.
Temporal aspects of heparin-induced thrombocytopenia.
Kelton et al., Hamilton, Canada. In N Engl J Med, 2001
We also investigated the persistence of circulating heparin-dependent antibodies by performing a platelet serotonin-release assay and an assay for antibodies against platelet factor 4. The outcome in seven patients who had previously had an episode of heparin-induced thrombocytopenia and were later treated again with heparin was also examined.
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