|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for PF4(NM_001363352.1) Search again
Product ID:
HQP104434
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CXCL4, PF-4, SCYB4
Gene Description:
platelet factor 4
Target Gene Accession:
NM_001363352.1(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
Platelet factor-4 is a 70-amino acid protein that is released from the alpha-granules of activated platelets and binds with high affinity to heparin. Its major physiologic role appears to be neutralization of heparin-like molecules on the endothelial surface of blood vessels, thereby inhibiting local antithrombin III activity and promoting coagulation. As a strong chemoattractant for neutrophils and fibroblasts, PF4 probably has a role in inflammation and wound repair (Eisman et al., 1990 [PubMed 1695112]).[supplied by OMIM].
Gene References into function
- a second epitope for heparin-induced thrombocytopenia/thrombosis antibodies is defined by epitope mapping
- Signaling transduction induced by PF4 in erythroleukemia cells was compared with that induced by TGFB1, which is also a potent inhibitor of HEL growth.
- PF4 inhibits T cell function by down-modulating cell proliferation and cytokine release and therefore has a potential role as a mediator of long-term effects in the regulation of inflammatory processes in vivo.
- CXCL4 at substimulatory dosages modulates CTAP-III- as well as CXCL7-induced adhesion of neutrophils to vascular endothelium.
- Platelet factor 4 induces human natural killer cells to synthesize and release interleukin-8.
- Platelet factor 4 inhibits FGF2-induced endothelial cell proliferation via the extracellular signal-regulated kinase pathway but not by the phosphatidylinositol 3-kinase pathway.
- PF4 may modulate the hematopoietic milieu both by promoting progenitor adhesion and by binding to or interfering with signaling caused by hematopoietically active chemokines, such as IL-8
- physiologically relevant concentrations of PF4 stimulate thrombin-dependent activated protein C generation in cultured vascular endothelial cells
- PREP1 regulates PF4 gene expression.
- Gene profiling identified PF4 from peripheral blood cells in coronary artery disease.
- results suggested a model by which PF4 bound to proximal (but distinct) sites to antithrombin (AT) resulting in steric interference of factor Xa binding to both polysaccharide and AT
- PF4 neutrophil adhesion is controlled by src-kinases and PF-4-mediated exocytosis requires activation of p38 MAP kinase and phosphatidylinositol 3-kinase
- correlation between PF4 deposition, lesion severity and symptomatic atherosclerosis; PF4 was commonly found in macrophages of early lesions
- Review: PF-4 isinteracts directly with angiogenesis growth factors and inhibits their interaction with cell surface receptors, perhaps playing a role as an endogenous angiogenesis regulator; role in cancer pathology
- PF4 promoters are transactivated by USF1 and 2 which may play an important role in megakaryocytic gene expression
- PF-4 acts on macrophages in a dual manner. PF-4 may play a crucial role in the induction and maintenance of an unspecific immune response.
- PF-4 strongly inhibited the VEGF(165)- and VEGF(121)-induced mitogen-activated protein (MAP) kinase signalling pathways
- The capacity of PF4 to form ultralarge complexes composed of multiple PF4 tetramers arrayed in a lattice with several molecules of unfractionated heparin may play a fundamental role in autoantibody formation, antibody-dependent platelet activation.
- Interactions with PF4 require structural motifs important in RANTES oligomerization and amplify RANTES-triggered effects on monocyte adhesion.
- Induction of E-selectin RNA in umbilical vein endothelial cells exposed to PF4 is time and dose dependent; PF4 induces E-selectin expression by activation of transcriptional activity
- Human platelet factor 4 stimulates proliferation of naturally anergic human CD4+CD25+ T regulatory cells while inhibiting proliferation of CD4+CD25- T nonregulatory cells.
- Expression of PF4 is up-regulated at the mRNA and protein level by thrombin and mediated by proteinase-activated receptors (PARs), resulting in a 32- to 128-fold higher mRNA level and leading to an up-to-sixfold increase of the peptide concentration.
- analysis of granule targeting sequence within platelet factor 4
- PTEN expression negatively regulates CXCR4-meidated chemotaxis of lymphoid mammalian cells via its lipid phosphatase activity
- cell-surface PF4 complexes are antigenic only over a restricted concentration range of PF4. Heparin is not required for HIT antibody binding but shifts the concentration of PF4 needed for optimal surface antigenicity to higher levels
- activated human skin mast cells (MCs) convert CTAP-III into biologically active NAP-2 through proteolytic cleavage by released chymase
- Salmonella could be used in vivo as a PF4 DNA delivery vector in the management of radiation injury
- a candidate tumor suppressor gene, platelet factor 4, was frequently silenced by promoter hypermethylation in MM (15 of 28) and MM cell lines (5 of 5)
- CXCL4 seals blood clots by altering the structure of fibrin
- CXCL4 and CXCL4L1 exhibit a distinct subcellular localization and are secreted in a differentially regulated manner, suggesting distinct roles in inflammatory or homeostatic processes.
- CXCL4 decreased serum levels in advanced MDS, suggesting the possibility of a concerted disturbance of transcription or translation of these chemokines in advanced MDS
- angiostatic non-ELR CXC chemokines may increase to balance angiogenic ELR+ CXC chemokines in which increased levels were shown in patients with inflammatory arthritides and CXCL4 may contribute to designate the chronicity of synovitis in patients with RA
- Several PF4 fragments and modified molecules exhibit antiangiogenesis properties and may become an alternative for further therapeutic angiogenesis.
- a high titer of antibodies to PF4 but no relationship was found between that and heparin induced thrombocytopenia or thrombosis in this Turkish population.
- PF4-stimulated immediate monocyte functions (oxygen radical formation) are regulated by p38 MAPK, Syk, and PI3K, whereas delayed functions (survival and cytokine expression) are controlled by Erk and JNK.
- Patients with isolated coronary artery ectasia (CAE) have raised levels of plasma P-selectin, beta-TG and PF4 compared with control participants with angiographically normal coronary arteries, suggesting increased platelet activation in patients with CAE
- These findings indicate that the equilibrium between angiostatic and angiogenic factors during inflammation and tumor progression is rather complex and differs depending on the chemokine, cell type, and stimulus.
- platelet-associated PF-4, but not its plasma counterpart, may represent a potential biomarker of early tumor presence
- This study demonstrates that PF4 protein levels are a good indicator for the recovery of blood count in the complete remission of acute myeloid leukemia.
- possible roles of CXCL4 in monocyte arrest and macrophage foam cell formation in atherosclerosis
- Literature analysis of commercial immunoassay results detecting platelet factor 4/heparin antibodies in healthy subjects.
- PF4 or anti-PF4 antibody alone did not alter neutrophil function, costimulation with both reagents resulted in approximately 3-fold increase in neutrophil cell surface antigens
- delayed pressure urticaria may be associated with increased secretion of platelet chemokines PF4 and beta-TG, similar to that observed in cold urticaria
- human umbilical vein endothelial cells adhere to immobilized CXCL4 through alphavbeta3 integrin, and also through other integrins, such as alphavbeta5 and alpha5beta1