Platelet factor 4 CXCL4, Human
- Known as:
- Platelet factor 4 CXCL4, Human
- Catalog number:
- Z03026-10
- Product Quantity:
- 10,0ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- Platelet factor 4 CXCL4 Human
Related genes to: Platelet factor 4 CXCL4, Human
- Gene:
- PF4 NIH gene
- Name:
- platelet factor 4
- Previous symbol:
- -
- Synonyms:
- SCYB4, CXCL4
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2017-12-06
- Gene:
- PF4V1 NIH gene
- Name:
- platelet factor 4 variant 1
- Previous symbol:
- -
- Synonyms:
- SCYB4V1, CXCL4V1, CXCL4L1
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2016-10-05
Related products to: Platelet factor 4 CXCL4, Human
Related articles to: Platelet factor 4 CXCL4, Human
- Megakaryopoiesis is an elaborate biological process that primarily occurs in the bone marrow. To gain deeper insights into molecular mechanisms driving normal megakaryopoiesis, we utilized an in vitro human megakaryocytic culture system based on mobilized peripheral blood-derived CD34 cells. Following fluorescence-activated cell sorting (FACS) isolation of CD41 and CD41 megakaryocyte (MK) subsets, mature MKs were confirmed through characterization of MK-specific surface markers, ploidy analysis, Giemsa staining, and immunofluorescence. Subsequent bulk RNA sequencing of these distinct populations enabled the identification of differentially expressed genes (DEGs) and enriched pathways. Based on our CD34-derived MK differentiation model, the expression of CD41 was found robustly induced by day 4 and further elevated by day 10. The CD41 population exhibited marked co-expression of CD42b and CD61, a significantly higher proportion of polyploid cells (≥16 N), along with characteristic morphological features of mature MKs, including proplatelet formation, cytoplasmic maturation, and cell size enlargement compared to the CD41 subset. Transcriptomic profiling of these two populations identified 1877 up-regulated and 1817 down-regulated DEGs in CD41 MKs. Protein-protein interaction (PPI) network analysis of the key DEGs revealed hub genes including VWF, PF4V1, SELP, PF4, GP1BA, CD40LG, PPBP, CLEC1B, P2RY12, and THBS1. Functional enrichment underscored the acquisition of migratory, adhesive, and secretory capacities, marked by significant upregulation of platelet activation and wound healing signatures. Pathway analysis further indicated coordinated activation of focal adhesion, cytoskeletal reorganization, glycerolipid metabolism, and neuroactive ligand-receptor interaction during maturation. This study provides an integrative transcriptomic blueprint of human MK maturation and highlights the novel candidate targets for thrombopoiesis. - Source: PubMed
Publication date: 2026/05/15
Zhang ZiyanWang YueLiu Peng - Over 60% of End Stage Renal Disease (ESRD) patients are relying on hemodialysis (HD) to survive, and the arteriovenous fistula (AVF) is the preferred vascular access method for HD. However approximately half of all newly created AVF fail to mature and cannot be used without a salvage procedure. We have recently demonstrated an association between AVF maturation failure and post-operative fibrosis, while our RNA-seq study also revealed that veins that ultimately failed during AVF maturation had elevated levels of platelet factor 4 (PF4/CXCL4). However, a link between these two findings was yet to be established. - Source: PubMed
Publication date: 2023/08/17
Xiao YuxuanMartinez LaiselZigmond ZacharyWoltmann DanielSinger Diane VSinger Harold AVazquez-Padron Roberto ISalman Loay H - Platelet factor 4 (CXCL4) is a chemokine abundantly stored in platelets. Upon injury and during atherosclerosis, CXCL4 is transported through the vessel wall where it modulates the function of vascular smooth muscle cells (VSMCs) by affecting proliferation, migration, gene expression and cytokine release. Variant CXCL4L1 is distinct from CXCL4 in function and expression pattern, despite a minor three-amino acid difference. Here, the effects of CXCL4 and CXCL4L1 on the phenotype and function of human VSMCs were compared in vitro. VSMCs were found to constitutively express CXCL4L1 and only exogenously added CXCL4 was internalized by VSMCs. Pre-treatment with heparin completely blocked CXCL4 uptake. A role of the putative CXCL4 receptors CXCR3 and DARC in endocytosis was excluded, but LDL receptor family members appeared to be involved in the uptake of CXCL4. Incubation of VSMCs with both CXCL4 and CXCL4L1 resulted in decreased expression of contractile marker genes and increased mRNA levels of KLF4 and NLRP3 transcription factors, yet only CXCL4 stimulated proliferation and calcification of VSMCs. In conclusion, CXCL4 and CXCL4L1 both modulate gene expression, yet only CXCL4 increases the division rate and formation of calcium-phosphate crystals in VSMCs. CXCL4 and CXCL4L1 may play distinct roles during vascular remodeling in which CXCL4 induces proliferation and calcification while endogenously expressed CXCL4L1 governs cellular homeostasis. The latter notion remains a subject for future investigation. - Source: PubMed
Publication date: 2022/01/06
Kaczor Dawid MKramann RafaelHackeng Tilman MSchurgers Leon JKoenen Rory R - The mainstay of control of the coronavirus disease 2019 (Covid-19) pandemic is vaccination against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Within a year, several vaccines have been developed and millions of doses delivered. Reporting of adverse events is a critical postmarketing activity. - Source: PubMed
Publication date: 2021/04/16
Scully MarieSingh DeepakLown RobertPoles AnthonySolomon TomLevi MarcelGoldblatt DavidKotoucek PavelThomas WilliamLester William - Exposure to hypoxia, through ascension to high altitudes (HAs), air travel, or human disease, is associated with an increased incidence of thrombosis in some settings. Mechanisms underpinning this increased thrombosis risk remain incompletely understood, and the effects of more sustained hypoxia on the human platelet molecular signature and associated functional responses have never been examined. We examined the effects of prolonged (≥2 months continuously) hypobaric hypoxia on platelets isolated from subjects residing at HA (3,700 meters) and, for comparison, matched subjects residing under normoxia conditions at sea level (50 meters). Using complementary transcriptomic, proteomic, and functional methods, we identified that the human platelet transcriptome is markedly altered under prolonged exposure to hypobaric hypoxia at HA. Among the significantly, differentially expressed genes (mRNA and protein), were those having canonical roles in platelet activation and thrombosis, including membrane glycoproteins (e.g. ), integrin subunits (e.g. ), and alpha-granule chemokines (e.g. ). Platelets from subjects residing at HA were hyperactive, as demonstrated by increased engagement and adhesion to fibrinogen, fewer alpha granules by transmission electron microscopy, increased circulating PF4 and ADP, and significantly enhanced clot retraction. In conclusion, we identify that prolonged hypobaric hypoxia exposure due to HA alters the platelet transcriptome and proteome, triggering increased functional activation responses that may contribute to thrombosis. Our findings may also have relevance across a range of human diseases where chronic hypoxia, platelet activation, and thrombosis are increased. - Source: PubMed
Publication date: 2019/02/05
Shang ChunxiangWuren TanaGa QingBai ZhenzhongGuo LiEustes Alicia SMcComas Kyra NRondina Matthew TGe Rili