PDGF â_Receptor (739_746) (phosphorylated) Formula C48H62N9O18PS Sequence Tyr(PO3H2)_Met_Ala_Pro_Tyr_Asp_Asn_Tyr
- Known as:
- PDGF â_Receptor (739_746) (phosphorylated) Formula C48H62N9O18PS Sequence L-tyrosine(PO3H2)_Met_Ala_Pro_Tyr_Asp_Asn_Tyr
- Catalog number:
- 89818
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- GLSChina
- Gene target:
- PDGF â_Receptor (739_746) (phosphorylated) Formula C48H62N9O18PS Sequence Tyr(PO3H2)_Met_Ala_Pro_Tyr_Asp_Asn_Tyr
Related genes to: PDGF â_Receptor (739_746) (phosphorylated) Formula C48H62N9O18PS Sequence Tyr(PO3H2)_Met_Ala_Pro_Tyr_Asp_Asn_Tyr
- Gene:
- PDGFA NIH gene
- Name:
- platelet derived growth factor subunit A
- Previous symbol:
- -
- Synonyms:
- PDGF1, PDGF-A
- Chromosome:
- 7p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
- Gene:
- PDGFRA NIH gene
- Name:
- platelet derived growth factor receptor alpha
- Previous symbol:
- -
- Synonyms:
- CD140a, PDGFR2, GAS9
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-19
- Date modifiied:
- 2019-04-23
- Gene:
- PDGFRB NIH gene
- Name:
- platelet derived growth factor receptor beta
- Previous symbol:
- PDGFR
- Synonyms:
- JTK12, CD140b, PDGFR1
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: PDGF â_Receptor (739_746) (phosphorylated) Formula C48H62N9O18PS Sequence Tyr(PO3H2)_Met_Ala_Pro_Tyr_Asp_Asn_Tyr
Paliperidone N-Oxide CAS: 761460-08-6 Formula: C23H27FN4O4 2,4-Dibromo-17,17-ethylenedioxy-1,3,5(10)-estratriene-3,16α-diol CAS: 90474-20-7 Formula: C20H24Br2O4 2,4-Dibromo-17,17-ethylenedioxy-1,3,5(10)-estratriene-3-ol CAS: Formula: C20H24Br2O3 3,3',5,5'-Tetraiodo Thyroformic Acid CAS: 2055-97-2 Formula: C13H6I4O4 3,5,3',5'-Tetrachlorobisphenol A CAS: 79-95-8 Formula: C15H12Cl4O2 4-(2,6,6-Trimethyl-2-cyclohexen-1-ylidene)-2-acetoxybut-2-ene CAS: 61693-39-8 Formula: C15H22O2 4-Benzyloxy-1-cyclohexanecarbonitrile (cis / trans mixture) CAS: 95233-32-2 Formula: C14H17NO 5-[(4-Methoxyphenyl)-diphenylmethylamino-6-methoxy-9H-purin-9-yl]-13C2, 15N-3-(phenylmethoxy)-2-[(phenylmethoxy)methyl]-cyclopentanol CAS: Formula: 6-Phenylhexylamine Hydrochloride CAS: 120375-57-7 Formula: C12H20ClN Paliperidone-d4 CAS: 1020719-55-4 Formula: C23H23D4FN4O3"Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP" Related articles to: PDGF â_Receptor (739_746) (phosphorylated) Formula C48H62N9O18PS Sequence Tyr(PO3H2)_Met_Ala_Pro_Tyr_Asp_Asn_Tyr
- BACKGROUND: Chronic migraine is a disabling neurological disorder with complex mechanisms. The trigeminal nucleus caudalis (TNC) is a critical relay in migraine pathogenesis, yet its cellular and molecular underpinnings remain unclear. METHODS: We applied single-nucleus RNA sequencing (snRNA-seq) to the TNC of a nitroglycerin (NTG)-induced chronic migraine mouse model and controls. Major neuronal classes were annotated, followed by subclustering of GABAergic neurons. We assessed cell-type abundance changes, reconstructed transcriptional trajectories, and applied network- and pathway-level analyses including high-dimensional weighted gene co-expression network analysis (hdWGCNA), pseudotime modeling, and CellChat-based intercellular communication profiling. RESULTS: We identified a previously unrecognized GABAergic subpopulation characterized by high Nox4 expression (GABA_Nox4). This subpopulation was significantly reduced in NTG-treated mice compared with controls (p = 0.018), a finding further validated by immunofluorescence staining. hdWGCNA identified a migraine-associated co-expression module enriched in GABA_Nox4 neurons, which was further supported by disease enrichment analysis. Pseudotime analysis showed that GABA_Nox4 neurons diverged into distinct transcriptional states under NTG treatment. Intercellular communication analysis revealed enhanced crosstalk of GABA_Nox4 neurons with astrocytes, endothelial cells, and OPCs in the NTG group, mediated by NTG-enriched ligand–receptor pairs such as Agrn–Dag1, Ncam1–Ncam2, and endothelial-derived Ncam1–L1cam, whereas VEH-specific interactions such as Pdgfa–Pdgfra and Pdgfa–Pdgfrb were diminished. CONCLUSIONS: Our integrative single-cell analysis identifies GABA_Nox4 neurons as a vulnerable and communication-active GABAergic subpopulation in the TNC that is selectively reduced and transcriptionally reprogrammed in chronic migraine. The disruption of inhibitory signaling and rewiring of ligand–receptor networks highlight this population as a potential cellular driver of migraine pathophysiology and a candidate target for therapeutic intervention. - Source: PubMed
Publication date: 2025/11/18
Xu YunhaoDeng YipingWu PeiyuTian MengkeLiu ChenLiu XuyangLiu DanhuaGuo YinanWang PengfeiXu YumingWang YonggangLi Yusheng - Epithelial ovarian cancer (OC) is the deadliest gynecological malignancy worldwide. Blocking angiogenesis with bevacizumab, an antibody targeting vascular endothelial growth factor (VEGF), shows efficacy in different lines of OC therapy. This study investigates the clinical impact of tumoral expression of angiogenesis-related genes and their association with bevacizumab response in OC in retrospective analysis of three independent cohorts. - Source: PubMed
Publication date: 2023/02/07
Wieser VerenaTsibulak IrinaReimer Daniel UweZeimet Alain GustaveFiegl HeidelindeHackl HubertMarth Christian - There is no effective treatment for the total recovery of myocardial injury caused by an anticancer drug, doxorubicin (Dox). In this study, using a Dox-induced cardiac injury model, we compared the cardioprotective effects of ventricular cells harvested from 11.5-day old embryonic mice (E11.5) with those from E14.5 embryos. Our results indicate that tail-vein-infused E11.5 ventricular cells are more efficient at homing into the injured adult myocardium, and are more angiogenic, than E14.5 ventricular cells. In addition, E11.5 cells were shown to mitigate the cardiomyopathic effects of Dox. In vitro, E11.5 ventricular cells were more migratory than E14.5 cells, and RT-qPCR analysis revealed that they express significantly higher levels of cytokine receptors , , , and . Remarkably, mRNA levels for and were also found to be elevated in the Dox-injured adult heart, as were the FGF1 and PDGFB protein levels. Addition of exogenous FGF1 or PDGFB was able to enhance E11.5 ventricular cell migration in vitro, and, whereas their neutralizing antibodies decreased cell migration. These results indicate that therapies raising the levels of FGF1 and PDGFB receptors in donor cells and or corresponding ligands in an injured heart could improve the efficacy of cell-based interventions for myocardial repair. - Source: PubMed
Publication date: 2021/11/03
Baguma-Nibasheka MarkFeridooni TiamZhang FeixiongPasumarthi Kishore B S - While the anti-PDGFRA antibody olaratumab failed to confirm an impact on survival in unselected advanced soft tissue sarcoma (STS) patients, the level of expression and the prognosis of platelet-derived growth factor (PDGF) receptors and ligands in STS remain unclear. - Source: PubMed
Publication date: 2021/01/29
Brahmi MLesluyes TDufresne AToulmonde MItaliano AMir OLe Cesne AValentin TChevreau CBonvalot SPenel NCoindre J-MLe Guellec SLe Loarer FKaranian MBlay J-YChibon F - Platelet Derived Growth Factor Receptor (PDGFR) signaling is a central mitogenic pathway in development, as well as tissue repair and homeostasis. The rules governing the binding of PDGF ligand to the receptor to produce activation and downstream signaling have been well defined over the last several decades. In cultured cells after a period of serum deprivation, treatment with PDGF leads to the rapid formation of dramatic, actin-rich Circular Dorsal Ruffles (CDRs). Using CDRs as a robust visual readout of early PDGFR signaling, we have identified several contradictory elements in the widely accepted model of PDGF activity. Employing CRISPR/Cas9 gene editing to disrupt the Pdgfra gene in two different murine cell lines, we show that in addition to the widely accepted function for PDGFR-beta in CDR formation, PDGFR-alpha is also clearly capable of eliciting CDRs. Moreover, we demonstrate activity for heterodimeric PDGF-AB ligand in the vigorous activation of PDGFR-beta homodimers to produce CDRs. These findings are key to a more complete understanding of PDGF ligand-receptor interactions and their downstream signaling consequences. This knowledge will allow for more rigorous experimental design in future studies of PDGFR signaling and its contributions to development and disease. - Source: PubMed
Publication date: 2020/11/09
Kadrmas Julie LBeckerle Mary CYoshigi Masaaki