PDGFR Tyrosine Phosphorylation Array
- Known as:
- PDGFR Tyrosine Phosphorylation Array
- Catalog number:
- MA3043
- Product Quantity:
- Kit
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- PDGFR Tyrosine Phosphorylation Array
Related genes to: PDGFR Tyrosine Phosphorylation Array
- 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: PDGFR Tyrosine Phosphorylation Array
105 kDa islet cell antigen,BEM-3,Brain-enriched membrane-associated protein tyrosine phosphatase,ICA105,PTP IA-2,PTPLP,Ptprn,Rat,Rattus norvegicus,Receptor-type tyrosine-protein phosphatase-like N,R-P12 Major types of paired cancer_normal array12 Major types of paired cancer_normal array12 Major types of paired cancer_normal array12 Major types of paired cancer_normal array12 Major types of paired cancer_normal array other12 Major types of paired cancer_normal array other14-3-3 epsilon. (1-255aa). Human. Recombinant. E Coli - Tyrosine 3-monooxygenase; tryptophan 5-monooxygenase activation protein. epsilon polypeptide N_A14-3-3 epsilon. (1-255aa). Human. Recombinant. E Coli - Tyrosine 3-monooxygenase; tryptophan 5-monooxygenase activation protein. epsilon polypeptide N_A14-3-3 gamma. (1-247aa). Human. Recombinant. E Coli - Tyrosine 3-monooxygenase; tryptophan 5-monooxygenase activation protein. gamma polypeptide; Protein kinase C inhibitor protein 1; KCIP-1 N_A14-3-3 gamma. (1-247aa). Human. Recombinant. E Coli - Tyrosine 3-monooxygenase; tryptophan 5-monooxygenase activation protein. gamma polypeptide; Protein kinase C inhibitor protein 1; KCIP-1 N_A14-3-3 tau. (1-245aa). Human. Recombinant. E Coli - Tyrosine 3-monooxygenase; tryptophan 5-monooxygenase activation protein. theta polypeptide N_A14-3-3 tau. (1-245aa). Human. Recombinant. E Coli - Tyrosine 3-monooxygenase; tryptophan 5-monooxygenase activation protein. theta polypeptide N_A15 Major types of cancer tissue array15 Major types of cancer tissue array Related articles to: PDGFR Tyrosine Phosphorylation Array
- Growth plate injuries in pediatric patients can lead to serious musculoskeletal complications, such as bony bar formation and potential growth arrest. Current clinical treatments have significant limitations, necessitating improved research models. The present study developed a highly reproducible drill-hole injury model in the mouse distal femur and introduces a quantitative scoring system for assessing bony bar formation. Using micro-computed tomography (μCT) and histological analyses, we demonstrate a progressive increase in bone tissue formation over a 42-day period. A 5-point grading system was developed to evaluate bony bar extent, validated through radiological and histological comparisons. We further examine the utility of the model by injuring either transgenic mice with lineage tracing for platelet-derived growth factor receptor alpha (Pdgfra) or beta (Pdgfrb). While not present before injury, both Pdgfra and Pdgfrb reporter+ cells migrate into sites of growth plate injury and participate in bony bar formation. In sum, this model offers a standardized, reproducible, and validated approach to quantitatively study growth plate injury mechanisms, facilitating the use of transgenic animal models or the development of new therapeutic strategies in pediatric orthopaedics. - Source: PubMed
Publication date: 2026/03/25
Li ZhaoZhou MylesXing XinDu BeichengArcher MaryRao ChunbaoZhu ManyuJames Aaron W - Circular RNAs (circRNAs) play critical regulatory roles in diverse biological processes of breast cancer. This study aimed to investigate the circRNAs potentially related to immunity in triple-negative breast cancer (TNBC). - Source: PubMed
Gao FengqinGong MingkaiCao YufengLiu XiaoyiCui JianDu BingDou RongrongWei ChuankuiSong Hongming - Heterogeneity is widely recognised across different cell types. Human oligodendrocyte progenitor cells (hOPCs), essential for myelination, exhibit considerable heterogeneity, which has not been fully characterised. In the current study, by examining the transcriptome of hOPCs at the single-cell level, three distinct subclusters were identified: PRE-OPCs, OPCs, and PRE-OLs. Single-cell RNA-sequencing and RNA-Scope detected high platelet-derived growth factor receptor alpha (PDGFRA) expression. PDGFR-α hOPCs exhibited greater myelination, migration, and proliferation capabilities compared to both unsorted hOPCs and PDGFR-α hOPCs. These enhanced functions may be associated with the activation of the PI3K-AKT-mTOR and TGF-β signalling pathways, which support oligodendrocyte differentiation. hOPCs were induced by hNSCs, their characteristics were identified. RNA-Scope and single-cell RNA Seq sequencing showed PDGFRA were highly expressed at mRNA and protein level. hOPCs were sorted by MACS using PDGFR-α beads. The myelination, migration, and proliferation abilities of PDGFR-α hOPCs were higher than that of un-sorting hOPCs and PDGFR-α hOPCs, possibly being associated with the activation of PI3K-AKT-mTOR and TGF-β signalling pathways, which support oligodendrocyte differentiation (Partly created with Scientific Image and Illustration Software BioRender). - Source: PubMed
Publication date: 2026/03/02
Ye DouZhou HaipengQu SuqingWang ZhaoyanZhang FanWang XiaohuaZhao YuanLiang JialanWang QianLuan ZuoYang Yinxiang - A type II Platelet-Derived Growth Factor Receptor Alpha PDGFRA) human kinase inhibitor , with antiplasmodium activity against asexual blood stage parasites (NF54 IC = 0.22 μM) was identified from the Kinase Chemogenomics Set, a collection of narrow-spectrum human kinase inhibitors. Medicinal chemistry progression of the hit focused on improving potency, selectivity, and ADME properties, leading to compounds , , and with improved microsomal metabolic stability and asexual blood stage antiplasmodium activity. Mechanism of action studies showed that this series inhibits hemozoin formation, killing late-stage trophozoites. - Source: PubMed
Publication date: 2025/12/26
Mmonwa Mmakwena MAudu OluwatosinMaepa KeletsoDziwornu Godwin AGovender PreshenTshaka LisoBurrows JamesTaylor DaleMasike KeabetsweNjoroge MathewWicht Kathryn JCoulson Lauren BChibale Kelly - Myeloid/Lymphoid Neoplasms with Eosinophilia and Tyrosine Kinase Gene Fusions (MLN-eo-TK) represent a distinct and heterogeneous group of hematologic malignancies characterized by recurrent gene fusions involving tyrosine kinases, such as PDGFRA, PDGFRB, FGFR1, JAK2, FLT3, ETV::ABL1 and other partner genes/variants. Among these, gene rearrangements involving PCM1::JAK2 are rare and may present diagnostic challenges, particularly when manifesting as acute lymphoblastic leukemia (ALL). We describe a case of a patient who presented with B-cell acute lymphoblastic leukemia (B-ALL) with a JAK2 rearrangement. After the induction therapy, strong myeloid proliferation in bone marrow without evidence of residual lymphoblasts was observed and JAK2 rearrangement was recognized to be a consequence of translocation t(8;9)(p22;p24)] resulting in PCM1::JAK2 fusion. This finding indicated the presence of an underlying chronic myeloid/lymphoid neoplasm, meeting criteria for MLN-eo-TK. Following an inadequate response to standard chemotherapy, salvage regimens incorporating targeted agents (JAK2 and BCL-2 inhibitors) and allogeneic bone marrow transplantation were administered, all of which unfortunately resulted in short-lived clinical benefit. The case highlights the importance of distinguishing de novo lymphoid malignancies from MLN-eo-TK, especially when JAK2 rearrangements are detected. Recognition of the clonal myeloid component during or after lymphoid-directed therapy has important diagnostic and therapeutic implications, supporting the use of targeted JAK2 inhibition in addition to standard chemotherapy. - Source: PubMed
Publication date: 2026/01/14
Čemažar LukaŠlajpah KlaraGredelj Šimec NjetočkaPodgornik Helena