Browse our anti-PDGFRA (PDGFRA) Antibodies

Mouse (Murine) Platelet-Derived Growth Factor Receptor, alpha Polypeptide (PDGFRA) interaction partners

1. PDGFRalpha in hepatocytes plays an important role in liver fibrosis by affecting PDGFRalpha expression in HSCs

2. PDGFRalpha has a role in in pathogenesis, progression and prognosis of NK/T-cell lymphoma

3. PDGFR signaling is necessary for postnatal tendon growth and remodeling and MT1-MMP is a critical mediator of tendon fibroblast migration.

4. PDGFR alpha beta and PDGFR beta beta dimers were strong inducers of random and directionally-persistent migration in mouse skin fibroblast, respectively, that was sustained for up to 24 h.

5. These findings revealed complexity in the behavior of the Pdgfra-lineaged cells as exemplified by their distinct contributions to myofibroblasts.

6. STMN1 is a PDGFRalpha phospho-regulated target; its mis-regulation confers sensitivity to vinblastine cytotoxicity in glioblastoma

7. PDGFRalpha enrichment in hepatic stellate cell-derived extracellular vesicles drives liver fibrosis by a SHP2-dependent mechanism

8. PDGFR activity is evenly distributed at different membrane microdomains, while integrin-mediated signaling events have inhibitory effects on the activation of PDGFR specifically located in lipid rafts but not outside rafts.

9. downregulate growth signals provided by PDGFRalpha to initiate oligodendrocyte differentiation and myelination

10. PDGFRA is not essential for the derivation and maintenance of extraembryonic endoderm stem (XEN) cell lines .

11. loss of Pdgfra in endothelial-derived mesenchyme in the outflow tract endocardial cushions leads to a secondary defect in neural crest migration during development.

12. Investigated the developmental process of mesenchymal stem cells (MSCs) in embryos using the gene Pdgfra as a marker. We traced cells expressing Pdgfra and other genes (brachyury, Sox1 and Pmx1) in various mutant embryos until the adult stage. Embryonic MSCs emerge in waves and almost all adult bone marrow MSCs and white adipose tissue MSCs originate from mesoderm and embryonic Pdgfralpha-positive cells.

13. PDGFRalpha/PDGFRbeta signaling balance determines progenitor commitment to beige (PDGFRalpha) or white (PDGFRbeta) adipogenesis.

14. our data establish that aberrant stromal PDGFRalpha signaling disrupts extracellular matrix homeostasis during mammary gland development, resulting in increased mammary stiffness and increased potential for tumor growth.

15. Spreading of PDGFR-alpha-deficient lung fibroblasts was insensitive to increased rigidity, and their migration was not reduced by Rac1-guanine exchange factor (GEF)-inhibition. PDGFR-alpha-expressing fibroblasts migrated toward stiffer regions within two-dimensional substrates by increasing migrational persistence (durotaxis).

16. Histone H3.3K27M and Trp53 loss and PDGFRA overexpression accelerates disease onset and increases tumor invasion.

17. PDGFRalpha(+) cells represent the in vitro counterpart of in vivo PrE precursors, and their selection from cultured mESCs yields pure PrE precursors.

18. The diabetes-induced increase in PDGFRalpha+ cells may be mediated by FOXO3 up-regulation via the inhibition of the PI3K/Akt signaling pathway in STZ-induced diabetic mice.

19. Constitutive activation of PDGFRalpha leads to expansion of cartilage underlying the coronal sutures, which contribute to suture closure through endochondral ossification, in a process regulated in part by PI3K/AKT signaling.

20. OLIG2 modulates growth factor signaling in two distinct populations of glioma stem cells, characterized by expression of either the epidermal growth factor receptor (EGFR) or platelet-derived growth factor receptor alpha.

Rabbit Platelet-Derived Growth Factor Receptor, alpha Polypeptide (PDGFRA) interaction partners

1. High PDGFR expression is associated with retinal neovascularization.

Human Platelet-Derived Growth Factor Receptor, alpha Polypeptide (PDGFRA) interaction partners

1. The current study shows that SH3BP2 is expressed in primary tumors and cell lines from Gastrointestinal stromal tumors (GISTs) patients and that SH3BP2 silencing leads to a downregulation of oncogenic KIT and PDGFRA expression and an increase in apoptosis in imatinib-sensitive and imatinib-resistant GIST cells.

2. gastrointestinal stromal tumors with PDGFRA mutation D842V mutation is resistant to imatinib, and non-D842V mutation can obtain benefit from imatinib treatment

3. Integrated analysis of genomic and transcriptomic data revealed several pathways related to PDGFRA, which could be a strategic target for anti-sarcoma therapy.

4. 16 novel PDGFRA mutations identified from different tumor types and identify three previously uncharacterized activating mutations that promote cell survival and proliferation, were characterized.

5. Describe the development of inflammatory fibroid polyps and gastrointestinal stromal tumors in familial PDGFRA-mutation syndrome.

6. PDGFRalpha has a role in in pathogenesis, progression and prognosis of NK/T-cell lymphoma

7. Protein expression of tumour and/or stromal cell PDGFRalpha, PDGFRbeta and PDGF-CC was evaluated in primary tumours (N = 489), synchronous lymph node metastases (N = 135) and asynchronous recurrences (N = 39) using immunohistochemistry in a prospectively maintained cohort of primary breast cancer patients

8. despite high PDGFRA expression, PDGFRalpha signaling was not essential to BCP-ALL cell survival ex vivo

9. joint bioinformatics analysis was performed to identify the differentially expressed genes (DEGs) in wildtype Gastrointestinal stromal tumors (GISTs)samples compared with KIT/PDGFRA mutant GIST samples

10. Hepatic stellate cells release PDGFRalpha-enriched extracellular vesicles. Alcoholic liver disease patients show an increase in PDGFRalpha enrichment in their serum extracellular vesicles.

11. In addition to replicating a previously identified genome-wide significant locus for corneal astigmatism near the PDGFRA gene, gene-based analysis identified three novel candidate genes, CLDN7, ACP2, and TNFAIP8L3, that warrant further investigation to understand their role in the pathogenesis of corneal astigmatism. (Meta-analysis)

12. The present study showed that PDGFRA amplification could be effectively targeted by pazopanib.

13. KIT and PDGFRA mutations account for 85-90% of GISTs; subsequent genetic studies have led to the identification of mutation/epimutation of additional genes, including the succinate dehydrogenase (SDH) subunit A, B, C, and D genes.

14. we compared the efficacy of first-line therapy, doxorubicin (DOX), and TRAB in a platelet-derived growth factor receptor-alpha (PDGFRA)-amplified PLPS. METHODS: We used a fresh sample of PLPS tumor derived from a 68-year-old male patient diagnosed with a recurrent Pleomorphic liposarcoma

15. PDGFRA D842V mutant binds imatinib with lower affinity with respect to wild-type structure, showing higher stability during the interaction with other type I TKIs (like crenolanib).

16. Altered SK3 channel expression observed in PDGFRalpha(+) cells in UPJ obstruction suggests that the impairment of SK3 activity across the UPJ may perturb upper urinary tract peristalsis in this urological condition

17. None of the 16 analyzable tumors showed mutations in PDGFRA. Thus, PDGFRA mutations probably do not play an important role in the development of sporadic lipomas of the intestines

18. Whole transcriptome sequencing followed by pathway analysis indicated that STXBP4 is involved in functional gene networks that regulate cell growth, proliferation, cell death, and survival in cancer. Platelet-derived growth factor receptor alpha (PDGFRalpha) was a key downstream mediator of STXBP4 function. In line with this, shRNA mediated STXBP4 and PDGFRA knockdown suppressed tumor growth in soft-agar and xenograft ...

19. We report a unique case of an SDH-deficient GIST case with an activating PDGFRA mutation. Oncogenic mutations in GIST are generally mutually exclusive; however documented exceptions exist which may have diagnostic and therapeutic implications.

20. Case Report: concurrent development of myeloproliferative hypereosinophilic syndrome and lymphomatoid papulosis associated with FIP1L1-PDGFRA gene fusion.