Browse our anti-PDGFRA (PDGFRA) Antibodies

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

1. PDGFRA/Pdgfra gene is regulated by at least seven first exons in human and mouse.

2. A subpopulation of oligodendrocyte lineage in the developing cortex is independent of PDGFRalpha signaling.

3. These findings demonstrate how Ca(2+) influx through TRPV4 channels can activate SK channels in PDGFRalpha(+) cells and prevent bladder overactivity during filling.

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

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

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

7. 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.

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

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

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

11. 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.

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

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

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

15. 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.

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

17. 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.

18. 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).

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

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

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. miR3423p was proposed to inhibit the proliferation, migration, invasion and G1/S phase transition of HTR8/SVneo cells by suppressing PDGFRA.

2. PDGFRA/Pdgfra gene is regulated by at least seven first exons in human and mouse.

3. our findings support a pathogenetic relationship between telocyte hyperplasia and both inflammatory fibroid polyp and PDGFRA-mutant gastrointestinal stromal tumour (GIST).

4. these findings are consistent with previous animal studies supporting potential interactions between the PDGFRA gene and maternal alcohol exposure.

5. detecting PDGFRA, PDGFRB, FGFR1 and PCM1-JAK2 rearrangements is a prerequisite for up-to-date WHO classification, and an essential step in the differential diagnosis of neoplasms with eosinophilia.

6. Results suggested that miR-19b-3p may be a promising target in inhibiting PDGFRalpha(+) muscle cell osteogenic differentiation and treatment of HO.

7. single-point mutations in the transmembrane (TM) region reshape the TM dimer ensemble and delineate the structural and dynamic determinants of spontaneous activation of PDGFRA via its TM domain

8. 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.

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

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

11. 16 novel PDGFRA mutations identified from different tumor types and identify three previously uncharacterized activating mutations that promote cell survival and proliferation, were characterized.

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

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

14. 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

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

16. 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

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

18. 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)

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

20. 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.