mProX™ Human PDGFRA Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 PDGFRA surface expression is controlled by cytoskeleton system.
Pharmacological inhibitors were used to impair the cytoskeletal organization of glioma cell lines #1, #2, and #3 that had high surface PDGFRA expression in order to evaluate the effects of the cytoskeleton on surface PDGFRA expression in living glioma cells.
Ref: Chen, Dongfeng, et al. "Glioma cell proliferation controlled by ERK activity-dependent surface expression of PDGFRA." PLoS One 9.1 (2014): e87281.
Pubmed: 24489888
DOI: 10.1371/journal.pone.0087281
Research Highlights
KIT or PDGFRA receptor tyrosine kinases are the sites of activating mutations found in most gastrointestinal stromal tumors (GIST). The KIT/PDGFRA tyrosine kinase inhibitor (TKI) imatinib's approval significantly enhanced the management of advanced GIST.
Bauer, Sebastian, et al. "Early and next-generation KIT/PDGFRA kinase inhibitors and the future of treatment for advanced gastrointestinal stromal tumor." Frontiers in Oncology 11 (2021): 672500.
Pubmed:
34322383
DOI:
10.3389/fonc.2021.672500
Among GISTs, PDGFRA IHC can be positive for inflammatory fibroid polyps and some other mesenchymal tumor types. It is also quite sensitive and somewhat selective for PDGFRA-mutant tumors. To identify the best course of treatment, epithelioid GISTs with PDGFRA positive could be categorized for PDGFRA sequencing.
Papke Jr, David J., et al. "PDGFRA immunohistochemistry predicts PDGFRA mutations in gastrointestinal stromal tumors." The American Journal of Surgical Pathology 46.1 (2022): 3-10.
Pubmed:
33859072
DOI:
10.1097/PAS.0000000000001720