Fig. 2: Oncogenicity of the NRIP1::PDGFRB fusion gene.
From: Promoter swapping of truncated PDGFRB drives Ph-like acute lymphoblastic leukemia
a Left panel shows Ba/F3 outgrowths transduced with NRIP1::PDGFRB compared to Ba/F3 cells transduced with a mock vector upon IL-3 withdrawal; right panel shows flow cytometry images of Ba/F3 cells transduced with a mock vector, including NRIP1::PDGFRB and PDGFRB WT; transformed clones were detected only in Ba/F3 cells transduced with NRIP1::PDGFRB and PDGFRB WT vectors; FSC forward scatter, SSC side scatter. b Western blot analyses of Ba/F3 cells transduced with NRIP1::PDGFRB or PDGFRB WT vectors; truncated form of PDGFRβ and phosphorylated PDGFRβ were shown on the left. c Ba/F3 cell sensitivities transduced with NRIP1::PDGFRB or PDGFRB WT vectors to imatinib, dasatinib, nilotinib, ponatinib, and vemurafenib; data are presented as the average of three independent experiments; vertical axis indicates viability as calculated by cell number. d Western blot analysis of Ba/F3 cells, transduced with NRIP1::PDGFRB, treated with ponatinib (1 nM) and vemurafenib (1 nM); after 24 h of tyrosine kinase inhibitor exposure, lysates were prepared and immunoblotted. e Structures of WT PDGFRB and NRIP1::PDGFRB predicted with AlphaFold2. TM transmembrane domain, JM juxtamembrane domain. f Schematic representation of PDGFRB fusion pattern; TM transmembrane domain, JM juxtamembrane domain.
