GPR34 truncation mutant confers resistance to apoptosis and transforming capacity. (A) Schematic illustration of GPR34 mutations seen in salivary gland MALT lymphoma. (B) Effect of GPR34 mutations on apoptosis induced by staurosporine. Isogenic Flp-InTRex293 cells that stably express a single copy of GPR34 or its various mutants were treated with 1.5 nM staurosporine in the absence or presence of LysoPS stimulation for 20 hours, and apoptosis was then measured by flow cytometry analysis of annexin V binding. Data are shown as mean ± standard deviation from 3 independent experiments. Statistical significance was analyzed by a two‐tailed unpaired Student t test, with significance indicated. (C) Transforming potential of GPR34 mutants determined by a soft agar colony formation assay. Isogenic Flp-INTRex293 cells that express a single copy of GPR34 or its various mutants were grown on soft agar for 3 weeks, and colonies were stained with a crystal violet and quantified. (D) Data are shown as mean ± standard deviation from 3 independent experiments. Statistical significance was analyzed by one‐way analysis of variance, with significance indicated. Control AQ19: the parental Flp-In T-REx-293 cell line. Wild-type (WT) or various mutations indicated: the derived stable expression cell line with single copy of WT or mutant GPR34.