Fig. 8
deletion of TXN1 attenuates HSPCs response to the stressor and reduces the survival of mice following sub-lethal dose of TBI. A P53 protein expression over time in response to 5 Gy radiation in EML/Cont and EML/TXN1KO cells. B BrdU cell proliferation. EML cells were transduced with Cas9 control, TXN1 specific CRISPR/Cas9, p53 specific CRISPR/Cas9 or both, and irradiated with 5 Gy. Cell proliferation was measured by BrdU incorporation. Data was plotted as mean ± SEM (n = 3, Data represents *p value < 0.01, **p value < 0.001).). C γ-H2AX expression in response to 5 Gy radiation in EML cell lines before and after deletion of TXN1 and/or TP53 genes. D Quantification of γ-H2AX expression using ImageJ software and normalized with βactin levels. (Data represent mean ± SD; n = 3). E Kaplan–Meier survival curve. TXN1fl/fl mice and ROSA-CreER-TXN1fl/fl mice were treated with TAM (75 mg/kg) i.p. daily for 5 days. Then the animals were exposed to 5 Gy radiation at day 7. Animal survival was monitored daily. F Western blot analyses of P53 protein expression in lysates prepared from (spleen, small intestine and bone marrow whole cells) from TXN1fl/fl mice and ROSA-Cre-TXN1fl/fl mice before and after 24 h of 5 Gy radiation exposure