Fig. 7: Sam68 knockdown promoted alternative splicing of Bcl-xl. | Laboratory Investigation

Fig. 7: Sam68 knockdown promoted alternative splicing of Bcl-xl.

From: Leukemia/lymphoma-related factor (LRF) or osteoclast zinc finger protein (OCZF) overexpression promotes osteoclast survival by increasing Bcl-xl mRNA: A novel regulatory mechanism mediated by the RNA binding protein SAM68

Fig. 7

A Expression of Sam68 mRNA in the cells infected with EGFP shRNA (control) or Sam68 shRNA lentivirus. The expression of Sam68 mRNA was assessed using RT-qPCR. B RT-PCR analysis of Bcl-xl and Bcl-xs isoforms in the cells infected with shEGFP or shSam68. C RT-qPCR analysis of Bcl-xl mRNA in the cells infected with shEGFP or shSam68. BMMs stimulated with RANKL for 48 h were infected with EGFP shRNA or Sam68 shRNA lentivirus. The cells were stimulated with RANKL for another 36 h and the expression of Sam68, Bcl-xl, or Bcl-x isoforms was assessed using RT-qPCR or RT-PCR. In RT-qPCR analysis, expression was normalized with Gapdh (n = 3). Data are presented as mean ± SD. Student’s t test was used for statistical analysis. **P < 0.01, *P < 0.05 compared to the cells infected with EGFP shRNA lentivirus (A, C).

Back to article page