Figure 6
Figure 6. AICAR induces BIM, NOXA, and PUMA proteins in CLL cells. (A) Cells were untreated (−) or treated (+) with 0.5mM AICAR for 9 hours. Cells were lysed and analyzed by Western blot. Total levels of the BCL-2 family members BIM, BNIP3, BNIP3L, MOAP1, BAX, NOXA, PUMA, MCL-1, and BCL-2 were analyzed. ERK was used as a control of protein loading. One representative sample is shown (n = 6). (B) BIMEL, BIML/β, NOXA, and PUMA protein levels from AICAR-treated cells for 9 hours were quantified by densitometry and normalized by the ERK protein levels. Data are mean ± SEM (n = 6), expressed as the fold induction compared with untreated cells. **P < .01, *P < .05, AICAR-treated versus untreated cells.

AICAR induces BIM, NOXA, and PUMA proteins in CLL cells. (A) Cells were untreated (−) or treated (+) with 0.5mM AICAR for 9 hours. Cells were lysed and analyzed by Western blot. Total levels of the BCL-2 family members BIM, BNIP3, BNIP3L, MOAP1, BAX, NOXA, PUMA, MCL-1, and BCL-2 were analyzed. ERK was used as a control of protein loading. One representative sample is shown (n = 6). (B) BIMEL, BIML/β, NOXA, and PUMA protein levels from AICAR-treated cells for 9 hours were quantified by densitometry and normalized by the ERK protein levels. Data are mean ± SEM (n = 6), expressed as the fold induction compared with untreated cells. **P < .01, *P < .05, AICAR-treated versus untreated cells.

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