Figure 6.
Figure 6. Antioxidants N-acetyl cysteine and tiron decrease Hu1D10 induced phosphorylation of AKT. CLL cells were treated as follows: (M) media only, (T) pretreatment with 10 mM tiron followed by Hu1D10 plus antihuman Fc antibody or (NAC) pretreatment with 25 mM N-acetyl cysteine followed by Hu1D10 plus antihuman Fc antibody (both 10 μg/mL). After a 15-minute treatment with cross-linked Hu1D10, the cells were lysed. Samples were immunoblotted using standard techniques. Blots were probed with anti–phospho-AKT (Ser473), stripped, and then reprobed with anti-AKT.

Antioxidants N-acetyl cysteine and tiron decrease Hu1D10 induced phosphorylation of AKT. CLL cells were treated as follows: (M) media only, (T) pretreatment with 10 mM tiron followed by Hu1D10 plus antihuman Fc antibody or (NAC) pretreatment with 25 mM N-acetyl cysteine followed by Hu1D10 plus antihuman Fc antibody (both 10 μg/mL). After a 15-minute treatment with cross-linked Hu1D10, the cells were lysed. Samples were immunoblotted using standard techniques. Blots were probed with anti–phospho-AKT (Ser473), stripped, and then reprobed with anti-AKT.

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