Figure 3.
Figure 3. Continuing inhibition of telomerase by AZT in HTLV-I–infected cells induces posttranscriptional stabilization of p53. (A) Western blot analysis for expression of p53 pathway regulators in untreated MT-2 and AZT-treated (18 weeks) MT-2 cells. Equal amounts (50 μg) of each extract were used and confirmed by β-tubulin. (B) Analysis of p53 mRNA expression by RT-PCR in MT-2 and after culture with AZT for 18 weeks. GAPDH was used as internal control for amplification. (C) Western blot analysis of p53 after 24 hours of AZT treatment. Equal amounts (50 μg) of each extract were used and confirmed by β-tubulin. (D) Increased expression of p53 detected by Western blot in several HTLV-I–infected cell lines (1185, C10MJ, LAF) treated for 4 weeks with AZT.

Continuing inhibition of telomerase by AZT in HTLV-I–infected cells induces posttranscriptional stabilization of p53. (A) Western blot analysis for expression of p53 pathway regulators in untreated MT-2 and AZT-treated (18 weeks) MT-2 cells. Equal amounts (50 μg) of each extract were used and confirmed by β-tubulin. (B) Analysis of p53 mRNA expression by RT-PCR in MT-2 and after culture with AZT for 18 weeks. GAPDH was used as internal control for amplification. (C) Western blot analysis of p53 after 24 hours of AZT treatment. Equal amounts (50 μg) of each extract were used and confirmed by β-tubulin. (D) Increased expression of p53 detected by Western blot in several HTLV-I–infected cell lines (1185, C10MJ, LAF) treated for 4 weeks with AZT.

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