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Results: 5

1.
Figure 2

Figure 2. From: A senescence rescue screen identifies BCL6 as an inhibitor of anti-proliferative p19ARF-p53 signaling.

The p19ARF–p53 pathway is intact in BCL6-immortalized MEFs. Western blot analysis of p53-pathway proteins in wild-type MEFs (P = 7) and BCL6-immortalized MEFs (P = 15), both before and 15 h after exposure to 40 μM cisplatin. Immortal MEFs of p19ARF−/− mice (ARF−/−) and spontaneously immortalized MEFs harboring a mutant p53 protein (mtp53) are shown for comparison.

Avi Shvarts, et al. Genes Dev. 2002 March 15;16(6):681-686.
2.
Figure 5

Figure 5. From: A senescence rescue screen identifies BCL6 as an inhibitor of anti-proliferative p19ARF-p53 signaling.

BCL6 confers a growth advantage to primary human B cells. (A) Two independent batches of primary human tonsillar B cells were infected with retroviral vectors expressing either GFP (●) or BCL6 and GFP (○). The percentage of GFP-positive cells was followed over time in culture. (B) Western blot analysis of BCL6, cyclin D1, and control CDK4 expression in primary human B cells in culture and BCL6-infected derivatives.

Avi Shvarts, et al. Genes Dev. 2002 March 15;16(6):681-686.
3.
Figure 4

Figure 4. From: A senescence rescue screen identifies BCL6 as an inhibitor of anti-proliferative p19ARF-p53 signaling.

BCL6 is unable to immortalize cyclin D1 knockout MEFs. Colony formation assay on primary MEFs at passage 5 infected with the BCL6 or BCL6 and cyclin D1 encoding retroviruses, and stained 10 d after infection. SV40 T antigen virus was used as a positive control (Large T). (Top four dishes) cyclin D1 knockout MEFs; (bottom four dishes) genotype-matched wild-type MEFs. Growth curves of cyclin D1−/− and matched wild-type control MEFs infected with the indicated retroviruses is shown at bottom. Passage numbers indicated reflect the number of passages after retroviral infection at P = 5.

Avi Shvarts, et al. Genes Dev. 2002 March 15;16(6):681-686.
4.
Figure 1

Figure 1. From: A senescence rescue screen identifies BCL6 as an inhibitor of anti-proliferative p19ARF-p53 signaling.

tsT-MEFs enter into a p53-dependent senescence program after shift to the nonpermissive temperature. (A) tsT-MEFs were cultured at 32°C, shifted to the nonpermissive temperature (39.5°C), and stained 10 d later. (Right) tsT-MEFs were infected with the E6 retrovirus at 32°C, shifted to nonpermissive temperature and stained 10 d later. (B) Abundance of SV40 T antigen and α-tubulin in tsT-MEFs at both temperatures was determined by Western blotting. (Bottom) Expression of senescence marker PAI-1 in tsT-MEFs at various time points after shift to the nonpermissive temperature. (C) The full-length BCL6 cDNA was cloned in pBabe-hygro retroviral vector and used to infect tsT-MEFs at 32°C. Expression of BCL6 was detected by Western blotting. After 2 d, infected cells were shifted to the nonpermissive temperature, and stained after 10 d. Growth curves are shown of tsT-MEFs infected with BCL6-expressing or control retrovirus at 32°C and 39.5°C. (D) Primary FVB MEF infected with BCL6 alone or in combination with a RAS oncogene escape replicative senescence. In contrast, control (pBabe-hygro infected) and RASV12-infected MEFs fail to proliferate. Growth curves of passage 5 MEFs infected with indicated retroviruses are shown. (♦) Bcl6; (▪) control; (▴) Bcl6/Ras V12; (●) Ras V12.

Avi Shvarts, et al. Genes Dev. 2002 March 15;16(6):681-686.
5.
Figure 3

Figure 3. From: A senescence rescue screen identifies BCL6 as an inhibitor of anti-proliferative p19ARF-p53 signaling.

BCL6 rescues senescence downstream of p53. (A) Western blot analysis of p21cip1 and p53 protein levels in tsT-MEFs expressing either BCL6 or control virus at indicated time points (days) after shift to the nonpermissive temperature. Cyclin E protein level was determined by Western blotting; Cyclin E-associated kinase activity was determined on cyclin E immunoprecipitates using histone H1 as a substrate. (B) (Left) Cells expressing either BCL6 or control virus were labeled with [35S]methionine and lysates were precipitated with either p21cip1 or CDK4 antibody and separated on SDS–polyacrylamide gels. (Lanes 1,3) FVB-MEFs (passage 5); (lanes 2,4) FVB MEFs expressing BCL6 (also at passage 5). (Right) [35S]methionine cell lysates of BCL6 cells were immunoprecipitated first with p21cip1 antibody in nonionic detergent, protein complexes were released by boiling in 1% SDS and reimmunoprecipitated with indicated antibodies. Individual proteins are indicated with arrows. (C) (Top) Western blot analysis for the expression of cyclin D1 and cyclin D2 in MEFs, human U2OS cells (osteosarcoma), and primary human embryonic kidney (HEK). (Lanes 1,3,5) Control; (lanes 2,4,6) BCL6-expressing derivatives. (Bottom) Northern blot analysis for the expression of cyclin D1 in Balb/c and FVB MEFs; (lanes 1,3) control; (lanes 2,4) BCL6-expressing MEFs.

Avi Shvarts, et al. Genes Dev. 2002 March 15;16(6):681-686.

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