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Fig. 4 | Cell Communication and Signaling

Fig. 4

From: A p53/TIAF1/WWOX triad exerts cancer suppression but may cause brain protein aggregation due to p53/WWOX functional antagonism

Fig. 4

Δ133p53γ is most potent in suppressing cancer cell migration, which correlates with SMAD promoter activation. a Nine representative p53 isoforms are shown. There are at least 12 isoforms [43,44,45,46]. The schematic graphs for Δ160p53, Δ160p53β and Δ160p53γ are not shown. Full-length p53 possesses two N-terminal transactivation acidic domains, a proline-rich domain, a central DNA-binding region, and a C-terminal domain, containing a nuclear localization signal, an oligomerization domain, and a basic region. TAD, transactivation domain; PrD, proline domain; NLS, nuclear localization signal; OD, oligomerization domain; BR, basic region. b MDA-MB-231 cells transfected with indicated p53 constructs by electroporation. Many p53 constructs significantly suppressed the cell migration (Mean ± S.D., n = 3). Δ133p53γ was most effective. c, d COS7 cells were transiently overexpressed with indicated p53 and isoform constructs, in the presence of an SMAD promoter construct with GFP as a reporter. Ectopic Δ133p53γ significantly induced the SMAD promoter activation (versus TIAF1si and scramble groups; Mean ± S.D., n = 3). TIAF1si and scramble constructs did not block the promoter activation. In controls, cells were subjected to mock electroporation with medium (negative), or a positive control construct (positive). e A schematic signaling event shows ectopic Δ133p53γ-mediated SMAD promoter activation may lead to inhibition of cell migration

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