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Protein & Cell

, Volume 10, Issue 12, pp 927–928 | Cite as

Correction to: Inhibition of p53 and/or AKT as a new therapeutic approach specifically targeting ALT cancers

  • Yuanlong Ge
  • Shu Wu
  • Zepeng Zhang
  • Xiaocui Li
  • Feng Li
  • Siyu Yan
  • Haiying Liu
  • Junjiu Huang
  • Yong ZhaoEmail author
Open Access
Correction

Correction to: Protein Cell  https://doi.org/10.1007/s13238-019-0634-z

In the original publication the labels in Fig. 4C and 4D are incorrectly published. The correct labels for Fig. 4C and 4D is provided in this correction.
Figure 4

AKT is phosphorylated in p53-dependent manner in ALT cells. (A) Western blot determination of total and phosphorylated AKT (S473) in p53-positive (VA13, U2OS) and p53-defective (SAOS2, SKLU-1) ALT cells. (B) Knockdown of p53 in U2OS or moderate expression of p53 in SAOS2 induces down or up-regulation of p-AKT, respectively. (C) Knockdown of ATM or ATR by siRNA decreases abundance of p53, phosphorylated p53 and p-AKT. (D) Quantitative-PCR determination of the level of ATR or ATM in U2OS cells transfected with siRNA to ATR or ATM, respectively. Scramble siRNA (Si-Ctl) was used as control. Data represent the mean ± SEM, n = 3-4. (E) ATM (KU60019) or ATR (VE-821) inhibitor decreases abundance of p-AKT in U2OS cells. U2OS cells were treated with indicated concentration of KU60019 or VE-821 for 24 h. (F) The expression of wt-p53, but not mutant p53 (p53-s269e) defective of transcription activity, increases the level of p-AKT. (G) PFTα,an inhibitor of p53 transcription activity, suppresses the phosphorylation of AKT. U2OS cells were treated with indicated concentration of PFTα for 24 h

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© The Author(s) 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

Authors and Affiliations

  • Yuanlong Ge
    • 1
    • 2
  • Shu Wu
    • 1
    • 2
  • Zepeng Zhang
    • 1
    • 2
  • Xiaocui Li
    • 1
    • 2
  • Feng Li
    • 1
  • Siyu Yan
    • 1
  • Haiying Liu
    • 1
    • 2
  • Junjiu Huang
    • 1
  • Yong Zhao
    • 1
    • 2
    Email author
  1. 1.MOE Key Laboratory of Gene Function and Regulation, State Key Laboratory of Biocontrol, School of Life SciencesSun Yat-sen UniversityGuangzhouChina
  2. 2.Collaborative Innovation Center of High Performance ComputingNational University of Defense TechnologyChangshaChina

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