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. 2019 Feb 22;10(11):854–855. doi: 10.1007/s13238-019-0613-4

Correction to: Developing potent PROTACs tools for selective degradation of HDAC6 protein

Zixuan An 1,#, Wenxing Lv 2,#, Shang Su 1, Wei Wu 1,, Yu Rao 2,
PMCID: PMC6834731  PMID: 30796636

Correction to: Protein Cell 10.1007/s13238-018-0602-z

In the original publication the title of X axis in Fig. 1G is incorrectly published as “Compound (µmol/L)”. The correct title of X axis in Fig. 1G should be read as “Compound (nmol/L)”

Figure 1.

Figure 1

Development of selective HDAC6-degrading PROTACs. (A) The principle of PROTAC. (B) The structure of PROTAC, as shown in the upper portion. A binding mode of PROTAC (ball stick), HDAC6 (PDB 5G0J, purple) and CRL4-CRBN (PDB 2HYE and 4CI3, colored cyan and gray) was simulated by Pymol. (C) Screen for a potent HDAC6 degrader. HeLa cells were treated as indicated for 24 h. (D) Characterization of NP8-induced degradation in HeLa cells. The degradation of HDAC6 was in a dose-dependent manner. The HDAC1, HDAC2 and HDAC4 levels were not affected within 24 h. (E) NP8 caused fast degradation of HDAC6 within 2 h in HeLa cells. (F) NP8-NC1 and NP8-NC2 failed to degrade HDAC6. NP8 induced degradation was rescued by single introduction of Nexturastat A (Nex A, 300 nmol/L), Pomalidomide (Poma, 10 µmol/L) or Carfilzomib (CARF, 1 µmol/L). The concentration of NP8-NC1, NP8-NC2 and NP8 were 300 nmol/L. HeLa cells were treated with Carfilzomib for 6 h and 24 h for the rest. (G) The degradation of HDAC6 by titration of NP8 for 24 h in MM.1S cells. (H) MM.1S cells were treated with NP8 or Nexturastat A (Nex A) for 72 h. Cell viability was determined by CCK-8 assay (n = 3)

Contributor Information

Wei Wu, Email: wwu@tsinghua.edu.cn.

Yu Rao, Email: yrao@tsinghua.edu.cn.


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