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. 2021 Sep 8;6(17):e149232. doi: 10.1172/jci.insight.149232

Figure 3. HDAC1 function is nonredundant in hGSCs and is not compensated for by its paralogue HDAC2.

Figure 3

(A) Log2 fold change of differential expression for the 11 HDACs (HDAC1–11) after short hairpin HDAC (shHDAC1) knockdown in 2 nontumorigenic (ihNPC and NHA) and 3 hGSC (BT145, GB3, BT187) cell lines. Blue bolded boxes indicate significant differential expression (adjusted P ≤ 0.05). (B) Representative immunoblot showing protein levels of HDAC1 and HDAC2 after acute HDAC2 knockdown (shHDAC2) in p53-WT (BT145) and p53-mutant (BT187) hGSCs. (C) Quantification of expression of HDAC2 and HDAC1 protein (normalized to Vinculin) after HDAC2 knockdown in BT145 (n = 4) and BT187 (n = 3). (D) Quantification of the percentage of viable hGSCs (BT145 and BT187) 7 days after HDAC2 knockdown, relative to shNT controls (n = 3). (E) Immunoblot comparing levels of acetylated p53 (K382) and HDAC1 and HDAC2 protein after HDAC1 and HDAC2 silencing in p53-WT hGSCs (BT145). For each cell line, the data are compiled from at least 3 independent experiments for each shRNA. Error bars indicate SEM. *P < 0.05, **P < 0.01, ****P < 0.0001. P values were calculated using unpaired 2-tailed t test. See also Supplemental Figure 4.