Fig. 4: NUDT1 knockout suppresses MYCN-driven neuroblastoma.
From: Therapeutic targeting nudix hydrolase 1 creates a MYC-driven metabolic vulnerability
a Targeting strategy for Nudt1 allele knockout in mice by CRISPR-Cas9. b Genotype analysis of Nudt1 knockout mice using PCR. PCR products clearly distinguish wild-type (single smaller band), homozygous (single larger band), and hemizygous (both bands) DNA fragments. c Immunoblot of NUDT1 in various organ lysates from Nudt1−/− mice and age-matched controls, with β-Actin as a loading control. d Breeding scheme for knockout of Nudt1 alleles in TH-MYCN transgenic mice. e Immunoblots of indicated proteins in primary sympathetic ganglia lysates from Nudt1−/− MYCN+/+ and age-matched Nudt1+/+ MYCN+/+ mice. Four mice were analyzed per group. f Kaplan–Meier survival curve of TH-MYCN+/+ mice with or without Nudt1 knockout. Significance was determined by log-rank test. g, h Representative histological images of 8-oxo-dG, γH2AX and c-Caspase 3 staining in paraffin-embedded tumor sections from TH-MYCN+/+ mice with or without Nudt1 knockout (g). Scale bar, 50 μm. Triangles denote positive-stained cells. Histological stain was quantified using ImageJ and plotted in (h). Data shown represent the means of four tumor samples (±SD). b, c these experiments were independently repeated three times with similar results. Statistical significance was determined by unpaired two-tailed Student’s t-test (h). Source data are provided as a Source Data file.
