Figure 4. Azin1 A-to-I–locked mice exhibit faster tissue recovery following ischemic injury compared with uneditable mice.

(A) Sanger sequencing chromatograms for wild-type (top), Azin1 A-to-I–uneditable (middle), and Azin1 A-to-I–locked homozygous mice (bottom). The CRISPR knockin strategy is depicted in Supplemental Figure 6A. (B) Serum creatinine levels 24 and 72 hours after a 20-minute bilateral IRI. (C) Kidney tissue Havcr1/kidney injury marker-1 (KIM1) levels as determined by RNA-Seq (counts per million). (D) Polyribosome profiling of kidneys from Azin1 A-to-I–locked and uneditable mice 24 hours after IRI. Two representative biological replicates are shown for each genotype. Mean polysome/monosome ratios for A-to-I–locked and uneditable genotypes are 3.3 and 2.8, respectively. (E) Hematoxylin and eosin staining 72 hours after IRI. Original magnification, ×40. (F) Western blotting for hypusine in the kidney after IRI.