Figure 5.
Favorable metabolic reprogramming of CD38KO NK cells. (A) Heat map of DEGs of significantly altered pathways (cholesterol biosynthesis and OXPHOS) as determined by IPA, based on normalized RNA-seq data of paired CD38WT and CD38KO NK cells (n = 6). (B) Principle components analysis (PCA) of DEGs, showing consistent effect of CD38 deletion for each donor despite wide interdonor variability. (C) Summarized data of metabolic analysis of paired CD38WT and CD38KO NK cells (n = 3; mean ± SD). (D) Graphical analysis of basal OCR, ECAR, OCR/ECAR, and spare respiratory capacity (SRC) derived from (C). All experiments were achieved using quintuplicate samples. FCCP, carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone; ROT/AA, rotenone and antimycin A.

Favorable metabolic reprogramming of CD38KO NK cells. (A) Heat map of DEGs of significantly altered pathways (cholesterol biosynthesis and OXPHOS) as determined by IPA, based on normalized RNA-seq data of paired CD38WT and CD38KO NK cells (n = 6). (B) Principle components analysis (PCA) of DEGs, showing consistent effect of CD38 deletion for each donor despite wide interdonor variability. (C) Summarized data of metabolic analysis of paired CD38WT and CD38KO NK cells (n = 3; mean ± SD). (D) Graphical analysis of basal OCR, ECAR, OCR/ECAR, and spare respiratory capacity (SRC) derived from (C). All experiments were achieved using quintuplicate samples. FCCP, carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone; ROT/AA, rotenone and antimycin A.

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