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. 2022 Apr 20;298(6):101961. doi: 10.1016/j.jbc.2022.101961

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© 2022 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

PMC Copyright notice

Methylation of EGLN1 on K297 promotes cellular hypoxia adaptation.A, quantitative real-time PCR (qPCR) analysis of PDK1 mRNA in EGLN1-deficient H1299 cells (EGLN1^−/−) reconstituted with EGLN1 or its mutant by lentivirus. Data show mean ± SEM; Student’s two tailed t test. B and C, colony formation of EGLN1-deficient H1299 cells (EGLN1^−/−) reconstituted with EGLN1 or its methylation-mimic mutant (EGLN1-K297F) by lentivirus (n = 3) cultured for 11 days by colony-formation assay. D and E, oxygen consumption rate (OCR) changes were measured by Seahorse XFe24 Extracellular Flux Analyzer in EGLN1-deficient H1299 cells (EGLN1^−/−) reconstituted with EGLN1 or its methylation-mimic mutant (EGLN1-K297F) by lentivirus (D). Statistics of basal respiration, maximal respiration, and spare respiratory capacity were presented in (E). EGLN, egg-laying defective nine.