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. Author manuscript; available in PMC: 2020 Aug 12.
Published in final edited form as: Nature. 2020 Feb 12;578(7796):621–626. doi: 10.1038/s41586-020-1998-1

Figure 3. TRIM21 mediates mechanically modulated PFKP degradation.

Figure 3.

a, Abundance of PFKP and ubiquitination in HBEC76 on stiff and soft substrates in the presence or absence of proteasome inhibitor MG132. Representative data from three independent experiments. b, Abundance of wildtype or mutant PFKP-GFP harboring K281R mutation (selected from Extended Data Fig. 5e) on stiff and soft substrates. Representative data from two independent experiments. c, Glycolytic rates, normalized to cell number, of HBEC76 expressing wildtype or K281R mutant PFKP on stiff and soft substrates (n = 6 independent cultures for each condition) from a single experiment. Bar graph indicates mean ± s.e.m. d, Abundance of PFKP in HBEC76 on stiff and soft substrates upon TRIM21 shRNA knockdown (shTRIM21). Representative data from two independent experiments. e, Abundance of PFKP in HBEC76 on stiff and soft substrates upon TRIM21-GFP over-expression. Representative data from two independent experiments. f, Abundance of PFKP in transformed H2009 cells upon TRIM21-GFP over-expression. Representative data from two independent experiments. Statistical significance was assessed using two-tailed Mann-Whitney test (c). Protein abundance was normalized to the abundance of GAPDH (a, b, e) or β-actin (d, f).