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. Author manuscript; available in PMC: 2024 Jan 19.
Published in final edited form as: Mol Cell. 2023 Jan 19;83(2):186–202.e11. doi: 10.1016/j.molcel.2022.12.022

Figure 2. ERRα mediates functional interactions of PGC-1α with CBP80, Mediator and P-TEFb, and is required for the P4RC to compete against Integrator for CBC binding.

Figure 2.

(A) WBs of lysates of WT or PGC-1α-KD MBs treated with DRB prior to lysis, before or after IP in the presence of RNase I using anti-CBP80 or, as a control, rIgG.

(B) Diagrams of human PGC-1α variants used in C, where red letters denote mutated amino acids in nuclear receptor (NR)-binding LxxLL/LLxxL motifs. RS, arginine- and serine-rich domain; CBM, CBP80-binding motif. Numbers specify amino acids.

(C) WBs of lysates of PGC-1α-KD MBs transiently transfected with the specified plasmid before or after IP in the presence (+) or absence (−) of RNase I using anti-FLAG. PABPC1 serves to control for RNase I-sensitive interactions.

(D) WBs of lysates of WT MBs that were transiently transfected with Errα or control (Ctl) siRNA and treated with DRB, before or after IP in the presence of RNase I using anti-PGC-1α, anti-CBP80 or, as a control, rIgG.

See also Figure S2 and Table S1.