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Fig. 3 | Genome Biology

Fig. 3

From: ARMC5 controls the degradation of most Pol II subunits, and ARMC5 mutation increases neural tube defect risks in mice and humans

Fig. 3

ARMC5 interacted with CUL3 and POLR2A. A A volcano plot showing ARMC5 interacted with endogenous CUL3 and POLR2A in HEK293 cells. HEK293 cells were transfected with ARMC5-FLAG-expressing plasmids. The anti-FLAG precipitates were analyzed by LC-MS/MS. The vertical line indicates twofold changes, and the horizontal line, FDR = 0.05, is based on three biological replicates. B,C ARMC5 interacted with endogenous POLR2A and CUL3 in SK-N-SH neuronal cells. SK-N-SH cells were transfected with a human ARMC5-HA-expressing plasmid or an empty vector. The presence of endogenous POLR2A (B) and CUL3 (C) in the immunoprecipitates was revealed by immunoblotting (IB) with anti-POLR2A and anti-CUL3 Abs. The presence of ARMC5-HA in the cell lysates and immunoprecipitates was confirmed by IB with anti-HA Ab (lower rows of B and C). The experiments were conducted more than three times, and representative results are shown

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