Fig 2: CLEC7A is the regulatory target of SNHG1. (A) Change of CLEC7A protein levels in VSMCs following treatment with rapamycin. (B) CLEC7A protein levels changes following silence and overexpression of SNHG1 in VSMCs. (C and D) RIP assays together with RT-qPCR showed that SNHG1 was pulled down by an anti-CLEC7A antibody. (E) RNA pulldown and western-blotting revealed the direct binding of CLEC7A proteins to SNHG1. Data were shown as mean ± standard deviation of a representative experiment performed in three independent replicates. **P<0.01. Input, sample control group; PRD, SNHG1 probe pull down CLEC7A protein group; NC, Negative control group (LacZ); CLEC7A, C-type lectin domain family 7 member A; VSMCs, vascular smooth muscle cells; SNHG1, small ribosome housekeeping gene RNA1; RIP, RNA-binding protein immunoprecipitation; RT-qPCR, reverse transcription-quantitative PCR.