Fig. 7: KLF9 positively regulates LncDACH1 transcription.

a The figure shows the relative positions of the full length (FL) and truncated fragments (P1, P2, P3) of the LncDACH1 promoter sequence (2 kb) reporter gene and the mutation site (M). P1, 684-2000 nt; P2, 1099–2000 nt; P3, 1500–2000 nt; M, 888–928 mut. b Binding of the full-length (FL) LncDACH1 promoter sequence (2 kb) to the transcription factor KLF9 was determined using luciferase activity assay (n = 5). c Binding of the LncDACH1 promoter truncation fragments (P1, P2, P3) to the transcription factor KLF9 was determined using luciferase activity assay (n = 3). d Binding of the M mutant vector to the transcription factor KLF9 was determined using luciferase activity assay (n = 3). e The figure shows the relative positions of the qPCR negative control probe and the predicted binding fragment probe in the ChIP-qPCR experiment. f, g Binding of the LncDACH1 promoter sequence to KLF9 was examined using ChIP-qPCR assay (n = 3). h Changes in mRNA expression of KLF9 during VSMC dedifferentiation using qRT-PCR (n = 6). i LncDACH1 expression levels were measured by qRT-PCR after transfection of si-KLF9 or scrambled siRNA in VSMC (n = 5). j LncDACH1 expression levels were measured by qRT-PCR after transfection of KLF9- pcDNA3.0 or pcDNA3.0-Vector in VSMC (n = 4). Promoter (P), mutant (M), transcription factor (TF), transcription start site (TSS), control (CTRL), negative control (NC), overexpression (OE), small interfering (SI). The n numbers represent biologically independent samples. Data are presented as mean values ± SD (b–d, f, h–j). P-values were determined by two-sided nonparametric tests (b, h–j) and two-sided 2way ANOVA (c, d, f) by Bonferroni’s multiple comparisons test. Source data are provided as a Source Data file.