Fig. 5: Foxp1 is a crucial link in LMO7-mediated regulation of TGF-β/CCL5. | Cell Death & Differentiation

Fig. 5: Foxp1 is a crucial link in LMO7-mediated regulation of TGF-β/CCL5.

From: LIM ___domain only 7: a novel driver of immune evasion through regulatory T cell differentiation and chemotaxis in pancreatic ductal adenocarcinoma

Fig. 5

a Transcription levels of Foxp1 after LMO7 knockdown (left) and overexpression (right). b Protein levels of Foxp1 after LMO7 knockdown (up) and overexpression (down). c Transcriptional levels of TGF-β and CCL5 after Foxp1 overexpression. d Extracellular protein levels of TGF-β and CCL5 after Foxp1 overexpression. e Transcriptional levels of TGF-β and CCL5 after Foxp1 knockdown. f Extracellular protein levels of TGF-β and CCL5 after Foxp1 knockdown. g Sequence logo and frequency matrix of the transcription factor Foxp1. h Regions in the TGF-β promoter where Foxp1 may bind. i Regions in the CCL5 promoter where Foxp1 may bind. j, k Luciferase activities of TGF-β promoter reporter vectors. Data presented as mean ± SEM (n = 3 independent biological replicates). l, m Luciferase activities of CCL5 promoter reporter vectors. n, o Luciferase assay for the TGF-β promoter mutation site (Red characters in the binding regions suggest the putative or mutated Foxp1 binding sequences). p, q Luciferase assay for the CCL5 promoter mutation site (Red characters in the binding regions suggest the putative or mutated Foxp1 binding sequences). ChIP-qPCR assay detecting the binding of Foxp1 to the TGF-β (r) and CCL5 (s) promoter. Data are presented as mean ± SEM (n = 3 independent biological replicates). Statistical significance was determined using two-tailed unpaired t-test. p < 0.05; **p < 0.01; ***p < 0.001.

Back to article page