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. 2010 Apr 7;15(4):970–982. doi: 10.1111/j.1582-4934.2010.01065.x

Fig 11.

Fig 11

(A) Schematic diagram of the DNA constructs of MLCK promoter (–2109 to –18) containing different combinations of Elk-1 binding sites. The Elk-1 binding sites (A) (GAAAATGGAAGTCCAAG) and (B) (TGGCCTTCCTCCCTC) are represented in black. (B) Effect of IL-1β on the deletion construct of MLCK promoter region (–929 to +118) lacking the downstream Elk-1 binding site (A). IL-1β caused a similar proportional increase in MLCK luciferase activity as compared to the FL construct (means ± S.E., n= 8). *P < 0.001 versus control. (C) IL-1β treatment caused a significant increase in MLCK promoter activity of the deletion construct (–313 to +118) containing only the cis-binding site (B) in Caco-2 monolayers (means ± S.E., n= 8). *P < 0.0001 versus control. (D) Site directed mutagenesis of Elk-1 binding site (B) (TGGCCTTCCTCCCTC) on MLCK –313 prevented the IL-1β-induced increase in MLCK –313 promoter activity (means ± S.E., n= 5). *P < 0.001 versus control. (E) Effect of Elk-1 siRNA co-transfection on the IL-1β-induced increase in MLCK –313 promoter activity. Elk-1 silencing completely prevented the IL-1β-induced increase in MLCK luciferase activity (means ± S.E., n= 8). *P < 0.0001 versus control; **P < 0.0001 versus IL-1β treatment.