(1) KLF5, 5'-AAAGUAUAGACGAGACAGUGC-3' (sense) and GCCTGTCTCGTCTTCTTT (antisense)
Immunoprecipitations were performed using the KLF5 antibody in the presence of BSA/salmon sperm DNA and a 50% slurry of protein A agarose beads.
In transient transfection assays, both Klf4 and Klf5 stimulated mouse Spdefpromoter activity (Gupta and Swamynathan, unpublished).
Severe phenotype observed when either Klf4 or Klf5 was disrupted in the ocular surface, keeping the other gene intact, suggested nonredundant functions for these two structurally related factors.
Effect of SC-MN on KLF4 and KLF5
Expression and Activation in NHBE Cells.
Matsuzaka et al., "Inhibition of ubiquitin ligase F-box and WD repeat domain-containing 7[alpha] (Fbw7[alpha]) causes hepatosteatosis through Kriippel-like Factor 5 (KLF5
)/Peroxisome Proliferator-activated Receptor [gamma]2 (PPAR[gamma]2) pathway but not SREBP-1c protein in mice," Journal of Biological Chemistry, vol.
Chen, "YAP promotes breast cell proliferation and survival partially through stabilizing the KLF5
transcription factor," American Journal of Pathology, vol.
Apart from them, transcription factors including CREB, Krox20, KLF5
, and STAT5 participate in the complex network of transcription regulation .
THSG reduces intima-media thickness in the aortic arch of SHRs, increases the vascular diastolic rate in response to acetylcholine, and reduces remodeling and fibrosis-related mRNA expression, such as that of genes ACTA2, CCL3, COL1A2, COL3A1, TIMP1 WISP2, IGFBP1, ECE1, KLF5
, MYL1 BMP4, FN1, and the plasminogen activator inhibitor-1 (PAI-1).
Transcription factors such as Klf5
, Gata4, Gata6, Ascl2, and Yy1 have been shown to control intestinal stem cell fate, and their deficiency causes disruption of intestinal architecture [14, 36].
is widely expressed in various tissues, including the intestinal epithelial cells, skin, and skeletal muscle cells, and is dysregulated in several cancer cell types.
Similarly, PPAR-p[gamma], CCAAT/enhancer binding protein (C/EBP) [alpha] and [beta], glucocorticoid receptor (GR), insulin, and Kruppel-like factor 5 (KLF5
) have been identified as critical regulators of adipogenesis .