Feb 14, 2005 · We showed that regulation of PPARγ expression by E2Fs is through direct binding to an E2F-responsive element in the PPARγ1 promoter.

Numerous studies had demonstrated that ligand activation of PPAR-γ activation inhibits the phosphorylation of Rb protein, which has been reported to lead to abrogation of E2F2 or directly decrease the DNA-binding activity of E2F/DP transcription factors .

We found that PPARα is associated with glioma grade and GBM survival. PPARα inhibits glioma cell proliferation, invasion, and aerobic glycolysis, and suppresses glioma growth in an orthotopic model via a positive feedback loop with E2F1 and miRNA-19a.

Mitosis-related genes that are predominantly regulated by E2F were induced to a higher level in HRAS-expressing Pparβ/δ-null keratinocytes compared to HRAS-expressing wild-type keratinocytes. Ligand-activated PPARβ/δ repressed expression of these genes by direct binding with p130/p107, facilitating nuclear translocation and increasing ...

Therefore, the findings suggest that wound healing process could be accelerated with enhanced M2 polarization through increased PPAR-γ expression in E2F1 knockout mice. Keywords: E2F1; PPAR-γ; macrophages; polarization; wound healing.

We show here that E2F1 induces PPAR gamma transcription during clonal expansion, whereas E2F4 represses PPARg amma expression during terminal adipocyte differentiation.

Jun 18, 2013 · Summary for the role of PPARβ in regulating liver regeneration through E2f-regulated pathway. PPARβ up-regulates Akt- and E2fs, which control glycolysis, fatty acid homeostasis as well as cell proliferation in regenerating livers.

May 23, 2008 · One of the first evidence for implication of PPARγ in the cell cycle regulation is the engagement to E2F transcription factor, which is known to prompt the G1/S transition. Transactivated PPARγ suppresses the transcriptional activity of E2F/DP complex by inhibiting the complex formation [4].

Nov 15, 1987 · The very important role that E2F/DP complexes have been shown to play in cell cycle progression strongly suggests that the PPARγ-linked decrease in the DNA-binding activity of these factors is linked causally to the differentiation-related cell cycle withdrawal.

We observed lower levels of PPAR-γ expression in nonkeratinizing NPC tissues compared with NPG tissues and determined an association between a low level of PPAR-γ expression with a more advanced tumor stage. Furthermore, strong E2F2 expression was detected in nonkeratinizing NPC tissues.