We show that inhibition of NF-kappaB (p65/RELA), either by overexpression of a mutant IkappaB (IkappaBSR) or a small-molecule inhibitor of NF-kappaB (parthenolide; IC(50)=500 nM in tamoxifen-resistant cells), synergistically restores sensitivity to 4-hydroxytamoxifen (4HT) in resistant MCF...
It has been demonstrated that MDM2 induces p65 expression in different cells; MDM2 overexpression was observed in AML, but its capacity to interact with NF-κB remains debated [99,100]. On the other hand, overexpression of negative regulator MDM2 inactivates p53, which is frequently inactivated ...
The NF-κB dimer, predominantly a heterodimer of p50-RelA/p65, translocates to the nucleus and binds DNA to stimulate the transcription of innate immunity, inflammatory, and cell survival genes. (Right) The noncanonical pathway is activated by BAFF, lymphotoxin-β (LTβ), CD40L, and LPS, ...
Silica NP significantly increased LC3BII abundance without affecting that of SQSTM1/p62 protein. On the contrary, LPS treatment did not modify the expression of the two autophagic markers, either in ASNP-exposed or not exposed cells. Figure 4. Effect of ASNP exposure on autophagic flux. ...
Similar to NF-κB, CBP acts as a transcriptional co-activator of Nrf2, binding its Neh4 and Neh5 domains, nevertheless with a lower affinity than to p65. Thus, both transcription factors compete for CBP accessibility: when p65 is overexpressed the amount of free CBP for Nrf2 is reduced ...
Pancreatic cancer is a disease in which deregulation of signaling pathways plays a key role, thus searching for their novel modulators is a promising therapeutic strategy. Hence, in this study, the effect of phytochemical combinations on the canonical an