Activating mTOR/NF-κB signaling pathway regulates the pathogenesis of diabetic encephalopathy, such as neuroinflammation, synaptic proteins loss, and synaptic ultrastructure impairment. The findings provide the implication that mTOR/NF-κB is potential new drug targets to treat diabetic encephalopathy.

Recent studies have shown the importance of reciprocal interactions between mammalian target of rapamycin (mTOR) and nuclear factor kappa B (NF-κB; two downstream molecules of Akt) in the regulation of tumor cells.

We show here that mTOR downstream from Akt controls NF-κB activity in PTEN-null/inactive prostate cancer cells via interaction with and stimulation of IKK. The mTOR-associated protein Raptor is required for the ability of Akt to induce NF-κB activity.

Our own research investigations have identified Nuclear factor-kappa B (NF-κB) pathway as a core central pathway that interacts with multiple upstream and downstream signaling pathways, including the PI3K/Akt/mTOR pathway, and plays an important role in invasion, angiogenesis and metastasis of human cancers in experimental models.

Jul 17, 2019 · Bioinformatics study revealed that dipeptidyl peptidase-4 (DPP4) was a target gene of NF-κB; DPP4 inhibitor, sitagliptin (10−500 μM) effectively inhibited the abnormal wound healing of PASMCs...

Mammalian target of rapamycin (mTOR) integrates signals from nutrients and growth factors to control protein synthesis, cell growth, survival and metabolism, and has been shown to regulate DDR in yeast and human cancer cells through the p53/p21 signaling cascade.

Dec 2, 2020 · Recent studies have shown the importance of reciprocal interactions between mammalian target of rapamycin (mTOR) and nuclear factor kappa B (NF-κB; two downstream molecules of Akt) in the regulation of tumor cells.

With the inhibition of mTOR or NF-κBbyeitherchemical inhibitor or short-hairpin RNA (shRNA)-expressing lentivirus-vector, we examined the effects of mTOR/NF-κBsignalingon proinflammatory cytokines and synaptic proteins.

In summary, the studies above focused on regulation of “canonical” signaling (e.g. JNK and NF-kB) by mTOR and Akt in control of macrophage activation. Later in the review, we discuss emerging studies that highlight the metabolic aspects of mTOR- …

Further mechanistic studies show that mTOR deficiency or inactivation increases phosphorylation and nuclear translocation of nuclear factor (NF)-κB, which results in an enhanced NF-kB binding to FANCD2 promoter to suppress FANCD2 expression.