Notably, TNFα activation of NF-κB was totally impaired after GPR108 knockout. engaged with GPR108 and promoted its degradation, knockout of GPR108 remarkably blocked GA inhibition of NF-κB

G Protein-Coupled Receptor D Induces Release of the Inflammatory Cytokine IL-6 and Is Dependent on NF-κB pathway, which results in an IkB kinases (IKK)-mediated canonical activation of nuclear factor kappa-B (NF-κB

hypersensitivity implicate potential contributions of mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB). MAPKs (extracellular signal-regulated kinase [ERK], p38) and redox-sensitive transcription factors (NF-κB mechanistic insight into how GPR183 signaling in the spinal cord produces hypersensitivity through MAPK and NF-κB We found that 7α,25-OHC-induced allodynia is dependent on MAPK and NF-κB signaling pathways and results

A series of evidence shows that TGR5 induces protein kinase B (AKT), nuclear factor kappa-B (NF-κB),

to IGF1R with ubiquitin E3 ligase MDM2, thereby activating its downstream signaling pathways such as NF-κB

mechanistic target of rapamycin kinase; MAPK: mitogen-activated protein kinase; 3-MA: 3-methyladenine; NFKB/NF-κB

We uncovered a novel neuroprotective mechanism involving interaction between neurotrophic factor-α1 (NF-α1 Treatment of 5-HTR1E stable cells with NF-α1/CPE increased pERK 1/2 and pCREB levels which prevented Molecular dynamics studies revealed that NF-α1/CPE interacts with 5-HTR1E via 3 salt bridges, stabilized Furthermore, after phosphorylating the C-terminal tail and intracellular loop 3 (ICL3) of NF-α1/CPE-5 Immunofluorescence studies showed 5-HTR1E and NF-α1/CPE are highly expressed and co-localized on cell

Regulation of nuclear factor κB activation by G-protein-coupled receptors.