KEAP1 (Kelch Like ECH Associated Protein 1)

Moreover, increased proapoptotic signaling (SK-MEL-1) was clearly observed, with increased expression of caspase-3 (UVA) and caspase-8 (CBG or UVA). Thus, CBG does not explicitly promote apoptosis but influences it by regulating oxidative and inflammatory processes in a cell-type-dependent manner.

A murine psoriasis model was induced by 6-day continuous topical imiquimod (IMQ) application; cellular models were established by stimulating keratinocyte lines with tumor necrosis factor-alpha (TNF-α)/interleukin-17A (IL-17A)...siNrf2 abolished Nef-mediated inhibition of NF-κB/ERK phosphorylation, cytokine down-regulation and ΔΨm loss. Neferine ameliorates psoriasis by inducing oxidative stress-driven apoptosis in hyper-proliferative keratinocytes and by activating Keap1-Nrf2-mediated anti-inflammatory signaling to block the IL-23/IL-17 axis, offering a promising small-molecule strategy for psoriasis management.

NSCLCs harboring ECD-ERBB2 mutations are associated with a unique clinico-genomic phenotype and improved outcomes with first-line chemoimmunotherapy. These findings have implications for optimizing treatment strategies in this disease.

In first-line ICI-treated stage IV NSCLC, KRAS-KEAP1 co-mutation, not KRAS or KEAP1 alone, identifies patients at high risk of early failure, whereas BRAF was associated with longer TTF. These findings highlight the importance of co-mutation profiling and warrant prospective validation with integrative models incorporating PD-L1 and TMB.

For large cell neuroendocrine carcinomas, the anti-Rb antibody can be helpful in determining patient treatment, in conjunction with KRAS, STK11, and KEAP1mutation testing. Finally, clones of these antibodies can show different results in terms of sensitivity and specificity, which are discussed in this work.

P1, N=52, Recruiting, M.D. Anderson Cancer Center | Trial completion date: Aug 2030 --> Dec 2026

Molecular docking studies and molecular dynamics simulations demonstrated that 18 exhibits a strong binding affinity and forms key stabilizing interactions within the Nrf2-binding domain of Kelch-like ECH-associated protein 1 (Keap1). These results demonstrate that quinazoline sulfonamide derivatives are promising oxidative stress modulators with tumor targeting ability.

These results suggest that CBG may protect melanocytes from UVA-induced oxidative changes and lipid peroxidation by activating the Nrf2-dependent antioxidant system and inhibiting NFκB-based pro-inflammatory signaling. CBG can therefore create favorable conditions for the physiological functioning of melanocytes after UVA exposure, ultimately reducing the risk of inflammatory skin responses and neoplastic transformation.

SE suppressed the PTX-induced increase in Keap-1 and enhanced Nrf-2 expression. In addition, SE treatment partially restored HO-1 expression, with statistically significant increases observed compared to the PTX group, although levels did not fully return to control values.

P2, N=100, Active, not recruiting, AstraZeneca | Recruiting --> Active, not recruiting | Phase classification: P3 --> P2 | N=280 --> 100 | Trial completion date: Mar 2031 --> Dec 2027 | Trial primary completion date: Aug 2027 --> Dec 2026

By merging molecular insights with technological advancements, this review explores the potential of phytochemicals in preventive and therapeutic strategies against chronic diseases. Future research should focus on personalized delivery systems, human efficacy, and harmonization to maximize their real-world impacts.

These findings demonstrate that Nrf2 signaling in macrophages fosters an immunosuppressive and pro-invasive microenvironment. The established MCT model provides a suitable platform to further unravel Nrf2-dependent mechanisms in the HCC TIME.