ATF2 (Activating Transcription Factor 2)

Notably, ATF2 mutants incapable of nuclear import can localise to the nucleus when co-expressed with c-Jun, indicating that c-Jun can facilitate ATF2 nuclear import via heterodimerisation. Together, these results establish that ATF2 enters the nucleus through IMPα recognition of two basic clusters and highlight the redundancy and complexity of ATF2 nuclear trafficking mechanisms.

In contrast, the activation or expression of the two other IFN transcription factors, the NF-κB subunit RelA and the AP-1 subunit ATF2, correlated with IFN-β induction. Our results suggest that during viral infection, activation of IRF3 does not automatically result in IFN responses at the level of individual cells, but that other factors, such as NF-κB and AP-1, are limiting for type I IFN induction.

It was found that it regulated cellular responses along with apoptotic mechanisms in cells without developing resistance in suppressing tumor growth by making changes on Atf2, Casp8, Bcl2 and Irf5 genes and proteins. As a result, the biotechnological drug potential of TRAIL was discovered in an aptamer-bound nanosystem for the treatment of triple-negative breast cancer and innovative applications for clinical use.

Inhibition of IRE1 with GSK2850163 suppressed these responses, whereas IRE1 activation with IXA4 reproduced the effects of BvrR. Findings indicate that BvrR from B. abortus activates IRE1, which subsequently stimulates ATF2 and NF-κB p65, leading to increased expression of IL-6 and TNF-α and the induction of inflammatory responses in HMC3 cells.

The pathway affects the cellular sensitivity to oxidative stress and ferroptosis, revealing a previously uncharacterized layer of epigenetic control in lipid quality control and damage repair. This positions the LORD pathway as a promising therapeutic target for diseases linked to chronic inflammation, neurodegeneration and cancer.

These findings highlight NKT cell differentiation as a strong prognostic indicator in OPSCC and support further exploration of epigenetic-immunologic interactions as potential therapeutic targets.

In addition, the results of biochemical indexes further verified that the overall changes in plasma ALT, AST, TBIL, DBIL, TRIG, ALP, LDH, GGT, CREA, UA, UREA, CK, HBD, and CHOL were significantly smaller in the TMF-treated groups than in the DDP-treated groups. These findings collectively position TMF as a promising therapeutic candidate combining robust antitumor efficacy with favorable safety characteristics for the treatment of cervical cancer.

Pretreatment with the antioxidant N-acetylcysteine inhibited not only ROS upregulation but also DR5 upregulation induced by bortezomib in Raji cells. Therefore, the results indicate that bortezomib may enhance Raji cell sensitivity to TRAIL via ROS-dependent upregulation of DR5, induce apoptosis through the MAPK signaling pathway, and subsequently inhibit cell proliferation. Additionally, bortezomib combined with TRAIL had a potential synergistic apoptosis-inducing effect in TRAIL-resistant BL cells.

Analysis of pan-cancer immunotherapy cohorts revealed a significant correlation between CXCR2 + VNN2 + Neu phenotypic transition and immunotherapy resistance in patients. We finally constructed a deep learning model named Deepsurv to accurately stratify pan-cancer patients based on the CXCR2 + VNN2 + Neu Phenotypic Transition Gene Regulatory Network (CVN-GRN) and predict the prognosis of the patients, which achieved the desired results.

These results illustrate that CSRP2 regulates the tumor microenvironment to promote HCC growth and drive lenvatinib tolerance via the CSRP2/ATF2/CCL28 axis. Targeting this pathway could synergize with lenvatinib to treat HCC more effectively.

FBXO45 promotes HCC lung metastasis by activating the TFG-ATF2-NF-κB-epithelial-mesenchymal transition signaling axis. In addition, we found that targeting the TP53-FBXO45-TFG-ATF2-NF-κB axis could be a novel approach for the treatment of metastatic HCC.