RAD23B (RAD23 Homolog B)

but direct functional impact on gene expression was not observed in this study. The observed promoter methylation and gene expression alterations provide preliminary evidence of epigenetic modifications in response to chronic LDIR.

OTUD1 cleaves the K63-linked ubiquitin chain of RAD23B and XPC, and enhances PRKN mediated K48-linked ubiquitination of RAD23B-XPC and the subsequent proteasomal degradation. The findings of this study highlighted that OTUD1 could be a potential therapeutic target for NSCLC.

RAD23B facilitates CRC metastasis through activation of the Talin1/Integrin αv/β1/PI3K/AKT/MMP9 signaling axis. These results provide novel insights into the role of RAD23B in CRC progression and identify it as a potential therapeutic target.

More specifically, RAD23B gains an allosteric H274/H323 copper-binding site to enable the transfer of copper from the universal copper transporter 1 (CTR1) uptake protein to all known copper metallochaperone pathways, while simultaneously making its canonical functions in DNA repair copper dependent. This layer of nutrient regulation allows organisms to withstand elevated levels of potentially toxic copper while augmenting metabolism in cells with high energetic needs across both physiology and disease, including neurons in the locus coeruleus, a key brain structure that regulates sleep, and cancer cells.

We also discuss the use of computer-aided methods to develop small molecule inhibitors targeting NER-related proteins, with a focus on structure-based virtual screening, and reflect on future perspectives on this topic. Although interesting results are obtained on cell models with various molecules, we believe new efforts are needed in order to validate the proof of concept in vivo and to translate the use of NER inhibitors in cancer patients.

Western blot analysis demonstrated that carbon ion-induced DNA damage repair involved a complex array of pathways, with the RAD51-mediated homologous recombination (HR) pathway being predominant, while the Rad23B-mediated nucleotide excision repair (NER) pathway and XRCC1-mediated base excision repair (BER) were more relevant in response to X-ray irradiation. These results suggest that carbon ion irradiation may overcome radioresistance by inducing more complex DNA damage and apoptosis, thus providing insights for targeting new strategies in combining gene therapy with radiotherapy.

The lack of DNase I cleavage at the lesions did not change upon adding Rad4. However, in the presence of Rad4, a footprint is observed on the 7-nucleotide region (5'-TGGTGAT-3') of the complementary strand to the 3' side of the lesion.

Furthermore, Twist1 could directly bind to the fmnl3 promoter to facilitate FMNL3 transcription. To conclude, this study indicated that FMNL3 acted as a pro-metastasis factor in breast cancer by promoting Twist1 stability to suppress CDH1 transcription.

This suggests the involvement of p38 MAPK/ATF-2/RAD23B axis as a signaling pathway under nutrition starvation in breast cancer cells. The RAD23B mediated proteasome activity was shown to be much higher under stress conditions indicating a crucial role of RAD23B as a target for breast cancer.

Experiments presented in this study reveal a previously unknown link between NTHL1 expression levels and cisplatin sensitivity of NSCLC tumor cells. These findings provide an opportunity to understand how altered NTHL1 expression levels and subcellular distribution can impact cisplatin sensitivity in NSCLC tumor cells.

Brains from DOX-RT-treated mice had upregulated Adar, E2f3, Erlec1, Gnb1, Srpr, Vim, and Pdgfra expression and downregulated Rock2 and Inpp5f expression compared to control brains. The gene expression changes demonstrated here highlight roles for neuronal transmission and oxidative stress in the pathogenesis of doxorubicin-related CRCI and inflammation in RT-related CRCI.

The differentially expressed genes (DEGs) in CRC markedly affected the survival time of patients. CircRNAs could be utilized as diagnostic markers of CRC, and the key genes in CRC could be screened out by bioinformatics, which would be helpful to understand the drug targets for the treatment of human immunodeficiency virus (HIV)-related CRC patients.