ATG3 (Autophagy Related 3)

Atractylon treatment for 12 h activated autophagic flux, because atractylon-induced autophagy was abolished by 3-methyladenine but was enhanced by chloroquine or bafilomycin A1. Furthermore, loss of MMP and activation of caspases upon atractylon treatment were abrogated by 3-methyladenine or autophagy-related gene 3 (ATG3) siRNA in HepG2 cells, suggesting that autophagy activation was required for induction of apoptosis. Altogether, atractylon disrupted the PI3K/AKT/mTOR signaling leading to autophagy-dependent apoptosis, which could be a promising candidate for anti-hepatoma therapy.

Our findings indicate autophagy activation in B3/TC and advanced Masaoka-Koga stage cases. Further studies are needed to explore the role of these autophagy related proteins as potential biomarkers and therapeutic targets in TETs.

Molecular docking studies demonstrated a strong binding affinity of compound 5b toward CDK4 and CDK6, supporting its role in cell cycle inhibition. Overall, these findings suggest that the synthetic chalcone derivatives 5b and 5c possess promising anticancer activity, modulating key pathways involved in cell cycle regulation, apoptosis, ferroptosis, and autophagy, and emerge as strong candidates for further investigation in the development of new therapeutic agents.

Autophagy blocker could prevent cells from autophagic cell death in response to high linear energy transfer radiation. We have outlined how autophagy can reverse complications of serious diseases in tumor cells and tumor microenvironment, which will contribute to a new direction for better treatment of diseases.

This study identified novel candidate risk genes for EOCRC, underscoring the role of rare variants and expanding our understanding of the genetic architecture of CRC. Future studies should include functional validation and replication studies on other ancestries to confirm and extend these results.

RETREG1 knockout abolishes degradation of ER-retained SERINC5, whereas endolysosomal turnover of surface SERINC5 remains partially intact, demonstrating that glycoGag utilizes dual ER-phagy and endolysosomal routes to suppress SERINC5. These findings expand the functional repertoire of RETREG1 in autophagy, identify that retroviruses repurpose micro-ER-phagy to circumvent SERINC5-mediated restriction, and reveal ER-phagy as an understudied battleground in the ongoing arms race between cellular restriction factors and viral accessory proteins.

Further experiments demonstrated that si-TNFAIP8 reduced the mRNA and protein levels of ATG3. Co-IP verified TNFAIP8 interacts with ATG3.TNFAIP8 may regulate AS autophagy by targeting ATG3.

Analysis of HADDOCK data showed that Lf interacted with the promoter of the genes. Lf, in addition to its effect on the expression of the genes, also interacts with the promoter of genes and their protein.

Our results provide novel insights into BL pathogenesis, emphasizing the interplay of age and EBV in shaping molecular landscapes. This study underscores the need for multi-omics integration to advance precision therapy strategies for BL subtypes.

Knockdown of ATG3 reversed the inhibitory effects of the polypeptide on cell proliferation and migration. These findings reveal that ENSG00000232259-ORF suppresses glioma progression by activating the autophagy pathway, providing a potential new target for tumor therapy.

An integrated assay toolbox-spanning surface plasmon resonance (SPR), dual-color LC3 flux reporters and disease-relevant phenotypes-now drives nanomolar optimization and safety profiling. We conclude by mapping future directions: covalent-reversible chemotypes, proteolysis-targeting chimera (PROTAC) degraders, targeted-delivery platforms and combination regimens poised to translate ATG12-ATG3 disruption into first-in-class therapeutics for oncology, immunology and infectious disease.

Importantly, our results indicate that CDK12 determines the oncogenic function of UPF3B. In conclusions, these results provide basis for research on liver cancer prevention and treatment.