EEF1A1 (Eukaryotic Translation Elongation Factor 1 Alpha 1)

Additionally, METTL16-mediated m6A modification of EEF1A1 mRNA activates the m6A-IGF2BP1 axis, resulting in increased EEF1A1 protein levels and enhanced resistance to ENZ-induced apoptosis. These findings uncover a novel UFL1-METTL16-EEF1A1 signaling pathway that drives ENZ resistance, suggesting that targeting this cascade may offer a promising therapeutic strategy for overcoming ENZ resistance in prostate cancer.

These insights emphasize the need to simultaneously preserve both target engagement and optimal permeability when modifying side chains in cell-permeable macrocyclic peptides, positioning compound 17 as a robust scaffold for future lead optimization. This work furnishes a blueprint for balancing drug-like properties with therapeutic potency in macrocyclic therapeutics.

Finally, MD simulations and pair-interaction energy analyses highlighted Lys84, Arg218, and Glu230 of eEF1A1 as key residues for driving its binding interactions to AKOS-04. These results reveal that AKOS-04, screened by SBVS against C234 of eEF1A1, represents a promising lead for eEF1A1-targeted pancreatic cancer therapy, highlighting the power of computational approaches in covalent drug discovery.

Further, RBPs like RPS8, RPL5, RPS3A, EEF1A1, and EIF4E1B were found to be strongly correlated with patients' overall survival. Taken together, our analyses identified several candidate RBPs which might serve as potential targets for oncological measures against gliomas.

ALB-EEF1A1 may play a pivotal role in the metastatic transformation of primary CRC and significantly increase the risk of death. The identified ALB-EEF1A1 fusion transcripts are promising novel molecular targets that may serve as prognostic and diagnostic biomarkers and treatment targets for mCRC in the future.

RNA-seq analysis additionally uncovered that SF-153 impaired lysosome acidification and inhibited autophagy to enhance the anti-leukemic activities. Taken together, our study characterized the multimodal mechanisms of inhibition by SF-153 in leukemia cells and laid the foundation for studying selective UHM inhibitors in future.

By addressing underlying patterning processes and plasticity networks as therapeutic vulnerabilities, our findings provide precision medicine strategies aimed at modulating glioma cell fates and overcoming therapeutic resistance. We suggest transition therapy toward neuronal-like lineage differentiation as a potential precision therapy to help stabilize pHGG plasticity and aggressivity.

Accordingly, the present work aims to examine their multifaceted modes of action more than just blocking protein synthesis. By unveiling these insights, our deepened knowledge of these eEF1A-binding inhibitors will inform the development of future eEF1A-targeted drugs for cancer treatment.

Comparison with unexposed controls demonstrated higher CHIP prevalence in WTC responders, particularly in those 55 or younger. Study highlights the potential utility of deep sequencing for CHIP detection with clinical, laboratory and exposure data to develop personalized risk-adapted screening programs for cancer and other CHIP-related conditions in individuals exposed to airborne carcinogens.

This study identifies specific blood transcriptomic profiles associated with the innate immune response and a key hub gene linked to treatment outcomes, suggesting an immune-related component in response to [177Lu]Lu-DOTA-TATE therapy. These findings may guide patient selection based on systemic immune markers and inform future therapeutic strategies.

Additionally, the limited efficacy of current smallpox antivirals, such as Tecovirimat and Brincidofovir, alongside growing concerns about the emergency of tecovirimat resistance mutants, underscores the need for new therapeutic options. These findings indicate plitidepsin as a promising candidate for mpox treatment. Further studies are needed to explore its potential as a standalone or combination therapy, supporting clinical evaluation for mpox treatment.

Additional Tap-tagging and mass spectrometry of components in Trus complexes isolated from Drosophila Kc cells identified Ribosomal protein subunit 2 (RpS2), which is coded by string of pearls (sop) in Drosophila, and Eukaryotic translation elongation factor 1 alpha 1 (eEF1α1) as interacting factors. We discuss the implication of these findings with respect to the similarity and differences in trus genetic null mutant phenotypes compared to the haplo-insufficiency phenotypes produced by heterozygosity for mutants in Minute genes and other genes involved in ribosome biogenesis.