NUP153 (Nucleoporin 153)

Targeting ASCOR with antisense oligonucleotides reverses chemoresistance in mouse models. Our study unveils an ascites circRNA-driven pathway underlying platinum resistance in HGSOC, suggesting targeting ASCOR is a promising strategy for HGSOC treatment.

Finally, we demonstrate that both SPOP-F102C and SPOP-F133L support targeted protein degradation in an engineered cellular system. These findings define the degradative capacities of SPOP mutants and highlight opportunities to repurpose these variants as mutant-selective E3 ligases for therapeutic applications.

Finally, we demonstrate that both SPOP-F102C and SPOP-F133L support targeted protein degradation (TPD) in an engineered cellular system. These findings define the degradative capacities of SPOP mutants and highlight opportunities to repurpose these variants as mutant-selective E3 ligases for therapeutic applications.

Gene expression analyses revealed that suppression reflected reduced expression of genes aberrantly activated following PRC2 inhibition. Together, these findings highlight conserved chromatin-regulatory pathways that intersect with Polycomb to maintain transcriptional balance and support developmental homeostasis.

We propose targeted therapies, including GSK3β inhibitors for ALS, antisense oligonucleotides for SCA2, and MTOR modulators for cancer, to restore ATXN2 function. By elucidating phosphocode of ATXN2, this work highlights novel avenues for precision medicine in neurodegenerative and oncogenic diseases.

Drug genomics analysis revealed that NUP153 expression predicted chemotherapy resistance, with imatinib and 4.5-dianilinophthalimide showing potential for inhibition in multiple cancers...The results indicate that NUP153 plays a key role in modulating the immune microenvironment and driving tumour progression, positioning it as a potential target for future therapeutic interventions. However, additional studies are required to elucidate the specific molecular mechanisms underlying NUP153's function in cancer and to explore its clinical applicability.

Structural variations within conserved TADs were associated with the expression of neuronal genes, including NUP153 and ID4, potentially driving cognitive and social adaptations. These findings provide novel insights into the molecular foundations of the convergent evolution of secondary aquatic adaptations in mammals.

Network and enrichment analysis identified the nucleoporins NUP54 and NUP153 as potential novel targets for TNBC. This study emphasizes the impact of ABI2 on nuclear proteins and suggests that targeting NUP54 and NUP153 could offer new therapeutic options for TNBC.

The model showed strong prognostic performance in 2088 newly diagnosed MM samples and predicted response to combination therapy (daratumumab, carfilzomib, lenalidomide, and dexamethasone) in patients who failed or relapsed from bortezomib-containing regimens, with an AUC of 0.9. Integrating the m6A risk model with the International Staging System (ISS) enhanced stratification accuracy. These insights support precision treatment of MM.

Altogether, our results demonstrate that SPOP regulates Nup153 levels and expands our understanding of the role of SPOP in protein and cellular homeostasis. [Media: see text] [Media: see text] [Media: see text].

We also show that U2OS osteosarcoma cells expressing the peptide-tagged myocardin-related transcription factor import this mechanosensitive protein to the nucleus at higher rates and display faster motility. Locally unstructured regions lower the free-energy barrier of protein translocation and might offer a control mechanism for nuclear mechanotransduction.

Although dsbNETs promote repair and survival, they are also co-opted during poly(ADP-ribose) polymerase (PARP) inhibition to restrain BRCA1-deficient breast cancer cells and are hyper-induced in cells expressing the aging-linked lamin A mutant progerin. In summary, our results advance understanding of nuclear structure-function relationships, uncover a nuclear-cytoplasmic DDR and identify dsbNETs as critical factors in genome organization and stability.