ATP1A1 (ATPase Na+/K+ Transporting Subunit Alpha 1)

These effects required both Na+/K+-ATPase-dependent endocytosis and autophagy, as rapamycin-induced autophagy alone did not remove surface CD63. Our findings reveal a previously unrecognized mechanism in which cardiac glycoside regulates EV cargo composition by coupling Na+/K+-ATPase-mediated endocytosis with autophagy. Given that endogenous and therapeutic cardiac glycosides are implicated in cardiovascular and cancer biology, this mechanism may broadly influence EV-mediated intercellular communication and represent a potential target for modulating EV functions.

ATP1A1 emerges as a potential therapeutic target, with functional implications in angiogenesis and immune modulation. These findings highlight the clinical relevance of the identified gene signatures and support the development of personalized treatment strategies for ccRCC patients.

The expression of ATP1A1, survivin, and SMAC did not differ by sex or diet, although an upregulation trend in both ATP1A1 and survivin was noted in the male-HFD group. There is sexual dimorphism in the response to HFD during the transition from senescence to the apoptosis-first apoptotic switch in MASH progression.

The integration of hepatic OATPs as MRI reporter proteins offers a translationally feasible platform for non-invasive, longitudinal imaging of therapeutic cells in clinical trials and medicine. This technology has the potential to improve safety, efficacy, and mechanistic understanding across a wide array of biomedical applications.

We confirmed the predominance of known somatic drivers and identified a uniquely high frequency of ATP2B3 variants, refining their clinical phenotype. These findings underscore the influence of population-specific genetic backgrounds and expand the global understanding of PA genetics.

In this study, we found that EGFR-TKI, including gefitinib and osimertinib, impaired WWP2-mediated proteasomal degradation of LAPTM4B. These compounds synergistically enhance the efficacy of EGFR-TKIs in NSCLC models in vitro and in vivo, with minimal toxicity. Integrative analyses of patient tissue samples, cellular models, an animal model, and cancer databases highlight the critical role of the LAPTM4B-ATP1A1-lysosomal acidification axis in EGFR-TKI resistance, providing a promising therapeutic avenue for overcoming resistance in EGFR-mutant NSCLC.

Furthermore, virtual screening identified several promising therapeutic candidates, including Ecteinascidin, Avodart, and Nilotinib, which demonstrated high binding affinity to pivotal molecular targets such as AIM2, HK3, ATP1A1, and ZAP70. This study provides novel insights into the carcinogenic mechanisms of PFAS in ccRCC and proposes new avenues for targeted therapy. However, further experimental and clinical validation is necessary to confirm these findings and translate them into improved patient outcomes, while also addressing broader environmental health concerns related to PFAS exposure.

Pancreatic digestive enzyme and osmoregulatory genes (atp1a1, aqp8) peaked in PC, whereas slc26a6 expression was negligible throughout. Crustacean shell meals are promising as sustainable feed ingredients for Atlantic cod, and the study offers novel insights into gut structure and function with implications for intestinal health in farmed cod.

This study supplements the current knowledge of the underlying mechanism behind acquired chemoresistance in OVCA. Four differentially methylated genes identified in this study may have the potential to serve as promising epigenetic clinical biomarkers for HGSC chemotherapy resistance.

Peptide deformylase regulates CYP11B2 expression and aldosterone production. The CALB1-calcium signaling pathway may mediate the effects of peptide deformylase on aldosterone overproduction.

Studies utilizing nude mouse models further confirmed that pNaktide significantly reduces tumor volume and weight, supporting its potential as a therapeutic agent. In summary, this study demonstrates that low ATP1A1 expression is a critical factor in ccRCC progression and that pNaktide, by restoring ATP1A1-like functions, presents a promising therapeutic strategy for ccRCC.

Uptake of the contrast agent is restricted to MBP-expressing cells, which is most highly expressed during myelin sheath formation, thereby allowing progenitor-mediated, and potentially oligodendrocyte-mediated, remyelination to be monitored non-invasively in vivo using MRI. These findings provide the foundation for the development of direct methods for assessing the efficacy of pro-remyelination therapies.