ATP1B1 (ATPase Na+/K+ transporting subunit beta 1)

Therapeutic strategies targeting lipid metabolism or the blood-brain barrier still face considerable challenges in clinical translation. Meanwhile, emerging tools such as lipidomics contribute to systematically analyzing the associated dysregulated lipid networks, thereby aiding in the identification of novel therapeutic targets.

This study elucidated the molecular mechanism by which JuA regulates mitochondrial energy metabolism and induces apoptosis in bladder cancer cells through targeted inhibition of ATP1A2. These findings reveal the crucial role of ATP1A2 in the energy metabolism and survival of bladder cancer cells, providing a new molecular perspective for a deeper understanding of the pathological mechanisms of bladder cancer.

Collectively, our bioinformatic and experimental findings indicate that ATP11B, RBBP7, DOCK10, and NUP160 are implicated in the pathogenesis and progression of sepsis. But their potential for sepsis biomarkers still requires further verification.

NRG1 fusions are a newly described clinically actionable target in solid tumors. We report the landscape of NRG1+ cancers and highlight the importance of RNA testing. NRG1+ PDAC is enriched in younger patients with KRAS wild-type disease and has a unique biology.

Arginine metabolism shapes neutrophil polarization in the LIHC TME. Targeting metabolic pathways may provide new therapeutic strategies to modulate the immune landscape and improve patient outcomes.

We identify subtype-specific protein signatures, with CD46, HNF1A, and ATP1B1 exclusively expressed in the aggressive group B. Finally, computational drug sensitivity prediction, validated by molecular docking, nominates Sunitinib as a potential therapy for group B patients. Our work provides a proteomic framework for improved prognostication and targeted therapy in high-risk HBV-HCC.

We constructed a risk prognostic model for UCEC based on a combination of lysosomal- and lipid metabolism-related genes. Our findings highlight the oncogenic potential of PLAAT1 in endometrial cancer and provide novel insights into the diagnosis and therapy of this cancer type.

Expanded human CECs expressed CEC functional markers, including Na+/K+-transporting ATPase subunit alpha-1 (ATP1A1), Zonula occludens-1 (ZO-1), and N-cadherin; they showed upregulated expression of YAP-regulated genes. Collectively, these findings support the development of efficient culture techniques for CEC expansion and may facilitate the advancement of therapeutic strategies for CEC-associated diseases.

IOPN exhibits distinct genetic alterations and a unique immune microenvironment. These features not only elucidate the mechanism underlying the relatively favorable prognosis of IOPN and IOPN-derived pancreatic cancers but also offer novel insights into immune regulation strategies for pancreatic cancer.

CEACAM5 defines a distinct immune-silent tumor phenotype and co-localizes with other vaccine-relevant genes such as EPCAM. This study provides a comprehensive immunogenomic rationale for CEACAM5-directed nanovaccine development and proposes EPCAM and ATP10B as co-targets based on tumor-specific and developmental expression profiles.

The results of the present study further elucidated the molecular processes underlying PDAC and highlight the crucial importance of manganese metabolism in its development. These biomarkers may provide significant prognostic insights and facilitate the advancement of targeted therapeutic strategies for PDAC.

The upregulation and externalization of S1PR1 on T cells mediated by ATP11B overexpression may be promising immunotherapeutic alternatives for GBM treatment.