Atp1b1-flox Mouse

ATP1B1, encoding the Na,K-ATPase β subunit, is a key regulator of the Na+ and K+ electrochemical gradients across the plasma membrane, which is essential for regulating cellular activity. It is involved in various biological processes and is associated with multiple pathways, such as those related to cell adhesion, antiviral innate immunity, and the regulation of cell proliferation, migration, and invasion [2,4,6].

In cancer research, ATP1B1 is overexpressed in diffuse large B-cell lymphoma (DLBCL) cell lines and its expression levels can impact the prognosis of DLBCL patients. Downregulation of ATP1B1 inhibits DLBCL cell proliferation, migration, invasion, and adhesion, and roxithromycin can rescue the higher proliferation ability in ATP1B1-overexpression cells [4]. In cytogenetically normal acute myeloid leukemia (CN-AML), high ATP1B1 expression is associated with shorter overall survival and event-free survival, and it may contribute to leukemogenicity through up-regulation of oncogenes/onco-microRNAs [6]. Rapamycin inhibits the progression of human acute myeloid leukemia by regulating the circ_0094100/miR-217/ATP1B1 axis [8]. In addition, in NRG1 fusion-driven tumors, ATP1B1 is identified as a fusion partner of NRG1, and drugs targeting the related pathways may be potential therapeutic strategies [1,3].

In antiviral innate immunity, ATP1B1 can be induced by DNA and RNA virus infections, inhibit viral replication, and increase the levels of IFNs, IFN-stimulated genes, and inflammatory cytokines by potentiating the ubiquitination of TRAF3 and TRAF6 [2].

In boar sperm, the relative mRNA expression level of ATP1B1 is significantly higher in fresh sperm of the group with good semen freezability, indicating it may be a promising cryotolerance marker [5].

In alveolar epithelial cells, a study identified proteins interacting with ATP1B1, providing new insights into its role in maintaining alveolar epithelial barrier integrity [7].

In astrocytes, the interaction of DCF1 with ATP1B1 impairs astrocyte structural plasticity via the P38 signaling pathway [9].

In Fuchs endothelial corneal dystrophy, intergenic variants are associated with decreased ATP1B1 expression [10].

In conclusion, ATP1B1 is crucial for maintaining normal cellular functions, and its dysregulation is involved in multiple diseases, including various cancers, viral infections, and corneal dystrophy. Research on ATP1B1, especially through studies in disease-relevant models, helps to understand the underlying molecular mechanisms, providing potential diagnostic biomarkers and therapeutic targets for these diseases.