ATP1B2

Last update 08 May 2025

Basic Info

Synonyms

Adhesion molecule in glia, AMOG, ATP1B2

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Introduction

This is the non-catalytic component of the active enzyme, which catalyzes the hydrolysis of ATP coupled with the exchange of Na(+) and K(+) ions across the plasma membrane. The exact function of the beta-2 subunit is not known. Mediates cell adhesion of neurons and astrocytes, and promotes neurite outgrowth.

100 Clinical Results associated with ATP1B2

100 Translational Medicine associated with ATP1B2

0 Patents (Medical) associated with ATP1B2

Literatures (Medical) associated with ATP1B2

01 May 2025·Neurotoxicology and Teratology

An in silico analysis of dicofol-induced neurotoxicity mechanisms in humans

Article

Author: Kuzu, Burak ; Karakuş, Fuat

Dicofol (DCF) is an organochlorine pesticide that has recently been recognized as a persistent organic pollutant. This study begins by investigating the neurotoxicity of DCF and its metabolites through in silico tools. It subsequently explores the molecular mechanisms and key targets associated with DCF-induced neurotoxicity in humans by employing network toxicology, multi-level bioinformatics approaches, and molecular docking analyses. The prediction results indicate that both DCF and its metabolites can traverse the blood-brain barrier, penetrating the central nervous system, and inducing neurotoxicity. A thorough analysis has identified 56 potential targets linked to DCF-induced neurotoxicity. Gene Ontology enrichment analysis revealed significant associations with pathways related to sodium ion transmembrane transport, sodium/potassium-exchanging ATPase complexes, and P-type calcium transporter activity. Pathway enrichment analysis suggests that DCF-induced neurotoxicity arises from disruptions in ion transport via P-type ATPases. Further examination of gene-gene and protein-protein interactions, along with centrality analysis, identified 11 hub targets, including ATP1A1, ATP1A2, ATP1A3, ATP1A4, ATP1B1, ATP1B2, and MAPK1, as key players. Notably, six of these targets are subunits of the Na⁺/K⁺-ATPase, a P-type ATPase. Molecular docking results demonstrated that DCF binds more effectively to the ATP1A3-ATP1B1 protein complex than to its natural ligand, ATP. These findings suggest that DCF may inhibit Na⁺/K⁺-ATPase through ATP1A3, resulting in an imbalance of sodium and potassium gradients and ultimately leading to neurotoxicity.

01 Jan 2025·General and Comparative Endocrinology

Thyroid hormones activate TH/E2 receptor/regulator system and drive Na+/K+-ATPase in the ovarian wall of hypothyroid air-breathing fish (Anabas testudineus Bloch)

Article

Author: Viswanath, Meenu ; Peter, M C Subhash ; Peter, M.C.Subhash

In fish, as in other vertebrates, thyroid hormones (THs) act on many biological processes including growth and reproduction. Primary THs such as thyroxine (T₄) and triiodothyronine (T₃) are known for their direct action on osmoregulatory organs regulating ion osmotic homeostasis in many teleost fishes. However, it is unclear how these hormones interact with estradiol-17β (E₂), an ovarian hormone that regulates the development of oocytes. We thus examined the short-term in vivo action of varied THs such as T_4, T₃ and T₂, a potent TH metabolite diiodothyronine, on the expression pattern of receptors of THs and E₂ in the ovarian wall of the hypothyroid climbing perch to identify the interactive pattern of TH/E₂ receptor system and the molecular dynamics of Na⁺/K⁺-ATPase (NKA) subunits in the ovarian wall that provides structural and functional support to ovary. We found differential pattern of transcript abundance of NKA subunits isoforms such as nkaα1a, nkaα1b, nkaα1c atp1b1, atp1b2 and fxyd3, fxyd5, fxyd6, TH receptor isoforms (tr<, trβ, tr2 receptor (er<, erβ, gper), aromatases (cyp19a1a, cyp19a1b) and steroidogenic enzymes (17β-hsd, sf-1, star) in ovarian wall in response to T₄, T₃ and T₂ administration in MMI-treated fish. The transcript abundance pattern provides evidence for a direct role of THs in the ovarian wall of hypothyroid fish. It confirms a targeted interaction of THs with ER/cyp19a1 and NKA systems. Pattern analysis further revealed that T₄ could produce maximum activation of the TR/Deo/Mct and ER/cyp19a1 systems among three iodinated tyrosines, bringing synergistic interaction between the TH and E₂ systems in the ovarian wall. This novel evidence of direct interaction between the TH/E₂ system and the NKA system in the ovarian wall further testifies to an ion osmotic role for THs in this ovarian structure.

01 Oct 2024·Brain Research Bulletin

Investigating the mechanisms of inflammation and immune alterations in Parkinson's disease using spatial transcriptomics techniques

Article

Author: Geng, Yifan ; Sun, Zhiyuan ; Bi, Jun ; Jiang, Xing ; Wang, Qinglu ; Zhang, Sen ; Tian, Xuewen ; Yan, Min

In recent years, overwhelming evidence has emphasized the crucial role of inflammation in the pathogenesis of PD. However, the exact mechanisms by which inflammation damages dopaminergic neurons in PD are still unclear. Therefore, we generated a MPTP-induced PD mouse model and performed spatial transcriptomic sequencing to provide more insight into the process of PD development at specific brain regions. Our results indicate that the pathological changes of PD are mainly manifested in the midbrain, especially in the substantia nigra region, with significant reductions in oligodendrocytes and Agt-labeled astrocytes and an increase in Gfap-labeled astrocytes. Macrophages displayed an increasing trend in the PD environment, indicating a pattern of immune modulation induced by PD. Moreover, pathway analysis revealed significant impairments in ion migration ability, abnormal Ca²⁺ channels, cAMP signaling, and synaptic damage in PD. Significant downregulation of Mt1 and Mt2 and upregulation of Atp1b2, Gpi1, and Cox6a1 in PD further underscored the occurrence of intense inflammation and immune alterations. On the basis of these findings, we have validated the significant accumulation of Ca²⁺ in the midbrain tissue in the PD environment by measuring its content. Additionally, we have demonstrated a close association between the reduction of dopaminergic neurons, represented by the midbrain region, and ferroptosis by evaluating the iron content, malondialdehyde (MDA) levels, and the protein expression of GPX4 and TH in the tissue. We propose the hypothesis that PD-related inflammation and immune changes can induce neuronal and oligodendrocyte damage through the induction of ferroptosis, thereby further accelerating the progression of PD.

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ATP1B2

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