ATP1B1 Membrane Protein Introduction

Introduction of ATP1B1

The protein encoded by ATP1B1 gene belongs to the family of Na+/K+ and H+/K+ ATPases beta chain proteins, which is the subfamily of Na+/K+ -ATPases. The beta subunit of Na+/K+-ATPase can be encoded by many genes. This gene encodes a beta 1 subunit. Alternatively, spliced transcript variants have been found encoding different isoforms, but their biological validity is unknown. This gene has a broad expression in kidney, brain and 14 other tissues.

Basic Information of ATP1B1
Protein Name Sodium/potassium-transporting ATPase subunit beta-1
Gene Name ATP1B1
Aliases Sodium/potassium-dependent ATPase subunit beta-1
Organism Homo sapiens (Human)
UniProt ID P05026
Transmembrane Times 1
Length (aa) 303

Functions of ATP1B1 Membrane Protein

ATP1B1 is the non-catalytic region of the active Na+/K+-ATPase, which catalyzes the ATP hydrolysis along with the exchange of Na+ and K+ ions across the cytomembrane. Na+/K+ -ATPase is an indispensable membrane protein, functioning in establishing and maintaining the Na and K ions electrochemical gradients across the plasma membrane. These gradients are necessary for osmoregulation, for electrical excitability of nerve and muscle, and for sodium-coupled transport of various organic and inorganic molecules. On the other hand, ATP1B1 may function, through the entire enzyme complex, in cell adhesion and in establishing cell polarity of epithelia. Fig.1 shows the role of ATP1B1 in the exchange of Na+ and K+ ions across the plasma membrane.

Schematic representation of ATP1B1 playing a role in the exchange of Na+ and K+ ions across the plasma membrane. Fig.1 Schematic representation of ATP1B1 playing a role in the exchange of Na+ and K+ ions across the plasma membrane. (Inchul Choi, 2012)

Application of ATP1B1 Membrane Protein in Literature

  1. Shi J.L., et al. Overexpression of ATP1B1 predicts an adverse prognosis in cytogenetically normal acute myeloid leukemia. Oncotarget. 2016, 7(3): 2585-95. PubMed ID: 26506237

    This article reveals that high ATP1B1 expression is associated with shorter overall survival (OS) and event-free survival (EFS) (P = 0.0068, P = 0.0039, respectively) within the primary cohort.

  2. Cui X., et al. Interaction between human cytomegalovirus UL136 protein and ATP1B1 protein. Braz J Med Biol Res. 2011, 44(12): 1251-5. PubMed ID: 22030864

    This article shows that ATP1B1 can interact with the UL136 protein by yeast two-hybrid, pull-down assay, and immunofluorescent co-localization. It is suggested that ATP1B1 may be a partner of the UL136 protein for the co-localization of UL136-EGFP and ATP1B1-DsRed in cell membranes.

  3. Prasad M.K., et al. A polymorphic 3'UTR element in ATP1B1 regulates alternative polyadenylation and is associated with blood pressure. PLoS One. 2013, 8(10): e76290. PubMed ID: 24098465

    This article demonstrates that the relative richness of the A2-polyadenylated ATP1B1 mRNA is lower in human kidneys lacking the T12GT 3GT6 allele than in those with at least one copy of this allele. Additionally, it identifies a new multi-allelic TRS in the ATP1B1 3'UTR, which may regulate its effect by mediating the polyadenylation of the ATP1B1 mRNA and may be associated with higher BP.

  4. Selvakumar P., et al. Epigenetic silencing of Na, K-ATPase β 1 subunit gene ATP1B1 by methylation in clear cell renal cell carcinoma. Epigenetics. 2014, 9(4): 579-86. PubMed ID: 24452105

    This report demonstrates that promoter hypermethylation has a connection with decreased ATP1B1 expression, which might have an influence on RCC initiation and/or disease progression, for the reason that treatment with 5-Aza-2'-deoxycytidine will rescue the expression of ATP1B1 mRNA.

  5. Faruque M.U., et al. Association of ATP1B1, RGS5 and SELE polymorphisms with hypertension and blood pressure in African-Americans. J Hypertens. 2011, 29(10): 1906-12. PubMed ID: 21881522

    This article provides a good support for the genetic role of ATP1B1, SELE, and RGS5 in hypertension and regulation of blood pressure.

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  1. I Choi, et al. (2012). Transcription factor AP-2γ is a core regulator of tight junction biogenesis and cavity formation during mouse early embryogenesis. Development. 139(24): 4623-32.

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