Home Primary Antibodies ATP1B1 Antibody [A23C23]

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ATP1B1 Antibody [A23C23]

Cat.No.: F2309

    Application: Reactivity:
    • F2309-wb
      Lane 1: Hela, Lane 2: MCF7, Lane 3: U251

    Usage Information

    Dilution
    1:1000-1:10000
    1:200
    Application
    WB, IP, IHC, IF
    Reactivity
    Human, Mouse, Sheep, Pig, Dog
    Source
    Mouse Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW Observed MW
    35 kDa ~42-55 kDa
    *Why do the predicted and actual molecular weights differ?
    The following reasons may explain differences between the predicted and actual protein molecular weight.
    Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

    Datasheet & SDS

    Biological Description

    Specificity
    ATP1B1 Antibody [A23C23] detects endogenous levels of total ATP1B1 protein.
    Clone
    A23C23
    Synonym(s)
    adenosinetriphosphatase; ATP1B1; ATPase beta subunit; ATPase, Na+/K+ transporting; MGC1798; Na+, K+-ATPase; OTTHUMP00000032537; OTTHUMP00000032538; Sodium Potassium ATPase; ATP1B; ATP1B1; Atp4b; Atpb; Atpb-1; NKbeta1
    Background
    ATP1B1, the β1 regulatory subunit of the Na+/K+-ATPase within the P-type ATPase β-subunit family, forms obligate heterotetramers with α1-4 catalytic subunits to establish transmembrane electrochemical gradients essential for excitable tissues and epithelial vectorial transport. Its single-pass transmembrane helix and large extracellular domain stabilize α-subunit maturation, plasma membrane trafficking, and voltage-sensitive conformational cycling between E1P (Na+-occluded) and E2P (K+-occluded) states, while allosterically modulating Na+ affinity and ouabain sensitivity through direct interactions with the α-subunit actuator domain. Circadian regulation via CLOCK:BMAL1 binding to promoter E-boxes drives rhythmic Atp1b1 expression antiphasic to blood pressure, where DEC1 repression lowers β1 levels to elevate vascular tone; conversely, DEC1 deficiency enhances pump density and reduces hypertension through sustained membrane hyperpolarization. In renal distal tubules, ATP1B1 coordinates paracellular Cl- permeability via modulation of claudin-2/4/7 expression, while cardiac β1 sustains diastolic relaxation through optimized sarcolemmal K+ influx during repolarization. Rare mutations disrupt α-β assembly, causing familial hemiplegic migraine, while heterozygous variants associate with PCOS through insulin resistance and granulosa cell dysfunction.
    References
    • https://pubmed.ncbi.nlm.nih.gov/30012868/
    • https://pubmed.ncbi.nlm.nih.gov/10411917/

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