ATP1B2 Antibody [G17J5] | Primary Antibodies

Application: Reactivity: Mouse, Rat, Human

Usage Information

Dilution
WB1:10000 - 1:50000 IP1:50 - 1:70 IHC1:2000

Application
WB, IP, IHC

Reactivity
Mouse, Rat, Human

Source
Rabbit 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
33 kDa

Positive Control	Human astrocytoma; Human cerebellum; Human retina; Rat cerebrum; Mouse retina; Rat retina; Mouse cerebrum; Y79 cells
Negative Control	Mouse liver; Human liver; Rat liver

Datasheet & SDS

Biological Description

Specificity
ATP1B2 Antibody [G17J5] detects endogenous levels of total ATP1B2 protein.

Clone
G17J5

Synonym(s)
ATP1B2; Sodium/potassium-transporting ATPase subunit beta-2; Adhesion molecule in glia; Sodium/potassium-dependent ATPase subunit beta-2; AMOG

Background
ATP1B2 (Sodium/potassium-transporting ATPase subunit beta-2) is the non-catalytic β2 subunit (heavily glycosylated) of the Na+/K±ATPase enzyme complex, predominantly expressed in neuronal tissues such as the brain and spinal cord. It is essential for assembling and stabilizing the catalytic α subunit in the plasma membrane, allowing active transport of 3 Na+ out and 2 K+ in per ATP hydrolyzed. ATP1B2 features a large extracellular domain with five conserved disulfide bonds and multiple N-linked glycosylation sites forming a protective “lid” over the ion-binding sites of the α subunit’s transmembrane helices, as well as a short cytoplasmic tail and a C-terminal motif that regulates ion affinity through tyrosine insertions favoring Na+ during E1/E2 conformational cycles. ATP1B2 modulates pump kinetics, promotes proper folding and trafficking of αβ heteromers from the ER/Golgi to the membrane, occludes K+ ions during conformational shifts, and enhances Na+ release extracellularly. These actions maintain electrochemical gradients crucial for neuronal resting potential, action potential firing, cell volume regulation, and secondary active transport (glucose and neurotransmitters). ATP1B2 also mediates glia-neuron adhesion and neurite outgrowth via homophilic interactions, linking ion homeostasis to synaptogenesis. Disease relevance includes epilepsy, where ATP1B2 variants impair pump assembly, leading to neuronal hyperexcitability due to Na+ overload, and potential involvement in neurodegeneration and cardiac dysfunction through disrupted ion gradients, similar to ATP1B1 or ATP1A2 mutations.

Background

ATP1B2 (Sodium/potassium-transporting ATPase subunit beta-2) is the non-catalytic β2 subunit (heavily glycosylated) of the Na+/K±ATPase enzyme complex, predominantly expressed in neuronal tissues such as the brain and spinal cord. It is essential for assembling and stabilizing the catalytic α subunit in the plasma membrane, allowing active transport of 3 Na+ out and 2 K+ in per ATP hydrolyzed. ATP1B2 features a large extracellular domain with five conserved disulfide bonds and multiple N-linked glycosylation sites forming a protective “lid” over the ion-binding sites of the α subunit’s transmembrane helices, as well as a short cytoplasmic tail and a C-terminal motif that regulates ion affinity through tyrosine insertions favoring Na+ during E1/E2 conformational cycles. ATP1B2 modulates pump kinetics, promotes proper folding and trafficking of αβ heteromers from the ER/Golgi to the membrane, occludes K+ ions during conformational shifts, and enhances Na+ release extracellularly. These actions maintain electrochemical gradients crucial for neuronal resting potential, action potential firing, cell volume regulation, and secondary active transport (glucose and neurotransmitters). ATP1B2 also mediates glia-neuron adhesion and neurite outgrowth via homophilic interactions, linking ion homeostasis to synaptogenesis. Disease relevance includes epilepsy, where ATP1B2 variants impair pump assembly, leading to neuronal hyperexcitability due to Na+ overload, and potential involvement in neurodegeneration and cardiac dysfunction through disrupted ion gradients, similar to ATP1B1 or ATP1A2 mutations.

References
https://pubmed.ncbi.nlm.nih.gov/31285960/ https://pubmed.ncbi.nlm.nih.gov/26847162/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%