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Key Documents

A9728

Sigma-Aldrich

Monoclonal Anti-ATP Synthase β antibody produced in mouse

1 mg/mL, clone 4.3E8.D10, purified immunoglobulin, buffered aqueous solution

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About This Item

MDL number:
MFCD03455681
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

200

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

4.3E8.D10, monoclonal

form

buffered aqueous solution

mol wt

antigen 50 kDa

species reactivity

human, mouse, rat

concentration

1 mg/mL

technique(s)

immunoprecipitation (IP): suitable
indirect immunofluorescence: suitable
western blot: suitable

isotype

IgG1

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... ATP5B(506)
mouse ... Atp5b(11947)
rat ... Atp5b(171374)

General description

ATP synthase is a highly conserved transmembrane protein that can catalyse the reversible synthesis of ATP from ADP and phosphate.
Detects the β subunit of ATP synthase and can be used as a mitochondrial marker.

Immunogen

intact rat mitochondria.

Application

Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Immunofluorescence (1 paper)
Western Blotting (1 paper)
Mouse Monoclonal Anti-ATP Synthase beta antibody can be used for western blot, indirect immunofluorescence and immunoprecipitation assays.
Pancreatic islet cells isolated from wither Wistar ratos or nondiabetic organ donors were fixed in 4% paraformaldhyde and permeabilized with 0.3% Triton-X for immunocytochemistry using monoclonal mouse anti- beta ATP synthase at a 1:1000 dilution.

Physical form

Solution in phosphate buffered saline containing 1.0 mg/mL bovine serum albumin and 0.05% sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class

10 - Combustible liquids

wgk_germany

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable

Osvědčení o analýze (COA)

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Navštívit knihovnu dokumentů

Esteban N Gurzov et al.
The Journal of biological chemistry, 285(26), 19910-19920 (2010-04-28)
Type 1 diabetes is an autoimmune disorder characterized by chronic inflammation and pancreatic beta-cell loss. Here, we demonstrate that the proinflammatory cytokine interleukin-1beta, combined with interferon-gamma, induces the expression of the Bcl-2 homology 3 (BH3)-only activator PUMA (p53 up-regulated modulator
J Alfonso Leyva et al.
Molecular membrane biology, 20(1), 27-33 (2003-05-15)
To couple the energy present in the electrochemical proton gradient, established across the mitochondrial membrane by the respiratory chain, to the formation of ATP from ADP and Pi, ATP-synthase goes through a sequence of coordinated conformational changes of its major
Sarah Engeham et al.
Journal of nutrition and metabolism, 2012, 989037-989037 (2012-04-27)
Maternal protein restriction in rat pregnancy is associated with impaired renal development and age-related loss of renal function in the resulting offspring. Pregnant rats were fed either control or low-protein (LP) diets, and kidneys from their male offspring were collected
Fabrice Moore et al.
PloS one, 7(2), e31062-e31062 (2012-02-22)
In the course of Type 1 diabetes pro-inflammatory cytokines (e.g., IL-1β, IFN-γ and TNF-α) produced by islet-infiltrating immune cells modify expression of key gene networks in β-cells, leading to local inflammation and β-cell apoptosis. Most known cytokine-induced transcription factors have
Mara Zilocchi et al.
Neurochemistry international, 118, 61-72 (2018-04-29)
Mitochondrial impairment is one of the most important hallmarks of Parkinson's disease (PD) pathogenesis. In this work, we wanted to verify the molecular basis of altered mitochondrial dynamics and disposal in Substantia nigra specimens of sporadic PD patients, by the
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