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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

Número MDL:
Código UNSPSC:
12352203
NACRES:
NA.41

fonte biológica

mouse

Nível de qualidade

conjugado

unconjugated

forma do anticorpo

purified immunoglobulin

tipo de produto de anticorpo

primary antibodies

clone

4.3E8.D10, monoclonal

forma

buffered aqueous solution

peso molecular

antigen 50 kDa

reatividade de espécies

human, mouse, rat

concentração

1 mg/mL

técnica(s)

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

Isotipo

IgG1

Condições de expedição

dry ice

temperatura de armazenamento

−20°C

modificação pós-traducional do alvo

unmodified

Informações sobre genes

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

Descrição geral

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.

Imunogênio

intact rat mitochondria.

Aplicação

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.

forma física

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

Exoneração de responsabilidade

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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Código de classe de armazenamento

10 - Combustible liquids

Classe de risco de água (WGK)

nwg

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


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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
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
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
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
Filio Billia et al.
Proceedings of the National Academy of Sciences of the United States of America, 108(23), 9572-9577 (2011-05-25)
Oxidative stress is caused by an imbalance between reactive oxygen species (ROS) production and the ability of an organism to eliminate these toxic intermediates. Mutations in PTEN-inducible kinase 1 (PINK1) link mitochondrial dysfunction, increased sensitivity to ROS, and apoptosis in

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