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Merck
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Documenti fondamentali

C5723

Sigma-Aldrich

Anti-Cytochrome c antibody produced in sheep

whole antiserum

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About This Item

Numero MDL:
Codice UNSPSC:
12352203
NACRES:
NA.41

Origine biologica

sheep

Livello qualitativo

Coniugato

unconjugated

Forma dell’anticorpo

whole antiserum

Tipo di anticorpo

primary antibodies

Clone

polyclonal

PM

antigen 14.4 kDa

Reattività contro le specie

human, rabbit, canine, rat

tecniche

immunoprecipitation (IP): suitable
indirect immunofluorescence: suitable
western blot: 1:5,000 using MCF-7, Rat-1, MDCK or Jurkat cell extracts

N° accesso UniProt

Condizioni di spedizione

dry ice

Temperatura di conservazione

−20°C

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

human ... CYCS(54205)
rat ... Cycs(25309)

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Immunogeno

rabbit cytochrome c

Applicazioni

Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Western Blotting (1 paper)

Descrizione del bersaglio

Cytochrome c is an electron transport protein released from mitochondria as an early committed event in apoptosis. Cytochrome c and dATP are cofactors for the mammalian apoptosome, which is composed of Apaf-1, Bcl-2, and procaspase 9. When caspase 9 is activated, activation of other caspases follow including the death protease caspase 3. The release of cytochrome c is inhibited by the presence of Bcl-2 on these organelles preventing the initiation of apoptosis. In cells induced by several apoptotic agents (such as UV irradiation, staurosporine, and overexpression of Bax), caspase inhibitors do not prevent cytochrome c release.

Esclusione di responsabilità

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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Raccomandato

Codice della classe di stoccaggio

10 - Combustible liquids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


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Certificati d'analisi (COA)

Lot/Batch Number

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Debolina Ghosh et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 32(17), 5821-5832 (2012-04-28)
The brain depends on redox electrons from nicotinamide adenine dinucleotide (reduced form; NADH) to produce ATP and oxyradicals (reactive oxygen species [ROS]). Because ROS damage and mitochondrial dysregulation are prominent in aging and Alzheimer's disease (AD) and their relationship to
Merrick S Reynolds et al.
American journal of physiology. Endocrinology and metabolism, 311(1), E186-E201 (2016-05-26)
β-Cell insulin secretion is dependent on proper mitochondrial function. Various studies have clearly shown that the Nr4a family of orphan nuclear receptors is essential for fuel utilization and mitochondrial function in liver, muscle, and adipose. Previously, we have demonstrated that
Mishra Suman et al.
Scientifica, 2016, 3675283-3675283 (2016-06-14)
Arginase regulates arginine metabolism, ornithine-urea cycle, and immunological surveillance. Arginase-I is predominant in cytosol, and arginase-II is localised in the mitochondria. A mitochondrial membrane-bound arginase has also been proposed to be adsorbed with outer membrane of mitochondria which gets released
Erik D Marchant et al.
International journal of molecular sciences, 23(15) (2022-08-13)
AIM: Mild heat stress can improve mitochondrial respiratory capacity in skeletal muscle. However, long-term heat interventions are scarce, and the effects of heat therapy need to be understood in the context of the adaptations which follow the more complex combination
Gina Sánchez et al.
PloS one, 15(5), e0233591-e0233591 (2020-05-27)
The heart is critically dependent on mitochondrial respiration for energy supply. Ischemia decreases oxygen availability, with catastrophic consequences for cellular energy systems. After a few minutes of ischemia, the mitochondrial respiratory chain halts, ATP levels drop and ion gradients across

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