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C5723

Sigma-Aldrich

Anti-Cytochrome c antibody produced in sheep

whole antiserum

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About This Item

MDL number:
MFCD01864291
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

sheep

Quality Level

200

conjugate

unconjugated

antibody form

whole antiserum

antibody product type

primary antibodies

clone

polyclonal

mol wt

antigen 14.4 kDa

species reactivity

human, rabbit, canine, rat

technique(s)

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

UniProt accession no.

P99999

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

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

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Immunogen

rabbit cytochrome c

Application

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

Target description

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.

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

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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
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
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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