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Merck
CN

C9616

Anti-Cytochrome c antibody produced in sheep

~0.5 mg/mL, affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-CYC

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About This Item

UNSPSC Code:
12352203
MDL number:
Conjugate:
unconjugated
Clone:
polyclonal
Application:
IF, IHC (p), WB
Citations:
10
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biological source

sheep

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 15 kDa

species reactivity

rabbit, rat, human, canine

concentration

~0.5 mg/mL

technique(s)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): 20-40 μg/mL using human heart tissue, indirect immunofluorescence: 5-10 μg/mL using human MCF-7 cells, western blot: 0.1-0.2 μg/mL using whole extracts of MCF−7, Jurkat, Rat−1, MDCK cells and extract of rat kidney or rat heart

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

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

General description

Anti-Cytochrome c produced in sheep using purified rabbit cytochrome c conjugated to keyhole limpet hemocyanin (KLH).
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.

Immunogen

rabbit cytochrome c.

Application

Anti-Cytochrome c antibody produced in sheep has been used in:
  • immunocytochemistry
  • immunostaining
  • immunoblotting
  • immunohistochemistry

Biochem/physiol Actions

Cytochrome c controls cellular electron transport and energy metabolism. It is involved in the transfer of electrons between complex III and complex IV in the mitochondrial electron transport chain. It is involved in apoptosis and activates the death protease caspase-3 (CCP32). The presence of Bcl-2 on the organelles inhibits the release of cytochrome c from mitochondria during apoptosis. Along with Apaf-1, and procaspase-9, it forms an essential component of vertebrate ”apoptosome”. Activation of caspase-9 and other capsases directs apoptosis. Serum cytochrome c is a sensitive apoptotic marker in vivo, and increased serum cytochrome c level can serve as a negative prognostic marker.

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 1% BSA and 15 mM 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

12 - Non Combustible Liquids

wgk

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable

Regulatory Information

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Related Content

Instructions


Differential control of growth, apoptotic activity and gene expression in human colon cancer cells by extracts derived from medicinal herbs, Rhazya stricta and Zingiber officinale and their combination
Elkady AI, et al.
World Journal of Gastroenterology, 20(41), 15275-15275 (2014)
Katarzyna Barczyk et al.
International journal of cancer, 116(2), 167-173 (2005-04-01)
Despite significant progress in cancer therapy, the outcome of the treatment is often unfavorable. Better treatment monitoring would not only allow an individual more effective, patient-adjusted therapy, but also it would eliminate some of the side effects. Using a cytochrome
R M Kluck et al.
Science (New York, N.Y.), 275(5303), 1132-1136 (1997-02-21)
In a cell-free apoptosis system, mitochondria spontaneously released cytochrome c, which activated DEVD-specific caspases, leading to fodrin cleavage and apoptotic nuclear morphology. Bcl-2 acted in situ on mitochondria to prevent the release of cytochrome c and thus caspase activation. During



Global Trade Item Number

SKUGTIN
C9616-200UL04061838104656