Product Description
Cytochrome C Antibody [6H2.B4] | 33-454 | ProSci
Host: Mouse
Reactivity: Human, Mouse, Rat
Homology: N/A
Immunogen: Rat full-length protein was used as the immunogen for the Cytochrome C antibody.
Research Area: Signal Transduction
Tested Application: WB, IP, Flow, IF
Application: Western blot: 1-2 ug/ml
Immunoprecipitation: 2 ug/mg of lysate
Flow Cytometry: 0.5-1 ug/million cells in 0.1ml
Immunofluorescence: 0.5-1 ug/ml
Optimal dilution of the Cytochrome C antibody should be determined by the researcher.
Specificiy: N/A
Positive Control 1: N/A
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: N/A
Validation: N/A
Isoform: N/A
Purification: Protein G affinity chromatography
Clonality: Monoclonal
Clone: 6H2.B4
Isotype: IgG1, kappa
Conjugate: Unconjugated
Physical State: Liquid
Buffer: PBS with 0.1 mg/ml BSA and 0.05% sodium azide
Concentration: 0.2 mg/mL
Storage Condition: Aliquot and Store at 2-8˚C. Avoid freez-thaw cycles.
Alternate Name: CYCS, CYC, HCS, THC4, Cytochrome c, Cytochrome c, somatic
User Note: Optimal dilutions for each application to be determined by the researcher
BACKGROUND: Cytochrome c is a well-characterized mobile electron transport protein that is essential to energy conversion in all aerobic organisms. In mammalian cells, this highly conserved protein is normally localized to the mitochondrial inter-membrane space. More recent studies have identified cytosolic cytochrome c as a factor necessary for activation of apoptosis. During apoptosis, cytochrome c is trans-located from the mitochondrial membrane to the cytosol, where it is required for activation of caspase-3 (CPP32) . Overexpression of Bcl-2 has been shown to prevent the translocation of cytochrome c, thereby blocking the apoptotic process. Overexpression of Bax has been shown to induce the release of cytochrome c and to induce cell death. The release of cytochrome c from the mitochondria is thought to trigger an apoptotic cascade, whereby Apaf-1 binds to Apaf-3 (caspase-9) in a cytochrome c-dependent manner, leading to caspase-9 cleavage of caspase-3.