Caspase-2 Antibody [10C6] | 36-178

Caspase-2 Antibody [10C6] | 36-178 | Gentaur UK, US & Europe Distribution

Host: Rat

Reactivity: Dog, Human, Monkey, Mouse, Rat

Homology: N/A

Immunogen: Recombinant human caspase-2 (p19 subunit) .

Research Area: Apoptosis, Cancer

Tested Application: E, Flow, ICC, IHC

Application: Flow Cytometry: (overexpressed in cell lines) . Immunocytochemistry: (10-20ug/ml; fix in 4% paraformaldehyde, 0.18% Triton-X100 for 10 min. prior to staining) . Immunohistochemistry: (frozen sections) . Optimal conditions must be determined individually for each application.

Specificiy: Recognizes an epitope in the p19 subunit of human, mouse, rat, monkey and dog caspase-2.

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: >95% (SDS-PAGE)

Clonality: Monoclonal

Clone: 10C6

Isotype: IgG2a, kappa

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Liquid. In PBS containing 0.02% sodium azide.

Concentration: 1 mg/ml

Storage Condition: Stable for at least 1 year after receipt when stored at -20˚C.

Alternate Name: CASP-2; Protease ICH-1; Neural Precursor Cell Expressed Developmentally Down-regulated Protein 2; NEDD-2

User Note: Optimal dilutions for each application to be determined by the researcher.

BACKGROUND: Caspase-2 is a Class I caspase with a long prodomain necessary for nuclear localization. Upon activation of the apoptotic pathway, the procaspase is cleaved into smaller fragments. Caspase-2 is the nuclear apoptotic respondent to cellular genotoxic stress or mitotic catastrophe and is involved in the activation cascade of caspases responsible for apoptosis execution. Activation occurs upon recruitment to a complex containing a p53-induced death domain protein, PIDD. This suggests caspase-2 can be a nuclear initiator caspase with a requirement for caspase-9 and caspase-3 activation in downstream apoptotic events. In apoptotic pathways resulting from UV-induced DNA damage, processing of caspase-2 occurs downstream of mitochondrial dysfunction and of caspase-9 and caspase-3 activation, extending a possible role for caspase-2 as a parallel effector caspase.