Product Description
Caspase-2 Antibody [11B4] | 36-179 | ProSci
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, IP, WB
Application: Immunoprecipitation: (1-5ug/ml) . Western Blot: (1-2ug/ml) . 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. Detects bands of ~51kDa (procaspase-2) , ~32kDa and ~18kDa (cleavage products) by Western blot.
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: 11B4
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.