Description
DELE Antibody | 6919 | Gentaur UK, US & Europe Distribution
Host: Rabbit
Reactivity: Human, Rat
Homology: Predicted species reactivity based on immunogen sequence: Mouse: (71%)
Immunogen: DELE antibody was raised against an 18 amino acid synthetic peptide near the amino terminus of human DELE.
The immunogen is located within the first 50 amino acids of DELE.
Research Area: Apoptosis
Tested Application: E, WB, IF
Application: DELE antibody can be used for detection of DELE by Western blot at 1 μg/mL. For immunofluorescence start at 20 μg/mL.
Antibody validated: Western Blot in rat samples and Immunofluorescence in human samples. All other applications and species not yet tested.
Specificiy: N/A
Positive Control 1: Cat. No. 1463 - Rat Brain Tissue Lysate
Positive Control 2: Cat. No. 10-301 - Human Brain Tissue Slide
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: DELE Antibody is affinity chromatography purified via peptide column.
Clonality: Polyclonal
Clone: N/A
Isotype: IgG
Conjugate: Unconjugated
Physical State: Liquid
Buffer: DELE Antibody is supplied in PBS containing 0.02% sodium azide.
Concentration: 1 mg/mL
Storage Condition: DELE antibody can be stored at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Alternate Name: DELE Antibody: DELE, DELE, Death ligand signal enhancer
User Note: Optimal dilutions for each application to be determined by the researcher.
BACKGROUND: DELE Antibody: DELE is a recently identified DAP3-binding protein that is thought to be important in the induction of death receptor-mediated apoptosis. Transfected cells that stably express DELE were found to be susceptible to apoptosis induction by TNF-α and TRAIL, whereas reducing DELE expression by siRNA rescued these cells from apoptosis induction. Furthermore, the reduction of DELE expression also inhibited the activation of caspase-3, caspase-8 and caspase-9 following stimulation by TNF-α, anti-Fas, or TRAIL, indicating the importance of DELE in apoptosis mediated by death receptors.