DELE Antibody | 6919

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.