Thermo Fisher Scientific DR3 Monoclonal Antibody (JD3), Biotin, eBioscience

Applications

Tested Dilution

Publications

Flow Cytometry (Flow)

Assay-Dependent

-

Product Specifications

Species Reactivity

Human

Host/Isotype

Mouse / IgG1, kappa

Recommended Isotype Control

Mouse IgG1 kappa Isotype Control (P3.6.2.8.1), Biotin, eBioscience™

Class

Monoclonal

Type

Antibody

Clone

JD3

Conjugate

Biotin Biotin Biotin

View additional formats

• Unconjugated
• PE
• Request custom conjugation

Form

Liquid

Concentration

0.5 mg/mL

Purification

Affinity chromatography

Storage buffer

PBS, pH 7.2

Contains

0.09% sodium azide

Storage conditions

4° C, store in dark, DO NOT FREEZE!

Shipping conditions

Ambient (domestic); Wet ice (international)

RRID

AB_466882

Product Specific Information

Description: The JD3 monoclonal antibody reacts with human DR3, also known as Apo-3, WSL-1, TRAMP, LARD, DDR3, and TR3. DR3, a novel death receptor is expressed at low level by monocytes and granulocytes. Interaction of DR3 with its ligand activates NF-kappa B pathway and induces apoptosis. Initially, DR3 was thought to be a receptor for TWEAK, but further studies have shown that TWEAK could induce apoptosis via receptors distinct from DR3. JD3 has been reported for use in flow cytometric analysis.

Applications Reported: The JD3 antibody has been reported for use in flow cytometric analysis.

Applications Tested: The JD3 antibody has been tested by flow cytometric analysis of human peripheral leukocytes and human DR3-transfected cells. It is recommended that the reagent be carefully titrated for optimal performance in the assay of interest.

Filtration: 0.2 µm post-manufacturing filtered.

Target Information

DR3/TNFRSF25 is a member of the TNF-receptor superfamily. This receptor is expressed preferentially in the tissues enriched in lymphocytes, and it may play a role in regulating lymphocyte homeostasis. This receptor has been shown to stimulate NF-kappa B activity and regulate cell apoptosis. The signal transduction of this receptor is mediated by various death domain containing adaptor proteins. Knockout studies in mice suggested the role of DR3/TNFRSF25 in the removal of self-reactive T cells in the thymus. Multiple alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported, most of which are potentially secreted molecules. The alternative splicing of this gene in B and T cells encounters a programmed change upon T-cell activation, which predominantly produces full-length, membrane bound isoforms, and is thought to be involved in controlling lymphocyte proliferation induced by T-cell activation.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.