![FACS analysis of CD261-transfected HEK-293 cells using GTX80183 DR4 antibody [DR-4-02] (FITC). FACS analysis of CD261-transfected HEK-293 cells using GTX80183 DR4 antibody [DR-4-02] (FITC).](https://www.genetex.com/upload/website/prouct_img/normal/GTX80183/GTX80183_20191025_AP_006_414_w_23061322_192.webp)
FACS analysis of CD261-transfected HEK-293 cells using GTX80183 DR4 antibody [DR-4-02] (FITC).
DR4 antibody [DR-4-02] (FITC)
GTX80183
ApplicationsFlow Cytometry
Product group Antibodies
TargetTNFRSF10A
Overview
- SupplierGeneTex
- Product NameDR4 antibody [DR-4-02] (FITC)
- Delivery Days Customer9
- ApplicationsFlow Cytometry
- CertificationResearch Use Only
- ClonalityMonoclonal
- Clone IDDR-4-02
- Concentration0.1 mg/ml
- ConjugateFITC
- Gene ID8797
- Target nameTNFRSF10A
- Target descriptionTNF receptor superfamily member 10a
- Target synonymsAPO2, CD261, DR4, TRAILR-1, TRAILR1, tumor necrosis factor receptor superfamily member 10A, TNF-related apoptosis-inducing ligand receptor 1, TRAIL receptor 1, TRAIL-R1, cytotoxic TRAIL receptor, death receptor 4, tumor necrosis factor receptor superfamily, member 10a
- HostMouse
- IsotypeIgG1
- Protein IDO00220
- Protein NameTumor necrosis factor receptor superfamily member 10A
- Scientific DescriptionThe protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor is activated by tumor necrosis factor-related apoptosis inducing ligand (TNFSF10/TRAIL), and thus transduces cell death signal and induces cell apoptosis. Studies with FADD-deficient mice suggested that FADD, a death domain containing adaptor protein, is required for the apoptosis mediated by this protein. [provided by RefSeq, Jul 2008]
- Storage Instruction2°C to 8°C
- UNSPSC12352203
References
- Yagolovich AV, Artykov AA, Karmakova TA, et al. Genetically Modified DR5-Specific TRAIL Variant DR5-B Revealed Dual Antitumor and Protumoral Effect in Colon Cancer Xenografts and an Improved Pharmacokinetic Profile. Transl Oncol. 2020,13(4):100762. doi: 10.1016/j.tranon.2020.100762Read this paper
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