Human TDAG8/GPR65 Antibody Summary
Accession # Q81IYL9
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Detection of Human TDAG8/GPR65 by Western Blot. Western blot shows lysates of NS0 mouse myeloma cell line either mock transfected or transfected with human TDAG8/GPR65. PVDF membrane was probed with 2 µg/mL of Mouse Anti-Human TDAG8/GPR65 Monoclonal Antibody (Catalog # MAB10077) followed by HRP-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # HAF018). Specific bands were detected for TDAG8/GPR65 at approximately 85-95 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.
TDAG8/GPR65 in THP‑1 and K562 Human Cell Lines. TDAG8/GPR65 was detected in immersion fixed THP‑1 human acute monocytic leukemia cell line (left panel, positive stain) and K562 human chronic myelogenous leukemia cell line (right panel, negative stain) using Mouse Anti-Human TDAG8/GPR65 Monoclonal Antibody (Catalog # MAB10077) at 8 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Mouse IgG Secondary Antibody (red; Catalog # NL007) and counterstained with DAPI (blue). Specific staining was localized to cell surfaces. View our protocol for Fluorescent ICC Staining of Non-adherent Cells.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Human G Protein-Coupled Receptor 65 (GPR65), also known as T-Cell Death-Associated Gene 8 Protein (TDAG8) and Psychosine Receptor, is a 337 aminoacids proton-sensing GPCR primarily expressed in lymphoid tissues and is uniquely expressed in Th17 cells; mice deficient in GPR65 are resistant to autoimmunity. GPR65 senses pH by protonation of histidine residues on its extracellular domain. Many pH-sensing G protein-coupled receptors have emerged as potential therapeutic agents in conditions that involve the response to acidotic stress.
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