Detection of RELT/TNFRSF19L in Raji Human Cell Line by Flow Cytometry.
Raji human Burkitt's lymphoma cell line was stained with Mouse Anti-Human RELT/TNFRSF19L Monoclonal Antibody (Catalog # MAB1385, filled histogram) or isotype control antibody (Catalog # MAB0041, open histogram), followed by Phycoerythrin-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # F0102B).
Preparation and Storage
Reconstitute at 0.5 mg/mL in sterile PBS.
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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.
RELT (Receptor Expressed in Lymphoid Tissues) is a type I transmembrane glycoprotein belonging to the tumor necrosis factor receptor superfamily (TNFRSF) and has been designated TNFRSF19-like (TNFRSF19L) (1, 2). It is primarily expressed in hematopoietic tissues and peripheral blood leukocytes. Human RELT cDNA encodes a 430 amino acid (aa) residue precursor protein with a putative 26 aa signal peptide, a 136 aa extracellular domain containing one TNF receptor cysteine-rich domain and one potential N-linked glycosylation site, a 21 aa transmembrane domain and a 247 aa cytoplasmic region containing no death domain. Human RELT shares 85% and 96% aa sequence homology with mouse RELT (Accession # BAC40459) and macaque RELT (Accession # Q9N092), respectively. Among TNFRSF members, the RELT extracellular domain is most closely related to that of TNFRSF19 and OX40. RELT has been shown to exclusively bind the adaptor protein TNF receptor-associated factor 1 (TRAF1). However, it has also been shown to activate the NF-kappa B pathway independently of TRAFs. Immobilized RELT can co‑stimulate T‑cell proliferation in the presence of CD3 signaling, suggesting a potential regulatory role in immune response.
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