Recombinant Human HVEM/TNFRSF14/CD270 Protein (Catalog#10334-H08H)
This antibody was obtained from a rabbit immunized with purified, recombinant Human HVEM/TNFRSF14/CD270 (rh HVEM/TNFRSF14/CD270; Catalog#10334-H08H; NP_003811.2; Met1-Val202) and conjugated with PE under optimum conditions, the unreacted PE was removed.
Monoclonal Rabbit IgG Clone #004
Aqueous solution containing 0.5% BSA and 0.09% sodium azide
10 μl/Test, 0.1 mg/ml
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
This antibody can be stored at 2℃-8℃ for twelve months without detectable loss of activity. Protected from prolonged exposure to light. Do not freeze ! Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.
Anti-HVEM Antibody (PE) (Rabbit Monoclonal 抗体) 图片
Flow cytometric analysis of Human HVEM(CD270) expression on human whole blood lymphocytes. Cells were stained with PE-conjugated anti-Human HVEM(CD270). The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.
Herpesvirus entry mediator (HVEM), also referred to as TNFRSF14, TR2 (TNF receptor-like molecule) and ATAR (another TRAF-associated receptor), is a member of type I transmembrane protein belonging to the TNF-receptor superfamily. It is expressed on many immune cells, including T and B cells, NK cells, monocytes, and neutrophils. Two TNF superfamily ligands lymphotoxin α (TNF-β) and LIGHT (TNFSF14) are identified as cellular ligands for HVEM and initiate the positive signaling. However, recent studies have revealed that HVEM is also involved in the unique inhibitory signaling pathway for T cells through activating tyrosine phosphorylation of the immunoreceptor tyrosine-based inhibitory motif (ITIM) in B and T lymphocyte attenuator (BTLA). HVEM provides a stimulatory signal following engagement with LIGHT (TNFSF14) on T cells. In contrast, it can also provide an inhibitory signal to T cells when it binds the B and T lymphocyte attenuator (BTLA), a ligand member of the Immunoglobulin (Ig) superfamily. Thus, HVEM may be viewed as a molecular switch, capable of facilitating both stimulatory and inhibitory cosignaling in T cells. Substantial evidence from both human disease and from experimental mouse models has indicated that dysregulation of the LIGHT-HVEM-BTLA cosignaling pathway can cause inflammation in the lung and in mucosal tissues.