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AN300320P

Recombinant HVEM/TNFRSF14/CD270 Monoclonal Antibody

Size

£361.80

Was £402.00

SKU:
AN300320P
Additional Names:
UNQ,PRO,Tumor Necrosis Factor Receptor-Like,Tumor Necrosis Factor Receptor Superfamily Member,Tnfrsf,CD270,Herpes Virus Entry Mediator A,Herpesvirus Entry Mediator A,TR2,Tumor Necrosis Factor Receptor Superfamily Member 14,Tumor Necrosis Factor Receptor-Like 2,HVEA,HVEM,TNFRSF14,UNQ329,PRO509
Application:
IF, ICC
Concentration:
1 mg/ml
Purification:
Protein A Purified
Storage Conditions:
-20[o]C/-70[o]C Avoid freeze/thaw cycles., 2-8[o]C Avoid freeze/thaw cycles.
Supplier:
Elabscience
Host:
Rabbit
Reactivities:
Human
Buffer:
PBS
Immunogen:
Recombinant Human HVEM/TNFRSF14/CD270 Protein
Clone:
B242
Uniprot:
Q92956
Synonyms:
ATAR;CD270;CD40-like protein;herpes virus entry mediator A;HVEA;HVEM;LIGHTR;TR2;tumor necrosis factor receptor superfamily member 14;tumor necrosis factor receptor superfamily, member 14 (herpesvirus entry mediator);Tumor necrosis factor receptor-like 2;tumor necrosis factor receptor-like gene2
Extra Details:
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 A Alpha (TNF-B Beta) 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.
Shipping Conditions:
Blue Ice