Respiratory Syncytial Virus / RSV (Fusion protein) Mouse Monoclonal Antibody [Clone ID: 0681]

Specifications

Product Data
Clone Name	0681
Applications	ELISA, IF
Recommend Dilution	ELISA: 1/20-1/200. Immunofluorescence: 1/10-1/50.
Reactivity	Respiratory Syncytial Virus
Host	Mouse
Clonality	Monoclonal
Specificity	This antibody is specific for the fusion protein of Respiratory Syncytical Virus (RSV). This clone has been reported for use in neutralising studies. Removal of Sodium Azide is recommended prior to use in Functional Assays.
Formulation	Phosphate buffered saline pH 7.2 containing 0.09% Sodium Azide as preservative. State: Purified State: Liquid purified IgG fraction.
Concentration	lot specific
Purification	Affinity Chromatography on Protein A.
Conjugation	Unconjugated
Storage Condition	Store the antibody undiluted at 2-8°C for one month or (in aliquots) at -20°C for longer. Avoid repeated freezing and thawing.
Background	Respiratory Syncytial Virus (RSV) Fusion (F) Glycoprotein is a Class I viral fusion protein. Under the current model, the protein has at least 3 conformational states: pre-fusion native state, pre-hairpin intermediate state, and post-fusion hairpin state. During viral and target cell membrane fusion, the heptad repeat (HR) regions assume a trimer-of-hairpins structure, positioning the fusion peptide in close proximity to the C-terminal region of the ectodomain. The formation of this structure appears to drive apposition and subsequent fusion of viral and target cell membranes. Directs fusion of viral and cellular membranes leading to delivery of the nucleocapsid into the cytoplasm. This fusion is pH independent and occurs directly at the outer cell membrane. The trimer of F1-F2 (protein F) interacts with glycoprotein G at the virion surface. Upon binding of G to heparan sulfate, the hydrophobic fusion peptide is unmasked and interacts with the cellular membrane, inducing the fusion between host cell and virion membranes. Notably, RSV fusion protein is able to interact directly with heparan sulfate and therefore actively participates in virus attachment. Furthermore, the F2 subunit was identifed as the major determinant of RSV host cell specificity. Later in infection, proteins F expressed at the plasma membrane of infected cells mediate fusion with adjacent cells to form syncytia, a cytopathic effect that could lead to tissue necrosis. The fusion protein is also able to trigger p53-dependent apoptosis.
Reference Data

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