MAB10207
Anti-Fusion Glycoprotein of Human parainfluenzavirus Type 3 Antibody, clone 9-4-3
ascites fluid, clone 9-4-3, Chemicon®
Synonym(s):
PI3
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General description
Human parainfluenza virus type 3 (PI3 virus) causes mild to severe respiratory tract infection in infants. PI3 virus is an enveloped RNA virus and possesses two glycoproteins, hemagglutinin-neuraminidase (HN) and fusion (F), at its external surface. These two glycoproteins are known to be responsible for initiation and progress of the infection process
Immunogen
Fusion (F) glycoprotein of human parainfluenzavirus type 3
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Antiviral effects of glycosylation and glucose trimming inhibitors on human parainfluenza virus type 3
Antiviral research, 72, 1-9 (2006)
Journal of virology, 74(24), 11792-11799 (2000-11-23)
Viral interference is characterized by the resistance of infected cells to infection by a challenge virus. Mechanisms of viral interference have not been characterized for human parainfluenza virus type 3 (HPF3), and the possible role of the neuraminidase (receptor-destroying) enzyme
Journal of virology, 83(13), 6900-6908 (2009-04-24)
Three discrete activities of the paramyxovirus hemagglutinin-neuraminidase (HN) protein, receptor binding, receptor cleaving (neuraminidase), and triggering of the fusion protein, each affect the promotion of viral fusion and entry. For human parainfluenza virus type 3 (HPIV3), the effects of specific
Virus genes, 56(1), 37-48 (2019-11-27)
Human parainfluenza virus type 3 (HPIV3) causes the majority of childhood viral pneumonia around the world. Fusing the viral and target cell membranes is crucial for its entry into target cells, and the fusion process requires the concerted actions of
PloS one, 10(8), e0136474-e0136474 (2015-08-26)
Human parainfluenza virus type 3 (HPIV3) can cause severe respiratory tract diseases in infants and young children, but no licensed vaccines or antiviral agents are currently available for treatment. Fusing the viral and target cell membranes is a prerequisite for
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