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MAB10207

Sigma-Aldrich

抗人副流感病毒3型融合糖蛋白抗体,克隆号9-4-3

ascites fluid, clone 9-4-3, Chemicon®

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别名:
PI3
UNSPSC代码:
12352203
eCl@ss:
32160702
NACRES:
NA.41

生物来源

mouse

质量水平

抗体形式

ascites fluid

抗体产品类型

primary antibodies

克隆

9-4-3, monoclonal

种属反应性

human

制造商/商品名称

Chemicon®

技术

immunofluorescence: suitable

同位素/亚型

IgG1

UniProt登记号

运输

wet ice

一般描述

人副流感病毒3型(PI3病毒)可引起婴儿轻度至重度呼吸道感染。PI3病毒是一种包膜RNA病毒,其外表面具有两种糖蛋白:血凝素-神经氨酸酶(HN)和融合(F)。已知这两种糖蛋白负责感染过程的开始和进展

免疫原

人副流感病毒3型融合糖蛋白

法律信息

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

WGK

WGK 1

闪点(°F)

Not applicable

闪点(°C)

Not applicable


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Antiviral effects of glycosylation and glucose trimming inhibitors on human parainfluenza virus type 3
Tanaka, Yoshikazu, et al
Antiviral research, 72, 1-9 (2006)
M A Horga et al.
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
Ying Liu et al.
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
Laura M Palermo et al.
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
Wenyan Xie et al.
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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