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腸道病毒71型抗體EV71 polyprotein VP1

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腸道病毒71型抗體EV71 polyprotein VP1研究領域腫瘤 免疫學
抗體來源Rabbit
克隆類型Polyclonal
交叉反應EV71
產品應用ELISA=1:500-1000 IP=1:20-100 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 (石蠟切片需做抗原修復)

腸道病毒71型抗體EV71 polyprotein VP1相關標記     Alexa Fluor 350   Alexa Fluor 488   Alexa Fluor 555   Alexa Fluor 647   AP   APC   Biotin   Cy3   Cy5  
Cy5.5   Cy7   FITC   Gold   HRP   PE   PE-Cy3   PE-CY5   PE-CY5.5   PE-CY7   RBITC  
英文名稱    EV71 polyprotein VP1
中文名稱    腸道病毒71型抗體
別    名    EV71; Enterovirus 71; Enterovirus 71 polyprotein VP1.
研究領域    腫瘤  免疫學  
抗體來源    Rabbit
腸道病毒71型抗體EV71 polyprotein VP1克隆類型    Polyclonal
交叉反應    EV71
產品應用    ELISA=1:500-1000 IP=1:20-100 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 (石蠟切片需做抗原修復) 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量    52kDa
性    狀    Lyophilized or Liquid
濃    度    1mg/1ml
免 疫 原    KLH conjugated synthetic peptide derived from EV71 polyprotein VP1
亞    型    IgG
純化方法    affinity purified by Protein A
儲 存 液    0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide
保存條件    Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
PubMed    PubMed
產品介紹    background:
Enteroviruses, such as enterovirus 71, are classified to be in the picornavirus family, pico [small] + RNA [ribonucleic acid] + virus. Picornaviruses are among the smallest and simplest ribonucleic acid containing viruses known (1). The RNA for many enteroviruses have now been cloned and complete genomic sequences have been obtained. The RNA from all sequenced enteroviruses are similar in length, about 7400 nucleotides, and have identical organization (1).
The human alimentary tract is the predominant site of enterovirus replication and these viruses were first isolated from enteric specimens. These viruses are the cause of paralytic poliomyelitis, aseptic meningitis-encephalitis, myocarditis, pleurodynia, hand-foot-and-mouth disease, conjunctivitis, and numerous other syndromes associated with extra-intestinal target organs. There are 67 numbered types of enteroviruses in the enterovirus family (1): three polioviruses, twenty-three coxsackieviruses A, six coxsackieviruses B, thirty-one echoviruses, and four other enteroviruses. 

Function:
Protein VP1: Forms, together with VP2 and VP3, an icosahedral capsid (pseudo T=3), 300 Angstroms in diameter, composed of 60 copies of each capsid protein and enclosing the viral positive strand RNA genome. Protein VP1 mainly forms the vertices of the capsid. VP1 interacts with host cell receptor to provide virion attachment to target cell. After binding to its receptor, the capsid undergoes conformational changes. VP1 N-terminus (that contains an amphipathic alpha-helix) is externalized, VP4 is released and together, they shape a virion-cell connecting channel and a pore in the host membrane through which RNase-protected transfer of the viral genome takes place. After genome has been released, the channel shrinks. 
Protein VP2: Forms, together with VP1 and VP3, an icosahedral capsid (pseudo T=3), 300 Angstroms in diameter, composed of 60 copies of each capsid protein and 
Protein VP3: Forms, together with VP1 and VP2, an icosahedral capsid (pseudo T=3), 300 Angstroms in diameter, composed of 60 copies of each capsid protein and enclosing the viral positive strand RNA genome.
Protein VP4: Lies on the inner surface of the capsid shell. After binding to the host receptor, the capsid undergoes conformational changes. VP4 is released, VP1 N-terminus is externalized, and together, they shape a virion-cell connecting channel and a pore in the host membrane through which RNase-protected transfer of the viral genome takes place. After genome has been released, the channel shrinks. 
Protein VP0: Protein VP0: VP0 precursor is a component of immature procapsids, which gives rise to VP4 and VP2 afer maturation. Allows the capsid to remain inactive before the maturation step. 
Protease 2A: cysteine protease that is responsible for the cleavage between the P1 and P2 regions. It cleaves the host translation initiation factor EIF4G1, in order to shut off the capped cellular mRNA transcription (By similarity). 
Protein 2B: Affects membrane integrity and cause an increase in membrane permeability. 
Protein 2C: Associates with and induces structural rearrangements of intracellular membranes. It displays RNA-binding, nucleotide binding and NTPase activities. 
Protein 3A, via its hydrophobic domain, serves as membrane anchor. It also inhibits endoplasmic reticulum-to-Golgi transport. 
Protease 3C: cysteine protease that generates mature viral proteins from the precursor polyprotein. In addition to its proteolytic activity, it binds to viral RNA, and thus influences viral genome replication. RNA and substrate bind cooperatively to the protease. 
RNA-directed RNA polymerase 3D-POL replicates genomic and antigenomic RNA by recognizing replications specific signals. 

Subunit:
Protein 2C N-terminus interacts with human RTN3. This interaction is important for viral replication.

Subcellular Location:
Protein VP2: Virion. Host cytoplasm (Potential). 
Protein VP3: Virion. Host cytoplasm (Potential). 
Protein VP1: Virion. Host cytoplasm (Potential). 
Protein 2B: Host cytoplasmic vesicle membrane; Peripheral membrane protein; Cytoplasmic side (Potential). Note=Probably localizes to the surface of intracellular membrane vesicles that are induced after virus infection as the site for viral RNA replication. These vesicles are derived from the endoplasmic reticulum. 
Protein 2C: Host cytoplasmic vesicle membrane; Peripheral membrane protein; Cytoplasmic side (Potential). Note=Probably localizes to the surface of intracellular membrane vesicles that are induced after virus infection as the site for viral RNA replication. These vesicles are derived from the endoplasmic reticulum. 
Protein 3A: Host cytoplasmic vesicle membrane; Peripheral membrane protein; Cytoplasmic side (Potential). Note=Probably localizes to the surface of intracellular membrane vesicles that are induced after virus infection as the site for viral RNA replication. These vesicles are derived from the endoplasmic reticulum. 
Protein 3B: Virion (Potential). 
Protease 3C: Host cytoplasm (Potential). 
RNA-directed RNA polymerase 3D-POL: Host cytoplasmic vesicle membrane; Peripheral membrane protein; Cytoplasmic side (Potential). Note=Probably localizes to the surface of intracellular membrane vesicles that are induced after virus infection as the site for viral RNA replication. These vesicles are derived from the endoplasmic reticulum.

Post-translational modifications:
Specific enzymatic cleavages in vivo by the viral proteases yield a variety of precursors and mature proteins. Polyprotein processing intermediates such as VP0 which is a VP4-VP2 precursor are produced. During virion maturation, non-infectious particles are rendered infectious following cleavage of VP0. This maturation cleavage is followed by a conformational change of the particle. 
VPg is uridylylated by the polymerase and is covalently linked to the 5'-end of genomic RNA. This uridylylated form acts as a nucleotide-peptide primer for the polymerase. 
Myristoylation of VP4 is required during RNA encapsidation and formation of the mature virus particle.

Similarity:
Belongs to the picornaviruses polyprotein family. 
Contains 2 peptidase C3 domains. 
Contains 1 RdRp catalytic domain. 
Contains 1 SF3 helicase domain.

Database links:
SwissProt: Q66478 HE71B 


Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. 

腸道病毒71型(Human enterovirus 71)簡稱EV71。腸病毒在病毒學上的分類是屬于微小病毒科(picornaviridae)中的腸病毒群(enterovirus)。
EV 71為目前腸病毒群中發現的病毒,其感染性強且致病率高,尤其是神經系統方面的并發癥。EV71主要引起手足口病,還可引起無菌性腦膜炎、腦干腦炎和脊髓灰質炎樣的麻痹等多種神經系統疾病。手足口病和中樞神經系統感染是EV71感染而引起的兩大常見臨床癥狀。
腸道病毒71型病毒從咽部或腸道侵入,在局部黏膜或淋巴組織中繁殖,并由局部排出,此時可引起局部癥狀。繼而病毒又侵入局部淋巴結,并由此進入血液循環導致*次病毒血癥。病毒經血循環侵入網狀內皮組織、深層淋巴結、肝、脾、骨髓等處大量繁殖并由此進入血液循環,引起第二次病毒血癥。病毒可隨血流進入全身各器官,如中樞神經系統、皮膚黏膜、心臟等處,進一步繁殖并引起病變。
Mol wt: 7.6kDa、141KDa
Antigen: bs-0983P, 0.2ug/100ul 
Primary: Antiserum, 1:500, 1:1000, 1:2000, 1:4000, 1:8000, 1:16000, 1:32000; 
Secondary: HRP conjugated Goat-Anti- Rabbit IgG(bs-0295G-HRP) at 1: 5000; 
TMB(C-0024) staining; 
Read the data in MicroplateReader by 450nm. 

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