Recombinant Coxsackievirus A16 Genome polyprotein

中文名稱：

Recombinant Coxsackievirus A16 Genome polyprotein
貨號(hào)：

CSB-YP731156CGAV
說明書：

MSDS Datasheet
規(guī)格：
來源：

Yeast
其他：

中文名稱：

Recombinant Coxsackievirus A16 Genome polyprotein
貨號(hào)：

CSB-EP731156CGAV
說明書：

MSDS Datasheet
規(guī)格：
來源：

E.coli
其他：

中文名稱：

Recombinant Coxsackievirus A16 Genome polyprotein
貨號(hào)：

CSB-EP731156CGAV-B
說明書：

MSDS Datasheet
規(guī)格：
來源：

E.coli
共軛：

Avi-tag Biotinylated
E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.
其他：

中文名稱：

Recombinant Coxsackievirus A16 Genome polyprotein
貨號(hào)：

CSB-BP731156CGAV
說明書：

MSDS Datasheet
規(guī)格：
來源：

Baculovirus
其他：

中文名稱：

Recombinant Coxsackievirus A16 Genome polyprotein
貨號(hào)：

CSB-MP731156CGAV
說明書：

MSDS Datasheet
規(guī)格：
來源：

Mammalian cell
其他：

產(chǎn)品詳情
產(chǎn)品評(píng)價(jià)
靶點(diǎn)詳情

產(chǎn)品詳情

純度：

>85% (SDS-PAGE)
基因名：

N/A
Uniprot No.：

Q65900
別名：

Genome polyprotein [Cleaved into: P1; Capsid protein VP0; VP4-VP2); Capsid protein VP4; P1A; Virion protein 4); Capsid protein VP2; P1B; Virion protein 2); Capsid protein VP3; P1C; Virion protein 3); Capsid protein VP1; P1D; Virion protein 1); P2; Protease 2A; P2A; EC 3.4.22.29; Picornain 2A; Protein 2A); Protein 2B; P2B); Protein 2C; P2C; EC 3.6.1.15); P3; Protein 3AB; Protein 3A; P3A); Viral protein genome-linked; VPg; Protein 3B; P3B); Protein 3CD; EC 3.4.22.28); Protease 3C; EC 3.4.22.28; Picornain 3C; P3C); RNA-directed RNA polymerase; RdRp; EC 2.7.7.48; 3D polymerase; 3Dpol; Protein 3D; 3D)]
種屬：

Coxsackievirus A16 (strain G-10)
蛋白長(zhǎng)度：

Full Length of Mature Protein
表達(dá)區(qū)域：

2-323
氨基酸序列

GSQVSTQRS GSHENSNSAS EGSTINYTTI NYYKDAYAAS AGRQDMSQDP KKFTDPVMDV IHEMAPPLKS PSAEACGYSD RVAQLTIGNS TITTQEAANI IIAYGEWPEY CKDADATAVD KPTRPDVSVN RFFTLDTKSW AKDSKGWYWK FPDVLTEVGV FGQNAQFHYL YRSGFCVHVQ CNASKFHQGA LLVAILPEYV LGTIAGGDGN ENSHPPYVTT QPGQVGAVLT NPYVLDAGVP LSQLTVCPHQ WINLRTNNCA TIIVPYMNTV PFDSALNHCN FGLIVVPVVP LDFNAGATSE IPITVTIAPM CAEFAGLRQA IKQ
蛋白標(biāo)簽：

Tag?type?will?be?determined?during?the?manufacturing?process.

The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
產(chǎn)品提供形式：

Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
復(fù)溶：

We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
儲(chǔ)存條件：

Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
保質(zhì)期：

The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
貨期：

Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
注意事項(xiàng)：

Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet ：

Please contact us to get it.

產(chǎn)品評(píng)價(jià)

靶點(diǎn)詳情

功能：

Forms an icosahedral capsid of pseudo T=3 symmetry with capsid proteins VP2 and VP3. The capsid is 300 Angstroms in diameter, composed of 60 copies of each capsid protein and enclosing the viral positive strand RNA genome. Capsid protein VP1 mainly forms the vertices of the capsid. Capsid protein VP1 interacts with host cell receptor to provide virion attachment to target host cells. This attachment induces virion internalization. After binding to its receptor, the capsid undergoes conformational changes. Capsid protein VP1 N-terminus (that contains an amphipathic alpha-helix) and capsid protein VP4 are externalized. Together, they shape a pore in the host membrane through which viral genome is translocated to host cell cytoplasm.; Forms an icosahedral capsid of pseudo T=3 symmetry with capsid proteins VP2 and VP3. The capsid is 300 Angstroms in diameter, composed of 60 copies of each capsid protein and enclosing the viral positive strand RNA genome.; Forms an icosahedral capsid of pseudo T=3 symmetry with capsid proteins VP2 and VP3. The capsid is 300 Angstroms in diameter, composed of 60 copies of each capsid protein and enclosing the viral positive strand RNA genome.; Lies on the inner surface of the capsid shell. After binding to the host receptor, the capsid undergoes conformational changes. Capsid protein VP4 is released, Capsid protein VP1 N-terminus is externalized, and together, they shape a pore in the host membrane through which the viral genome is translocated into the host cell cytoplasm.; Component of immature procapsids, which is cleaved into capsid proteins VP4 and VP2 after maturation. Allows the capsid to remain inactive before the maturation step.; Cysteine protease that cleaves viral polyprotein and specific host proteins. It is responsible for the autocatalytic cleavage between the P1 and P2 regions, which is the first cleavage occurring in the polyprotein. Cleaves also the host translation initiation factor EIF4G1, in order to shut down the capped cellular mRNA translation. Inhibits the host nucleus-cytoplasm protein and RNA trafficking by cleaving host members of the nuclear pores. Counteracts stress granule formation probably by antagonizing its assembly or promoting its dissassembly. Cleaves and inhibits host IFIH1/MDA5, thereby inhibiting the type-I IFN production and the establishment of the antiviral state. Cleaves and inhibits host MAVS, thereby inhibiting the type-I IFN production and the establishment of the antiviral state.; Plays an essential role in the virus replication cycle by acting as a viroporin. Creates a pore in the host reticulum endoplasmic and as a consequence releases Ca2+ in the cytoplasm of infected cell. In turn, high levels of cytoplasmic calcium may trigger membrane trafficking and transport of viral ER-associated proteins to viroplasms, sites of viral genome replication.; Induces and associates with structural rearrangements of intracellular membranes. Displays RNA-binding, nucleotide binding and NTPase activities. May play a role in virion morphogenesis and viral RNA encapsidation by interacting with the capsid protein VP3.; Localizes the viral replication complex to the surface of membranous vesicles. Together with protein 3CD binds the Cis-Active RNA Element (CRE) which is involved in RNA synthesis initiation. Acts as a cofactor to stimulate the activity of 3D polymerase, maybe through a nucleid acid chaperone activity.; Localizes the viral replication complex to the surface of membranous vesicles. It inhibits host cell endoplasmic reticulum-to-Golgi apparatus transport and causes the disassembly of the Golgi complex, possibly through GBF1 interaction. This would result in depletion of MHC, trail receptors and IFN receptors at the host cell surface. Plays an essential role in viral RNA replication by recruiting ACBD3 and PI4KB at the viral replication sites, thereby allowing the formation of the rearranged membranous structures where viral replication takes place.; Acts as a primer for viral RNA replication and remains covalently bound to viral genomic RNA. VPg is uridylylated prior to priming replication into VPg-pUpU. The oriI viral genomic sequence may act as a template for this. The VPg-pUpU is then used as primer on the genomic RNA poly(A) by the RNA-dependent RNA polymerase to replicate the viral genome. Following genome release from the infecting virion in the cytoplasm, the VPg-RNA linkage is probably removed by host TDP2. During the late stage of the replication cycle, host TDP2 is excluded from sites of viral RNA synthesis and encapsidation, allowing for the generation of progeny virions.; Involved in the viral replication complex and viral polypeptide maturation. It exhibits protease activity with a specificity and catalytic efficiency that is different from protease 3C. Protein 3CD lacks polymerase activity. Protein 3CD binds to the 5'UTR of the viral genome.; Major viral protease that mediates proteolytic processing of the polyprotein. Cleaves host EIF5B, contributing to host translation shutoff. Cleaves also host PABPC1, contributing to host translation shutoff. Binds and inhibits host IFIH1/MDA5, thereby inhibiting the type-I IFN production and the establishment of the antiviral state. Cleaves host MAP3K7/TAK1, resulting in inhibition of TRAF6-triggered NF-kappa-B induction. Cleaves host NLRP1, triggers host N-glycine-mediated degradation of the autoinhibitory NLRP1 N-terminal fragment.; Replicates the viral genomic RNA on the surface of intracellular membranes. May form linear arrays of subunits that propagate along a strong head-to-tail interaction called interface-I. Covalently attaches UMP to a tyrosine of VPg, which is used to prime RNA synthesis. The positive stranded RNA genome is first replicated at virus induced membranous vesicles, creating a dsRNA genomic replication form. This dsRNA is then used as template to synthesize positive stranded RNA genomes. ss(+)RNA genomes are either translated, replicated or encapsidated.
基因功能參考文獻(xiàn)：
1. The carboxyl terminus-mediated self-oligomerization is fundamental to 2C ATPase activity and EV71 replication. PMID: 28508043
2. A glutamine at position 145 of the VP1 capsid protein was identified as a key determinant of infectivity. PMID: 29743570
3. 1-94aa of the RNA-dependent RNA polymerase are the transcriptional activation domain. PMID: 30001577
4. Human enterovirus 71 2BC physically and specifically interacted with syntaxin-17, synaptosome associated protein 29, LC3B and LAMP1 proteins. PMID: 28677644
5. The results indicate that an equilibrium between ZAP and enterovirus 3C protease controls viral infection. PMID: 29182509
6. The authors identified a natural virulence determinant of 3C protease and revealed the mechanism of attenuated virulence is mediated by N69D substitution. PMID: 28217559
7. Remarkably, the Enterovirus 71 protease 3C directly targets GSDMD and induces its cleavage, which is dependent on the protease activity. PMID: 28679757
8. study determined that a VP1 mutation (K244E) was needed for Enterovirus 71 virulence in adult AG129 mice PMID: 27440896
9. Heparin-binding phenotype was completely abolished with VP1-E98-E145, but was restored by an E98K or E145Q substitution. PMID: 27875780
10. findings reveal that EV71 2C forms a complex with PP1 and IKKbeta to maintain IKKbeta in an unphosphorylated and inactive state, resulting in the inactivation of the TNF-alpha-mediated NF-kappaB signaling pathway. We provide evidence that the 2C proteins of the enteroviruses PV, CVA16, and CVB3 suppress IKKbeta phosphorylation through the same mechanism involving PP1 PMID: 26962213
11. results demonstrate that the three VP1 residues (98E, 145A and 169F ) cooperate to effectively interact with the mSCARB2 protein on murine cells and permit the virus to infect murine cells PMID: 27329847
12. Taken together, these data highlight the importance of positively charged residues in VP1 for production of infectious particles. PMID: 26512078
13. These results demonstrate the anti-enterovirus 71 ability of IFN-gamma and the immunoediting ability by enterovirus 71 2A and 3D, which attenuate IFN-gamma signaling through different mechanisms. PMID: 25926657
14. The last 7 amino acids at the C-terminal of 3AB is essential for the RNA chaperone activity. [3AB] PMID: 25113906
15. Authors demonstrate that enterovirus 71 3C interacts with TAB2 and TAK1 and suppresses cytokine expression via cleavage of the TAK1 complex proteins. PMID: 24942571
16. Authors reported that enterovirus 71 VP1 protein could bind to vimentin intermediate filaments expressed on the host cell surface. PMID: 24623428
17. The VP1 gene of EV71 strains circulating in the Asia-Pacific region during 1994-2013, showed polymorphisms and divergence with very slow evolution rate. PMID: 23933074
18. These findings demonstrate that only the 3D-S264L mutation attenuates human enterovirus 71 in mice, suggesting that the high replication fidelity phenotype is not essential for virulence attenuation in this model. PMID: 23856384
19. Data suggest that PSGL1 (selectin P ligand) on human leukocytes is binding site for VP1 in Enterovirus 71; mutation of conserved lysine residue at VP1-244 abolishes virus binding; mutation of conserved lysine residue VP1-242 greatly reduces binding. PMID: 23935488
20. In the present study, the authors report that enterovirus 71 downregulates IRF7 through the 3C protein, which inhibits the function of IRF7. PMID: 23175366
21. These findings indicate that enterovirus 71 can hamper the host innate defense by blocking selectively type I interferon synthesis through the 3C viral protein. PMID: 22997081
22. VP1 is a type II transmembrane protein efficiently stimulated both humoral and cellular immunities. PMID: 22728446
23. Viruses expressing the VP1-Q145E were virulent in BALB/c mice with 100% mortality. PMID: 22647370
24. Mouse adaptation of human enterovirus 71 is associated with a lysine to glutamic acid substitution at position 244 in protein VP1. PMID: 22575826
25. 2A protease encoded by EV71 as an antagonist of IFNB1 and the protease activity is required for reducing IFNAR1 levels. PMID: 22258259
26. The residues between 144 and 151 are critical for SCARB2 binding to VP1 of EV71 and seven residues from the human receptor could convert murine SCARB2, an otherwise inefficient receptor, to an efficient receptor for EV71 viral infection. PMID: 22219187
27. In this study, the authors showed that human annexin II (Anx2) protein could bind to the enterovirus type 71 virion via the capsid protein VP1. PMID: 21900167
28. The complex structures of enterovirus 71 and coxsackievirus A16 3Cs with rupintrivir, a specific human rhinovirus 3C protease inhibitor, were solved. PMID: 21795339
29. The authors demonstrated that catalytic Glu71 is irreplaceable for maintaining the overall architecture of the active site and, most importantly, the productive conformation of catalytic His40. PMID: 21813612
30. TRIF cleavage mediated by human enterovirus 71 3C protease may be a mechanism to impair type I interferon production in response to Toll-like receptor 3 (TLR3) activation. PMID: 21697485
31. The crystal structure shows that enterovirus 71 3C(pro) has a typical chymotrypsin-like fold that is common in picornaviral 3C(pro). PMID: 21396941
32. Together, these results suggest that inhibition of RIG-I-mediated type I IFN responses by the enterovirus 71 3C protein may contribute to the pathogenesis of enterovirus 71 infection. PMID: 20519382
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亞細(xì)胞定位：

[Capsid protein VP0]: Virion. Host cytoplasm.; [Capsid protein VP4]: Virion.; [Capsid protein VP2]: Virion. Host cytoplasm.; [Capsid protein VP3]: Virion. Host cytoplasm.; [Capsid protein VP1]: Virion. Host cytoplasm.; [Protein 2B]: Host cytoplasmic vesicle membrane; Peripheral membrane protein; Cytoplasmic side. 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. 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. 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 3AB]: Host cytoplasmic vesicle membrane; Peripheral membrane protein; Cytoplasmic side. 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.; [Viral protein genome-linked]: Virion. Host cytoplasm.; [Protease 3C]: Host cytoplasm.; [Protein 3CD]: Host nucleus. Host cytoplasm. Host cytoplasmic vesicle membrane; Peripheral membrane protein; Cytoplasmic side. 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.; [RNA-directed RNA polymerase]: Host cytoplasmic vesicle membrane; Peripheral membrane protein; Cytoplasmic side. 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.
蛋白家族：

Picornaviruses polyprotein family
數(shù)據(jù)庫(kù)鏈接：

KEGG: vg:1461111