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Recombinant Influenza A virus Protein PB1-F2 (PB1)

Recombinant Influenza A virus Protein PB1-F2 (PB1)

Code
MSDS	MSDS
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Target Background

Product Details

Purity

>85% (SDS-PAGE)

Target Names

PB1

Uniprot NO.

P0C0U1

Species

Influenza A virus (strain A/Puerto Rico/8/1934 H1N1)

Source

Yeast

Expression Region

1-87

Target Protein Sequence

MGQEQDTPWI LSTGHISTQK RQDGQQTPKL EHRNSTRLMG HCQKTMNQVV MPKQIVYWKQ WLSLRNPILV FLKTRVLKRW RLFSKHE

Protein Length

full length protein

Tag Info

N-terminal His-tagged/Tag-Free

Storage

Store at -20°C, for extended storage, conserve at -20°C or -80°C.

Shelf Life

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.

Notes

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

Description

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Target Background

Function

Plays an important role in promoting lung pathology in both primary viral infection and secondary bacterial infection. Promotes alteration of mitochondrial morphology, dissipation of mitochondrial membrane potential, and cell death. Alternatively, inhibits the production of interferon in the infected cell at the level of host mitochondrial antiviral signaling MAVS. Its level of expression differs greatly depending on which cell type is infected, in a manner that is independent of the levels of expression of other viral proteins. Monocytic cells are more affected than epithelial cells. Seems to disable virus-infected monocytes or other host innate immune cells. During early stage of infection, predisposes the mitochondria to permeability transition through interaction with host SLC25A6/ANT3 and VDAC1. These proteins participate in the formation of the permeability transition pore complex (PTPC) responsible of the release of mitochondrial products that triggers apoptosis.

Gene References into Functions

results constitute an important step forward in the understanding of the cell type-dependent function of PB1-F2. PMID:26896002
Influenza A virus protein PB1-F2 translocates into mitochondria via Tom40 channels and impairs innate immunity. PMID:25140902
Mutations in PB1-F2 gene is associated with virulence. PMID:24699508
NLRX1 enhances macrophage antiviral immunity by interacting with influenza virus PB1-F2 protein, as well as preventing mitochondrial-induced apoptosis PMID:24799673
PB1-F2 inhibits the activation of NF-kappaB dependent signalling pathways. PMID:23704945
MIF and GNbeta2 interacted with influenza A H1N1 virus PB1-F2 protein. PMID:23043599
PB1-F2 protein of influenza A virus interacts with human MOAP-1 protein. PMID:23236846
PB1-F2 contribute to superinfection with Gram-positive respiratory pathogens. PMID:22674997
Using a flow cytometry-based assay, the authors demonstrate that the PB1-F2 protein inhibits MAVS-mediated IFN synthesis by decreasing the mitochondrial membrane potential (MMP). PMID:22674996
PB1-F2 protein of influenza A viruses exhibits a type I IFN-antagonistic function by interfering with the RIG-I/MAVS complex, which contributes to an enhanced pathogenicity in vivo PMID:22050228
PB1-F2 in the context of pH1N1 moderately modulates viral replication, lung histopathology, and local cytokine response in pigs. PMID:22379102
PB1-F2 is of limited importance for the pathogenesis of primary viral infection with human seasonal H1N1 viruses. PMID:22318139
PB1-F2 strongly influences the early host response during influenza A virus infection. PMID:21901097
characterized the anti-interferon function of PB1-F2 and suggest that this activity contributes to the enhanced pathogenicity seen with PB1-F2 N66S- expressing influenza viruses. PMID:21695240
Intranasally infected groups of mice with either influenza A virus PR8 or a genetically engineered virus that expresses the 1918 PB1-F2 protein on a PR8 background, PR8-PB1-F2(1918). PMID:21379324
Genome annotations of this virus identified a stop mutation replacing serine at codon 12 (S12Stop) of the PB1-F2 protein; the significance of this in host specialization was discussed. PMID:19934602
Alternate mechanisms besides alterations to replication are likely responsible for the enhanced virulence in mammalian hosts attributed to PB1-F2 in previous studies. PMID:19828614
structural characterization and oligomerization of PB1-F2 PMID:17052982