Influenza A NP 383-391 (HLA-B*27:05) SRYWAIRTR
€210.00*
Description
The Influenza A NP 383–391 peptide (Sequence: SRYWAIRTR) is an exceptionally well-studied, immunodominant epitope derived from the viral Nucleoprotein (NP) of Influenza A virus (UniProt ID: P03466).
Primarily presented by HLA-B*27:05, this canonical peptide is a cornerstone tool in cellular immunology for monitoring CD8+ cytotoxic T-lymphocyte (CTL) activation, investigating viral immune escape, and profiling allele-specific T-cell responses. Reactivity has additionally been reported in select studies for related alleles, including HLA-B*27:03 and HLA-B*27:04.
Key Scientific Highlights
- Extensive Literature Validation: Supported by an exceptional scientific corpus including 58 publications, 74+ functional T-cell assays, and 75 MHC ligand binding studies (IEDB Epitope ID: 60867).
- High-Resolution Structural Data: Structural binding interactions are fully resolved in available 3D crystal structures (PDB ID: 2BST), facilitating structure-based TCR interaction studies.
- Recall Assay Reference: Widely recognized as a benchmark viral antigen for testing memory T-cell responses in HLA-B*27-positive donor samples.
Cross-Referenced Control Pools
Streamline your assay workflows by sourcing this epitope as an individual catalog peptide or as a verified component within our off-the-shelf peptides&elephants control panels:
TechData
| Sequence: | SRYWAIRTR |
| Gene: | NP |
| Delivery: | 1-3 days |
| C-Terminus: | OH |
| N-Terminus: | H |
| Amount: | 1 mg |
| Counterion: | TFA |
| Protein: | Nucleoprotein |
| UniProt Id: | P03466 |
| Species: | Influenza A virus |
| Allele: | HLA-B*27:05 |
| Application: | T-cell assays, Immune monitoring, Antigen specific T-cell stimulation, T-cell expansion, Cellular immune response |
| Indication: | Infectious disease |
| Purity: | 95% HPLC-MS |
Documents
References
Boon, A C M et al. “The magnitude and specificity of influenza A virus-specific cytotoxic T-lymphocyte responses in humans is related to HLA-A and -B phenotype.” Journal of virology vol. 76,2 (2002): 582-90. doi:10.1128/jvi.76.2.582-590.2002
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