BTN2A1 Blocking Peptide, Blocking Peptides
- Known as:
- BTN2A1 Blocking Peptide, Blocking Peptides
- Catalog number:
- 33R-8900
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- BTN2A1 Blocking Peptide Peptides
Related genes to: BTN2A1 Blocking Peptide, Blocking Peptides
- Gene:
- BTN2A1 NIH gene
- Name:
- butyrophilin subfamily 2 member A1
- Previous symbol:
- -
- Synonyms:
- BT2.1, BTF1, BTN2.1
- Chromosome:
- 6p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-27
- Date modifiied:
- 2016-10-05
Related products to: BTN2A1 Blocking Peptide, Blocking Peptides
Related articles to: BTN2A1 Blocking Peptide, Blocking Peptides
- This study conducted a meta-analysis across three large European cohorts (UKBB, FinnGen, and REPAIR), including 12,660 rheumatoid arthritis (RA) cases, 2,446 radiographic axial spondyloarthritis (r-axSpA) cases, and over 530,000 shared controls. - Source: PubMed
Publication date: 2026/04/23
Cabrera-Serrano Antonio JoséCarretero-Fernández MaríaPérez-Rojo BegoñaTer Horst RobCañadas-Garre MarisaCanhão HelenaQuartuccio LucaSorensen Signe BGlintborg BenteFilipescu IleanaPérez-Pampin EvaConesa-Zamora PabloSwierkot Jerzyden Broeder Alfons Ade Vita SalvatoreBrix Petersen Eva RabingLi YangCoenen Marieke J HBogunia-Kubik KatarzynaAndersen VibekeFonseca João EuricoLund Hetland MereteLópez Nevot Miguel ÁngelLópez-Medina ClementinaReyes-Zurita Fernando JesúsNetea Mihai GEscudero AlejandroCáliz RafaelCollantes-Estévez EduardoSánchez-Maldonado José ManuelSainz Juan - Anti-GD2 monoclonal antibody effectively treats high-risk neuroblastoma (HR-NB) by recruiting NK cells for antibody-dependent cellular cytotoxicity (ADCC). We recently developed a cell product containing mature, cytotoxic γδ T and NK cells (GADEKILL), and its potential use as a novel immunotherapy for HR-NB has been investigated. - Source: PubMed
Publication date: 2026/01/30
Morandi FabioDella Lastra MartinaPastorino FabioCiampi EleonoraFaraci MauraBrignole ChiaraGiardino StefanoAiroldi Irma - Phosphoantigens (pAgs) are phosphate-containing small molecules that elicit an immune response. The pAgs bind to the intracellular domain of butyrophilin 3 (BTN3), enabling interactions with other butyrophilins to form complexes that trigger the T cell receptor (TCR) of Vγ9Vδ2 (γ9δ2) T cells. Despite multiple reports on this process, the conditions that regulate pAg levels leading to their detection remain unclear. Here we reveal a novel stress detection pathway, a type of lymphoid stress-surveillance response, in which mild cold stress triggers endogenous pAgs to engage with BTN family proteins, leading to the activation of γ9δ2 T cells. This stress response is dependent upon endogenous pAgs, as inhibition of HMG-CoA reductase abrogates the effect. It is also dependent upon BTN proteins, as depletion of BTN3A1 reduces the response. The ability of BTN2A1/BTN3A1 to respond is enhanced by the presence of BTN3A2 or BTN3A3. Furthermore, the internal domains of BTN2A1, BTN3A1, and BTN3A3 display differing abilities to dimerize, with BTN2A1 a constitutive dimer, BTN3A1 a monomer, and BTN3A3 a concentration dependent dimer. Full length BTN2A1/3A1 hybrid proteins additionally reveal that appropriately spaced multimers of BTN2A1 and BTN3A1 are critical in engaging the γ9δ2 TCR. In summary, our study uncovers a novel γ9δ2 T cell activation pathway mediated by cell stress and mevalonate pathway intermediates and highlights the critical roles of the BTN family members and their spacing in this process. - Source: PubMed
Publication date: 2026/01/22
Jin YimingNguyen KhiemBashir SidraPawge GirijaStrand Reagan MHsiao Chia-Hung ChristineVinogradova OlgaWiemer Andrew J - Schizophrenia (SCZ) has strong genetic underpinnings, yet the functional impact of associated genetic variants remains unclear. We computationally analyzed SCZ-associated missense single-nucleotide polymorphisms (SNPs) from the National Human Genome Research Institute-European Bioinformatics Institute (NHGRI-EBI) Genome-Wide Association Studies (GWAS) Catalog to identify variants with significant functional consequences. From 5083 SCZ-associated SNPs, we prioritized five genes harboring highly deleterious missense SNPs: STX2, BTN2A1, and UGT1A8/9/10. We integrated pathogenicity predictions, protein stability assessments, structural analyses, and protein-protein interaction networks to understand how these SCZ-associated missense variants may contribute to disease pathogenesis. Amino acid changes, or variants, of the five genes were consistently predicted to decrease protein stability. The STX2 variant affects the syntaxin N-terminus domain, crucial for neurotransmitter release and implicated in antipsychotic pharmacology. The BTN2A1 variants disrupt immunoglobulin-like domains involved in T-cell regulation. The UGT1A8/9/10 variant impacts the UDP-glycosyltransferase domain, potentially altering drug metabolism. Protein interaction analyses revealed connections to synaptic signaling, immune regulation, and xenobiotic metabolism pathways implicated in SCZ. Our findings illuminate potential molecular mechanisms by which these genetic variants may contribute to SCZ pathophysiology and highlight promising targets for therapeutic development. - Source: PubMed
Publication date: 2026/01/14
Coppin Fatimah MKwon MichelleBakhteri AriyaAbugaliyeva Aziza - The effectiveness of immunotherapies against glioblastoma (GB) remains limited. A major obstacle in advancing new strategies is the reliance on non-autologous systems, which do not accurately mimic the true extent of inter-patient heterogeneity in both immune responses and tumor susceptibility. This often leads to misleading conclusions about therapeutic efficacy and targetability. - Source: PubMed
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