Nectin2 Recombinant Protein (BV)
- Known as:
- Nectin2 Recombinant Protein (BV)
- Catalog number:
- HA264050
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Viagen
- Gene target:
- Nectin2 Recombinant Protein ()
Related genes to: Nectin2 Recombinant Protein (BV)
- Gene:
- NECTIN2 NIH gene
- Name:
- nectin cell adhesion molecule 2
- Previous symbol:
- HVEB, PVRL2
- Synonyms:
- PVRR2, PRR2, CD112
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-15
- Date modifiied:
- 2016-02-12
Related products to: Nectin2 Recombinant Protein (BV)
Related articles to: Nectin2 Recombinant Protein (BV)
- Acute myeloid leukemia (AML) remains challenging to treat and often requires intensive chemotherapy. In contrast to other hematologic malignancies, the development of effective antibody-based and cellular immunotherapies for AML has been limited by the scarcity of suitable target antigens. - Source: PubMed
Publication date: 2026/09/12
Hashimoto KojiKonetzki VerenaGaritano-Trojaola AndoniKraus SabrinaFriedel Sabrina RHudecek MichaelPeng HaiyongRader Christoph - [This corrects the article DOI: 10.1371/journal.pone.0356726.]. - Source: PubMed
Publication date: 2026/09/25
Klaihmon PhatchanatMuangtate PattaratornThongphayong SudaratSaetan PuretatChanthateyanonth SupasornThuwajit ChanitraIssaragrisil SurapolPhannasil Phatchariya - Dementia is clinically and biologically heterogeneous, and genetically supported plasma protein associations across dementia subtypes remain incompletely characterized. We aimed to genetically prioritize plasma proteins associated with overall dementia and major dementia subtypes using proteome-wide Mendelian randomization (MR) and Bayesian colocalization. We used the UK Biobank Pharma Proteomics Project (UKB-PPP) as a harmonized source of cis-protein quantitative trait loci (cis-pQTLs) for 2,941 Olink-measured plasma analytes. The European-ancestry discovery cis-pQTL analysis included up to 34,557 participants, whereas 54,219 participants were profiled in the overall UKB-PPP. Outcomes included FinnGen R10 genome-wide association studies (GWAS) for dementia, Alzheimer's dementia, vascular dementia, frontotemporal dementia, and unspecified dementia, plus a European GWAS for dementia with Lewy bodies. At the nominal threshold of P < 0.05, 134, 132, 102, 78, 101, and 112 exploratory protein-outcome signals were observed for dementia, Alzheimer's dementia, vascular dementia, frontotemporal dementia, dementia with Lewy bodies, and unspecified dementia, respectively; 23 associations remained significant after outcome-specific Benjamini-Hochberg false discovery rate (FDR) correction. Key FDR-significant proteins included APOE, NECTIN2, PVR, SERPINF2, GRN, TREM2, and ATXN2L. The strongest risk and protective associations were NECTIN2 with Alzheimer's dementia (odds ratio [OR] = 2.650, 95% confidence interval [CI]: 1.875-3.744, FDR-adjusted P = 1.58 × 10) and ATXN2L with dementia (OR = 0.408, 95% CI: 0.255-0.654, FDR-adjusted P = 0.0370), respectively. Strong colocalization support was observed for selected SERPINF2 and TREM2 associations. These findings genetically prioritize several plasma proteins as candidate biomarkers and potential therapeutic targets across dementia subtypes, but do not establish that circulating protein abundance directly mediates dementia risk. - Source: PubMed
Publication date: 2026/09/07
Yan XinyangZhang LongxiaoLi JiaxiSong Jinning - USP5 is a deubiquitinating enzyme whose role in anti-PD-L1 resistance in breast cancer remains unclear. This study investigated whether USP5 contributes to resistance against the anti‑PD‑L1 antibody (atezolizumab) by regulating the FOXM1/Nectin2 axis. Anti-PD-L1-resistant and lung metastatic mouse models were established, combined with in vitro cellular assays, clinical sample analyses, and bioinformatics approaches. The results showed that USP5 was upregulated in breast cancer and stabilized FOXM1 via deubiquitination, which led to increased Nectin2 expression and resistance to CD8⁺ T cell-mediated killing. Knockdown of USP5 or its pharmacological inhibition with G9 synergized with anti-PD-L1 to suppress tumor growth, an effect that was reversible by Nectin2 overexpression. In conclusion, USP5 promotes breast cancer progression and anti-PD-L1 resistance by deubiquitinating FOXM1, thereby upregulating Nectin2 expression. Targeting USP5 enhances the efficacy of anti-PD-L1 therapy, offering a novel strategy to overcome immunotherapy resistance in breast cancer. - Source: PubMed
Publication date: 2026/09/22
Li GuangyanSu ZhiyuanZhang YutongDu QiguangXu ZhongkaiCui HeZhang Jianguo - Given the distinct pathogenic mechanisms of early-onset Alzheimer's disease (EOAD) and late-onset Alzheimer's disease (LOAD), identifying disease-specific therapeutic targets for each subtype is particularly critical. - Source: PubMed
Publication date: 2026/03/04
Chen LinSun HongxuFang Ming-JuanCheng NanXu Yin