Recombinant Human PVRL1 /CD111 Protein
- Known as:
- Recombinant Human PVRL1 /CD111 Protein
- Catalog number:
- cd-784
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human PVRL1 /CD111 Protein
Related genes to: Recombinant Human PVRL1 /CD111 Protein
- Gene:
- NECTIN1 NIH gene
- Name:
- nectin cell adhesion molecule 1
- Previous symbol:
- HVEC, ED4, PVRL1
- Synonyms:
- PRR, PRR1, PVRR1, SK-12, HIgR, CLPED1, CD111, OFC7
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-15
- Date modifiied:
- 2016-02-12
Related products to: Recombinant Human PVRL1 /CD111 Protein
Related articles to: Recombinant Human PVRL1 /CD111 Protein
- Puncta adherentia junctions (PAJs) have been observed at glutamatergic excitatory synapses on glutamatergic excitatory neurons (E→E synapses) in the mouse hippocampus and are considered to be the mechanical adhesion sites between axon terminals and dendritic shafts. However, it remains unclear whether they are present at other types of synapses, such as glutamatergic synapses on GABAergic inhibitory neurons (E→I synapses) and GABAergic synapses on excitatory neurons (I→E synapses) and inhibitory neurons (I→I synapses). We showed here that the PAJ components, such as nectin-1, nectin-3, l-afadin, N-cadherin, β-catenin, and αN-catenin, were observed at all four types of synapses in cultured mouse hippocampal neurons. In the adult mouse hippocampus, these PAJ components were observed at a subset of I→I synapses on parvalbumin-positive GABAergic inhibitory neurons, similarly to their presence at E→E synapses in the CA1 and CA3 regions. In contrast, several PAJ components, including nectin-3, l-afadin, N-cadherin, β-catenin, and αN-catenin, were observed at E→I and I→E synapses, whereas nectin-1 was absent. These results indicate that the PAJs are formed at a subset of I→I synapses in addition to E→E synapses, where all examined PAJ components are present, whereas E→I and I→E synapses exhibit only partial localization of these components, reflecting molecular diversity among different synapses in the adult mouse hippocampus. - Source: PubMed
Katanazaka KimitakaShiotani HajimeMiyata MuneakiKameyama TakeshiKedashiro ShinKomaki RyouheiNishii ShotaKashiwagi YutaroSato YukaOkabe ShigeoChihara NorioMatsumoto RikiMizutani KiyohitoTakai Yoshimi - Herpes simplex encephalitis (HSE) is a life-threatening disease of the central nervous system caused by herpes simplex virus type 1 (HSV-1). Despite being a standard treatment, antiviral acyclovir and its derivatives often face limitations in clinical application due to their side effects and viral drug resistance. Inspired by viral entry through recognition of nectin-1 on the host cell surface, we engineered enucleated mesenchymal stem cells with high nectin-1 expression (eMSCs) to serve as "decoys" for capturing HSV-1. We found that eMSCs competitively captured the virus in the presence of neurons while inhibiting its replication and spread by removing the nucleus in advance. Interestingly, due to the absence of nuclei, eMSCs capturing the virus trigger macrophage efferocytosis through intrinsic apoptosis after approximately 60 h, thereby accelerating existing viral clearance. This is a property lacking in current antiviral drugs, including ACV. In summary, this strategy significantly improved the quality of life of HSE mice. - Source: PubMed
Publication date: 2026/03/12
Zhou LeiSong QingyingCao MengnianQin MengjiaoWang ZhenyaSun YiwenXue DayuZhang ZhenzhongShi JinjinLiu Junjie - Herpes simplex virus 1 (HSV-1) entry is a complex interplay of viral and host factors. The mechanisms of its regulation remain undefined. HSV-1 entry occurs via multiple distinct and cell-type dependent pathways, further complicating study of this process. HSV-1 strains with atypical entry properties aid in the elucidation of entry determinants. HSV-1 strain ANG path exhibits entry in Vero cells at 4 °C, whereas wild-type strains do not. We investigated the determinants of low temperature entry by HSV-1 ANG path in several cell types. The receptor nectin-2 mediated 4 °C entry of HSV-1 ANG path into CHO-K1 cells, but the related receptor nectin-1 did not, suggesting that gD-binding receptors are a determinant of HSV-1 entry at low temperatures. In HaCaT cells, both HSV-1 ANG path and wild-type strain KOS entered at 4 °C, while HSV-1 chimera 27/III, which contains KOS strain gB in the ANG path virus background, did not. This suggests that gB functions as a determinant of low temperature entry of HSV-1. Together, the findings suggest that there are multiple determinants and mechanisms of HSV-1 low temperature entry and that the requirements differ by cell type. - Source: PubMed
Publication date: 2026/01/27
Lynch Colleen MHull McKenna ANicola Anthony V - Autoimmune Polyendocrine Syndrome Type 1 (APS-1) is a rare monogenic disorder caused by mutations in the autoimmune regulator (AIRE) gene. Although AIRE is essential for central immune tolerance, how distinct APS-1-associated mutations differentially affect medullary thymic epithelial cell (mTEC) biology remains incompletely understood. Here, we investigated the molecular and functional consequences of three Aire/AIRE variants using complementary murine mTEC models. To define transcriptional effects, we performed single-cell RNA sequencing (scRNA-seq) on mTECs carrying a heterozygous genomic Aire c.735delG mutation generated by CRISPR-Cas9. This analysis revealed reduced transcriptional heterogeneity, decreased expression of tissue-restricted antigens (TRAs) mRNAs (including Col4a3, Col7a1, and Neto2), and downregulation of key mTEC lineage markers (Epcam, Cldn4, Krt14). Mutant cells also displayed altered expression of mRNAs involved in chemokine-mediated migration (Ccl25, Cxcl16), extracellular matrix and cell adhesion (Fn1, Lama5, Col4a1, Nectin1, Cdh1), and actin cytoskeleton organization (Gsn, Rac1, Wasl, Actn1), indicating broad disruption of pathways governing mTEC identity and cell-cell interactions. Guided by these findings, we assessed mutation-specific functional outcomes using a CRISPR-derived Aire functional knockout and lentiviral expression of the human AIRE missense variants p.G229W and p.C313Y in wild-type mTECs. Functional assays revealed mutation-dependent alterations in mTEC morphology, thymocyte migration, and adhesion, with the p.C313Y variant exerting the strongest effects. Together, these data demonstrate that heterozygous and missense AIRE mutations exert distinct yet convergent effects on mTEC transcriptional programs and cellular behavior, providing mechanistic insight into AIRE-dependent immune tolerance failure in APS-1. - Source: PubMed
Tanaka Pedro ParanhosCotta-Almeida ViniciusDonadi Eduardo AntônioWesterberg LisaPassos Geraldo Aleixo - Triple-negative breast cancer (TNBC) represents the most aggressive breast cancer subtype, with its highly heterogeneous tumor microenvironment posing substantial challenges for precision diagnosis and therapy. To address this, we aim to construct a novel prognostic framework based on tumor-immune interactions. Through integrative analysis of single-cell RNA sequencing data from 30 TNBC samples (106,132 cells), we identify key tumor expression metaprograms and uncover their interaction with an immunosuppressive dendritic-cell subset, a process associated with the NECTIN1-NECTIN4 axis. Leveraging these interactions, we developed and validated two immunological prognostic models using multi-cohort transcriptomic data, including the stress response tumor cell and pDC_CLEC4C prognostic model (SPSM) and the immune response tumor cell and pDC_CLEC4C prognostic model (IPSM). These models effectively stratified TNBC patients into distinct risk groups, with the low-risk group characterized by an immunologically active microenvironment and elevated expression of immune checkpoint genes, suggesting a potential responsiveness to immunotherapy. Furthermore, we identified several potential therapeutic agents, including imatinib and bortezomib. Collectively, our dual-model framework provides a tool for risk stratification, offers translational insights for precision treatment, and presents new directions for understanding TNBC heterogeneity and therapeutic development. - Source: PubMed
Publication date: 2026/02/03
Lin ShihuaWang HongjiuWang ZhenzhenXiao YuxuanPatrice Menoudji DjetoyomWang LiLi XiaZhang Yunpeng