Human Cupidin (CPD)ELISA Kit
- Known as:
- Human Cupidin (CPD)Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-2799
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Cupidin (CPD)ELISA Kit
Related genes to: Human Cupidin (CPD)ELISA Kit
- Gene:
- HOMER2 NIH gene
- Name:
- homer scaffold protein 2
- Previous symbol:
- -
- Synonyms:
- CPD, Cupidin, Vesl-2, HOMER-2B, HOMER-2, HOMER-2A, DFNA68
- Chromosome:
- 15q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-28
- Date modifiied:
- 2018-03-01
Related products to: Human Cupidin (CPD)ELISA Kit
Related articles to: Human Cupidin (CPD)ELISA Kit
- The central nervous system responds to acute injury with plastic remodeling of its network. However, the temporal and structural dynamics of this response in the denervated dentate gyrus remain poorly understood. Therefore, we examined the transcriptional programs activated after perforant path transection, focusing on the outer molecular layer (OML) and the granule cell layer (GCL). - Source: PubMed
Publication date: 2026/05/19
Schlaudraff JessicaDel Turco DomenicoKey JanaDeller ThomasAuburger Georg - INTRODUCTION: Sarcoidosis is an inflammatory disease driven by immune-mediated mechanisms, characterized by the formation of epithelioid cell granulomas and a wide range of clinical manifestations. Its phenotype is the result of a complex interplay of genetic and environmental factors, the precise roles and interactions of which remain poorly defined. AIM: To identify candidate genes and risk loci associated with sarcoidosis from large population datasets. To estimate the genetic heritability of the phenotype in selected ancestries. POPULATION AND METHODS: Public summary statistics from the FinnGen release 12 (European ancestry), pan UK BioBank Project (UKBB - European and African ancestry), Million Veteran Program (MVP - European and African ancestry), and Japan BioBank (East Asian ancestry) were included for European, African and multi-ancestry meta-analysis through sample size-based analysis. Novel risk loci and single nucleotide polymorphisms (SNPs) significantly associated with the disease were critically reviewed on the basis of the available literature. For each risk locus, SNPs highly correlated with the lead SNP were selected based on Combined Annotation Dependent Depletion (CADD) scores. Genetic heritability (h2) scores were obtained through ancestry-specific linkage-disequilibrium score calculation. RESULT: Overall 9659 cases (7559 European, 1880 African, 220 East Asian) and 1,665,804 controls (1,361,726 European, 126,411 African, 177,667 East Asian) were analysed. Nineteen and two risk loci were identified in European and African ancestry, respectively; h2 scores were 0.25 (European) and 0.19 (African). Candidate non-MHC genes for further explorations through functional studies included IL23R, PUS10, ACOXL, PLCL1, FAM117B, BMPR2, PPARG, ESYT2, ANXA11, CCDC88B, ATXN2, CCL24, RP11−540O11.1, HOMER2, CD19, UBASH3A, RNF215, and others. Interferon gamma signaling, meiotic recombination/condensation of prophase chromosomes, and DNA methylation were the most enriched gene sets in European and multi-ancestry meta-analysis. Multi-ancestry meta-analysis was confronted with FinnGen+UKBB+MVP meta-analysis (released by FinnGen freeze 12) yielding consistent results (18 risk loci identified) CONCLUSION: Nineteen and two risk loci were significantly associated with sarcoidosis for European and African ancestries, respectively. Moderate genetic heritability was observed for both ancestries. A set of significantly associated non-MHC genes and SNPs was obtained to investigate functional validation. Although further studies are warranted, epigenetic alterations may contribute to the risk of developing sarcoidosis - Source: PubMed
Publication date: 2025/12/29
Ricci AndreaAndolfi FedericaSabbatini DanieleGozzi FilippoBetto Giada DiVentura PaoloBuzzetti ElenaPietrangelo AntonelloClini EnricoTonelli RobertoAndrisani Dariode Guzman Marinduque Brent JuliusBergamini ElisaVecchi ChiaraPegoraro ElenaGregori DarioCorradini ElenaCerri Stefania - There is a lack of objective evaluation tools for assessing upper limb motor dysfunction in ischemic stroke patients (ULMD-IS). This study aimed to develop and validate a diagnostic nomogram for diagnosing the severity of ULMD-IS using functional near-infrared spectroscopy (fNIRS) data. - Source: PubMed
Publication date: 2025/12/04
Liu MenghuiWan ChunxiaoWang ChunyanLi XinyiShang Mengmeng - Heterozygous variant in HOMER2 is associated with autosomal dominant nonsyndromic hearing loss (ADNSHL), designated as the locus of DFNA68. Only five pathogenic variants in HOMER2 have been identified to date. - Source: PubMed
Publication date: 2025/12/05
Peng Li-TingWang Wei-QianHuang Sha-ShaLiu MinYang Su-YanKang Dong-YangWang XiangGao XueYuan Yong-YiXu Jin-Cao - At the neuromuscular junction, nicotinic acetylcholine receptor (nAChR) dynamics are regulated in a nerve- and activity-dependent manner. Correlated local alterations in myoplasmic [Ca], induced by IP-sensitive subsynaptic Ca stores, have been proposed to signal motor endplate adaptation to motor neuron stimulation. Accordingly, there is evidence for a modulatory role of Ca/calmodulin-dependent protein kinase IIβ (CaMKIIβ) in the sorting, targeting, and/or incorporation of nAChRs into the postsynaptic membrane. As the scaffold protein Homer 2 emerges as a key player in integrating downstream postsynaptic signaling pathways, this study investigated the possible involvement of Homer 2 in the molecular mechanism controlling nAChR dynamics. Using Homer 2 transgenic mice, it was found that Homer 2 ablation leads to a chronic adaptation of the endplate characterized by: ) reduction in nAChR activity due to slower insertion of nAChRs into the endplate; ) reduced subsynaptic IPR1 content and IP-releasable Ca; and ) impaired colocalization of CaMKIIβ with nAChRs. Overall, the present results demonstrate that Homer 2 ablation produces a significant alteration in endplate nAChR dynamics, which is associated with impaired organization of the subsynaptic IP-driven Ca signaling mechanism. This research sheds light on the role of Homer 2 in organizing the subsynaptic microdomain, where nAChRs, IPR1s, and CaMKIIβ assemble to regulate nAChR dynamics. The present results point to a novel type of endplate instability, which may have implications for understanding neuromuscular junction function and related disorders. - Source: PubMed
Publication date: 2025/11/19
Lorenzon PaolaAmoretti StefanoFurlan SandraRavara BarbaraBernareggi AnnalisaSciancalepore MarinaSacchetto RobertaMegighian AramZampieri SandraNori AlessandraVolpe Pompeo