OPCML IHC Antibody
- Known as:
- OPCML Immunohistochemistry Antibody
- Catalog number:
- IW-PA1131
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- IHC
- Gene target:
- OPCML IHC Antibody
Related genes to: OPCML IHC Antibody
- Gene:
- OPCML NIH gene
- Name:
- opioid binding protein/cell adhesion molecule like
- Previous symbol:
- -
- Synonyms:
- OPCM, OBCAM, IGLON1
- Chromosome:
- 11q25
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-13
- Date modifiied:
- 2016-06-17
Related products to: OPCML IHC Antibody
Related articles to: OPCML IHC Antibody
- Colon cancer (CC) is a highly prevalent malignant tumor with a high mortality rate worldwide. Despite recent advancements in diagnosis and treatment, the overall prognosis for patients remains poor, especially for those with metastasis. Exploring key genes associated with the prognosis of patients with colon cancer, establishing effective molecular models, and validating their functions are necessary to optimize patient management and develop novel therapeutic strategies. This study aimed to reveal the role of the key gene SERPINE1 in the progression of colon cancer and its potential clinical application value through bioinformatics analysis and experimental validation. - Source: PubMed
Publication date: 2026/05/05
Li XinLi NanaWang YujieHan QixiangLi XiaodongTu QiushiSun BoshiYang HaoGao Yuan - Cerebrospinal fluid (CSF) biomarkers are central to Alzheimer's disease (AD) diagnosis and research. However, CSF composition is shaped not only by neurodegeneration, but also by underlying physiological and pathological processes that remain poorly characterized. By integrating multi-omics data from the deeply characterized memory-clinic ACE CSF cohort (N=1,372), the Global Neurodegeneration Proteomics Consortium (N=1,863), and publicly available quantitative trait data, we reveal that 73.2-85.9% of the molecular variance in CSF omics data is driven by two main factors: one reflecting CSF turnover rate, and another representing blood-brain barrier (BBB) integrity. CSF turnover mainly determines brain-derived molecules, while BBB damage leads to increased blood-derived protein abundance. CSF turnover/clearance severely impacted core AD biomarker levels, affecting the classification of subjects in the A/T framework. Adjusting biomarker levels for OPCML, a novel reference marker, improved biomarker-based prediction of AD progression and removed confounded associations, revealing a proteomic signature of sporadic AD pathology that closely resembles that of autosomal dominant AD. Finally, using the ACE CSF cohort as discovery (N=1,221) and Knight ADRC as replication (N=1,073), we report a curated AD signature comprising 446 unique proteins. Our findings identify CSF dynamics as a major source of molecular variation, reshaping the interpretation of CSF biomarkers. - Source: PubMed
Publication date: 2026/02/03
García-González PabloPuerta RaquelDehairs JonasYang ChengranWang CiyangTimsina Jigyashade Rojas ItziarOlivé ClaudiaValenzuela AlejandroBayón-Buján PaulaRovira MartaMontrreal LauraCapdevila MariaMuñoz-Morales ÁlvaroCalm BertaValero SergiAlegret MontseMarquié Marta Morris John CSchindler Suzanne EHoltzman David MSanz PilarTárraga LluísKhan AsifSáez Maria ESmets BartOrellana AdelinaMontalbán XavierBoada MercèCano AmandaLiu MenghanAli MuhammadCruchaga CarlosSwinnen Johannes VFernández VictoriaCabrera-Socorro AlfredoRuiz Agustín - (opioid-binding protein/cell adhesion molecule-like), a glycosylphosphatidylinositol (GPI)-anchored IgLON adhesion molecule with brain-enriched expression, has tumor-suppressive roles in several epithelial cancers; however, its role in glioblastoma (GBM) biology is unclear. - Source: PubMed
Publication date: 2026/01/05
Liu ZhixinXu ChunhuaZhou WuLin BilinLiu YihaoWu Wenrui - Adolescents and young adults (AYA) with papillary thyroid carcinoma (PTC) often present with more extensive cervical lymph node metastasis (LNM) than older adults (AD). We aimed to identify age-associated molecular and immune features that might explain this phenotype and to explore potential translational implications for managing aggressive AYA PTC. We analyzed clinical and transcriptomic data from 501 PTC cases in The Cancer Genome Atlas (TCGA), stratified as AYA (<30 years, n = 64) and AD (≥30 years, n = 437). An institutional RNA-seq cohort (n = 13; 7 AYA, 6 AD) was used to screen for differentially expressed genes (DEGs). DEGs were defined by ≤ 0.05 and |log2 fold change| ≥ 1. Intersection with invasion- and dissemination-related gene sets yielded a final age-related DEG list. Functional enrichment (GO/KEGG via DAVID), PPI network analysis (STRING, Cytoscape/cytoHubba), and immune deconvolution (CIBERSORT LM22) were performed. Protein-level validation was carried out by immunohistochemistry (IHC) in an independent cohort (n = 56; 28 AYA, 28 AD). Statistical comparisons used chi-square/Fisher's exact tests for categorical variables, -tests or nonparametric tests for continuous variables, and EdgeR with FDR correction for transcriptomic analyses. In TCGA, LNM was more frequent in AYA than in AD (62.1% vs. 47.8%, = 0.031). From intersected analyses, we identified 239 core DEGs distinguishing highly invasive, age-related tumors. Key upregulated genes in AYA included , and ; downregulated genes included , , and . Enriched pathways involved extracellular matrix organization, cell adhesion, calcium signaling and canonical oncogenic cascades (PI3K-Akt, MAPK, Wnt, Ras). Immune deconvolution showed reduced naïve B cells, M1 and M2 macrophages and resting mast cells and an increased proportion of M0 macrophages in AYA tumors. IHC validated differential protein expression for seven markers. Collectively, the data indicate an immune-suppressed, immune-excluded microenvironment in AYA PTC. AYA PTC exhibits distinct molecular and immune features that may underlie its propensity for lymphatic dissemination. These findings support evaluation of translational strategies, such as CXCR4 inhibition, restoration of antigen presentation, and macrophage reprogramming, to convert "cold" tumors into immune-permissive lesions. Validation in larger, prospective, multicenter cohorts is required. - Source: PubMed
Publication date: 2025/11/21
Ao WeiChen ShuqianLiu TenghongWang BoZhao Wenxin - Synaptic plasticity in the central nervous system enables the encoding, storing, and integrating new information. AMPA (alpha-amino-3-hydroxyl-5-methyl-isoxazole-4-propionic acid)-type glutamate receptors (AMPARs) are ligand-gated ion channels that mediate most fast excitatory synaptic transmission in the brain, and plasticity of AMPARs signaling underlies the long-lasting changes in synaptic efficacy and strength important for learning and memory. Recent work has indicated that the enigmatic N-terminal domain (NTD) of AMPARs may be a critical regulator of synaptic targeting and plasticity of AMPARs. However, few synaptic proteins have been identified that regulate AMPAR plasticity through interactions with AMPAR NTDs. Moreover, the scope of AMPAR NTD interactors that are important for synaptic plasticity remains unknown. Here, we present the dynamic, extracellular interactome for AMPARs during synaptic plasticity. Using surface-restricted proximity labeling and BioSITe-based proteomics, we identified 70 proteins that were differentially labeled by APEX2-tagged AMPARs after induction of chemical long-term potentiation of synapses in cultured neurons. Included in this list, were four members of the IgLON family of GPI-anchored proteins (Ntm, OBCAM/Opcml, Negr1, Lsamp). We show OBCAM and NTM directly interact with the extracellular domains of AMPARs. Moreover, overexpression of NTM significantly attenuates the mobility of surface AMPARs in dendritic spines. These data represent a significant step at uncovering the unexplored extracellular regulation of AMPARs, with broad implications for synapse function and synaptic plasticity. - Source: PubMed
Publication date: 2025/11/17
Merrion Hana GoldschmidtBarber Casey NRenuse SantoshCutler JevonKreimer SimionBygrave Alexei MMeyers David JHale W DylanPandey AkhileshHuganir Richard L