Ask about this productRelated genes to: CADM3 antibody
- Gene:
- CADM3 NIH gene
- Name:
- cell adhesion molecule 3
- Previous symbol:
- IGSF4B
- Synonyms:
- BIgR, FLJ10698, TSLL1, NECL1, SynCAM3, Necl-1
- Chromosome:
- 1q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-24
- Date modifiied:
- 2016-10-05
Related products to: CADM3 antibody
Related articles to: CADM3 antibody
- This systematic review aims to comprehensively evaluate the clinicopathological and molecular features of superficial CD34-positive fibroblastic tumour (SCD34FT), a recently described intermediate-grade soft-tissue neoplasm recognised in the 5th edition of the WHO classification of soft tissue tumours. - Source: PubMed
Publication date: 2026/04/11
Das SumantaPerret RaulKhan Adil AzizMishra PallaviAhlawat Sunita - Chagas disease, caused by , affects over seven million people worldwide. Vertical transmission during pregnancy contributes to the urban spread of the disease, including in non-endemic regions. Although the placenta constitutes a critical barrier against fetal infection, the molecular mechanisms underlying congenital transmission remain poorly understood. To identify placental factors associated with transmission, we performed a transcriptomic analysis of placental tissues from deliveries of congenitally infected (M+B+), exposed but uninfected (M+B-), and unexposed/uninfected (M-B-) newborns. Differential gene expression analysis comparing M+B+ and M-B- placentas revealed overexpression of CEMIP (cell migration-inducing hyaluronidase 1), involved in extracellular matrix (ECM) remodeling and intracellular transport, together with ENSG00000304767, a novel long non-coding RNA located intronically within . In contrast, PRRX1 (paired related homeobox 1), CADM3 (cell adhesion molecule 3), and CDH11 (cadherin 11), genes associated with transcriptional regulation and cell-cell adhesion, were underexpressed. In the M+B- versus M-B- comparison, MIR4300HG, a long non-coding RNA hosting , was overexpressed, whereas CGB5 (chorionic gonadotropin subunit beta 5), essential for pregnancy maintenance, was underexpressed. Direct comparison between M+B+ and M+B- placentas showed overexpression of the -associated lncRNA and CGB5, accompanied by downregulation of CADM3, NEGR1, PDPN, and CDH11, implicating altered adhesion and structural pathways in transmission. Overall, these findings indicate that placental cell adhesion and ECM integrity are disrupted in transmitting placentas. Gene set enrichment analysis using the Gene Ontology library revealed alterations of immune-related pathways in both infected mother groups, while highlighting ECM-related processes-particularly collagen organization and metabolism-as key contributors to transmission events. Cell type enrichment analysis showed overrepresentation of extravillous trophoblasts in M+B+ placentas, with the opposite pattern observed in M+B- cases. Conversely, syncytiotrophoblasts and villous cytotrophoblasts were enriched in non-transmitting placentas relative to controls. Immune-associated placental cell types were consistently reduced in both infected groups. Co-expression network analysis further confirmed compromised placental signaling and structural integrity in transmitting cases, identifying ENPP1 and SLC16A10 as central hub genes. Together, these RNA-seq data define key placental transcriptional alterations associated with congenital transmission which, upon future experimental validation may provide insights into molecular mechanisms governing fetal protection or susceptibility. - Source: PubMed
Publication date: 2026/03/18
Apodaca SofiaCampos Emiliano ECalupiña Kevin DDavies CarolinaLucero Raúl HLonghi Silvia AKamenetzky LauraZago Maria PaolaSchijman Alejandro G - Chronic exposure to benzo[a]pyrene (BaP), a Group 1 IARC carcinogen, is a major driver of lung carcinogenesis; however, how sustained subcytotoxic exposure reprograms bronchial epithelium toward preneoplastic states remains poorly defined. Here, we subjected BEAS-2B human bronchial epithelial cells to 12 weeks of continuous BaP at environmentally relevant concentrations (0.1 and 1.0 µM) and interrogated the resulting phenotypes using an integrated multi-scale framework encompassing functional toxicology, RT-qPCR, RNA-seq, phospho-kinase/NF-κB arrays, and organotypic air-liquid interface (ALI) cultures. Cells maintained metabolic competence throughout, evidenced by sustained CYP1A1 and CYP1B1 induction at both acute (4 h) and chronic (12-week) timepoints, while accumulating genotoxic stress as demonstrated by dose-dependent nuclear γ-H2AX foci formation and ATM phosphorylation (Ser1981). RNA-seq revealed a dose-dependent transcriptional shift: 0.1 µM BaP yielded 119 differentially expressed genes (DEGs; |log2FC| ≥ 1, FDR < 0.05), whereas 1.0 µM generated 255 DEGs. Downregulated transcripts were enriched for extracellular matrix and cell-adhesion programs (COL14A1, ADAMTS2, CSMD3, CADM3), while upregulated genes encompassed inflammatory, calcium-signaling, and vesicle-trafficking modules (NFATC4, CSF2RA, SYT1, PCLO). Phospho-kinase/NF-κB arrays confirmed a p53/NF-κB signaling nexus, with concurrent activation of MAPK/ERK (Thr202/Tyr204) and PI3K/Akt (Ser473) pathways. Despite persistent genotoxic stress, cells did not acquire anchorage-independent growth and remained non-tumorigenic in vivo. Critically, ALI organotypic cultures derived from BaP-exposed cells exhibited histological dysplasia, nuclear pleomorphism, and disrupted apical-basal polarity. These findings mechanistically link chronic BaP exposure to an initiation-like preneoplastic state and establish a validated 2D/3D multi-omics platform for PAH-driven lung carcinogenesis research. - Source: PubMed
Publication date: 2026/03/22
Andrade-Madrigal CristianRojas-Fuentes CeciliaDíaz-Mijares JavierCalaf Gloria MSantoro Pablo MCorvalán Alejandro HMedina Francisca JTorres Cristian GRomero-Vicencio PaulaTapia Julio CAcevedo Mónica LSoto-Rifo RicardoBoccardo EnriqueAguayo Francisco - Abnormal paternal methylation of imprinted genes is associated with preeclampsia. C19MC is an imprinted miRNA cluster that plays an important role in placental development. Thus, the present study investigated methylation of C19MC in the spermatozoa and placentae and, its expression in the placentae of early-onset preeclampsia (EOPE). The study was carried out with n = 25 (controls) and 14 (EOPE cases). Methylation study of C19MC differentially methylated region (DMR) was performed by pyrosequencing of spermatozoa and placental villi samples. Expression levels of C19MC miRNAs in the placental villi were measured by small RNA sequencing on Illumina NovaSeq 6000. Publicly available datasets of EOPE were examined. The mRNA targets of differentially expressed miRNAs (DEMs) that were expressed in these datasets were subject to gene ontology analysis. The expression levels of target genes were quantified by qPCR. C19MC was not differentially methylated in the preeclampsia group spermatozoa. The DMR showed hypomethylation and, elevated expression of miR-518a-5p/527 and miR-520a-5p in the placental villi of the case group. The targets DAB2IP, ACAA2, TRAF2, VCAM1, CADM3, TWIST1 and CUL3 were significantly downregulated in the preeclamptic placentae. Birth weight and systolic blood pressure had a significant association with methylation in placental villi. The study is the first to explore methylation of C19MC in the spermatozoa and placentae from EOPE couples. Aberrant expression of C19MC miRNAs and their targets could be associated with pathophysiology of EOPE. The study paves the way for assessment of C19MC DEMs and target mRNAs as potential therapeutic targets for EOPE. - Source: PubMed
Publication date: 2026/03/09
Nair SwetaJoseph ShainiWarke HimangiBansal VandanaPatil AnushreeNishi KumariBalasinor Nafisa H - Atherosclerosis, the main driver of cardiovascular disease (CVD), is influenced by a plethora of risk factors, including age, gender, and diabetes, that correlate with socio-economic status and may vary across ethnicities. These factors fail to fully explain observed ethnic disparities in CVD burden. For example, coronary artery calcification increases with age regardless of ethnicity, yet CAC is more prevalent in individuals of European descent. As these findings may be confounded by self-reported ethnicity, genome-informed ancestry offers a more accurate lens through which to study these ancestral differences. Yet, the biological basis of atherosclerotic plaque development and composition across ancestries remains essential underexplored. We hypothesized that genetically determined ancestry is associated with morphological and molecular features of atherosclerotic plaques. Leveraging the Athero-Express Biobank Study, an ongoing Dutch cohort with deep histological and transcriptomic profiling of plaques, we analyzed data from 1944 patients after genotype quality control and ancestry inference using principal component analysis against 1000 Genomes. Two ancestry groups were identified, European (n = 1866) and non-European (n = 51), reflecting Netherlands' migratory history. Demographics were largely comparable between groups, however, ordinal logistic regression showed non-European ancestries had higher odds of increase plaque vulnerability (OR = 1.67, 95% CI 1.01-2.77, p = 0.0450), a finding that remained robust after down sampling. Differential gene expression analysis highlighted NLGN4X and CADM3 among the top differentially expressed genes, representing biologically relevant pathways related to synaptic and cell-cell adhesion. Pathway and single-cell enrichment analyses, including through integration with genome-wide association study data, further revealed consistent enrichment of inflammation-related biological processes and diseases. Our findings support that genetic ancestry correlates with morphological and molecular plaque composition, with non-European patients showing more inflammatory, higher-risk plaque features, including inflammatory signatures. Increased ancestral diversity in vascular biology research is critical for understanding atherosclerotic pathophysiology and develop equitable and personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/02/13
Fahim NimaSakkers Tim Rvan der Zalm Floor B HHoekstra Joostde Kleijn Dominique P VMokry MichalVerdezoto Mosquera JosePasterkamp Gerardden Ruijter Hester MMiller Clint Lvan Setten Jessicavan der Laan Sander W