Ask about this productRelated genes to: LMNB2 antibody
- Gene:
- LMNB2 NIH gene
- Name:
- lamin B2
- Previous symbol:
- LMN2
- Synonyms:
- -
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-04-09
- Date modifiied:
- 2016-04-25
Related products to: LMNB2 antibody
Related articles to: LMNB2 antibody
- Extensive evidence suggests overlapping pathological mechanisms in the brain of individuals with Parkinson's disease dementia, Down syndrome dementia, and Alzheimer's disease. For these neurodegenerative dementias, we observed that the chronological age did not align with their biological age, which was determined based on hippocampal transcript levels (i.e., transcriptional age). Subsequently, we performed a transcriptomic analysis that corrected for the transcriptional age in the hippocampus of affected individuals, highlighting common underlying pathogenic mechanisms. There were 45 common differentially expressed genes (DEGs), whereas enriched functional terms were related to lysine -methyltransferase activity and intermediate filament. Co-expression network analysis displayed a module that was significantly downregulated in the non-demented control group only. This module identified and as hub genes, which were also common DEGs. Overall, these findings uncover shared functional insights in the hippocampus, while specifically highlighting and as potential universal biomarkers or disease-altered targets across neurodegenerative dementias. - Source: PubMed
Publication date: 2026/04/29
Crans René A JFructuoso MartaBascón-Cardozo KarenRecaioglu HaticeSotelo-Fonseca JesusVermeiren YannickStrydom AndréVan Dam DebbyDe Deyn Peter PRodríguez-Martín BernardoPotier Marie-ClaudeDierssen Mara - Brain metastasis (BM) represents a significant clinical challenge in advanced breast cancer, yet the molecular mechanisms driving breast cancer brain metastasis (BCBM) remain incompletely characterized. This study aims to identify key molecular pathways and hub genes specifically associated with BCBM through comprehensive bioinformatic analyses. Gene Set Enrichment Analysis (GSEA), differential gene expression analysis, and weighted gene co-expression network analysis (WGCNA) were performed using two independent GEO datasets (GSE191230 and GSE43837). Protein-protein interaction (PPI) networks were constructed to visualize functional interconnections among dysregulated genes. Survival analyses were conducted using the Kaplan-Meier Plotter database to evaluate the prognostic significance of identified hub genes. GSEA revealed significant upregulation of metabolic pathways (mTORC1 signaling, glycolysis, oxidative phosphorylation) and downregulation of immune-related pathways in BCBM compared to primary tumors. Integrative analysis identified 34 consistently dysregulated genes across datasets, from which 12 hub genes were validated. Among these, RRM2, CDCA8, CCNB1, LMNB2, FANCI, NCAPH, YWHAZ, and ESPL1 demonstrated brain-specific over-expression compared to other metastatic sites. Functional enrichment analysis highlighted cell cycle dysregulation as a critical mechanism in BCBM, and all hub genes showed significant association with poor prognosis in breast cancer patients. This study identifies a unique molecular profile of BCBM characterized by cell cycle dysregulation, metabolic reprogramming, and immune microenvironment alterations. The brain-specific expression patterns of these hub genes represent potential biomarkers for BCBM risk assessment and novel therapeutic targets, providing a basis for precision medicine development. - Source: PubMed
Publication date: 2026/04/13
Ting Wei-YiLu Yueh-HsunLin Che-Ming - [This retracts the article DOI: 10.3727/096504019X15615433287579.]. - Source: PubMed
Publication date: 2026/04/22
- Prostate cancer (PCa) is a leading cause of cancer mortality in men. Lamin B2 (LMNB2) has been implicated in various cancers, but its functional role and molecular mechanisms in PCa progression remain poorly characterized. - Source: PubMed
Publication date: 2026/04/21
Liu ZhiyuLi YuqiWang JuanZeng YangWu QilongZhu XinyaoZhou TaoDeng Qingfu - Epigenetic regulation of chromatin structure is a key determinant of transcriptional control and nuclear organization in cancer. Among histone lysine methyltransferases, SUV39H1 and SUV39H2 catalyze the trimethylation of histone H3 lysine 9 (H3K9me3), establishing repressive heterochromatin domains that are important for genomic stability. However, their pan-cancer expression dynamics, prognostic value, and structural implications remain poorly defined. In this study, we performed an integrative analysis of SUV39H1 and SUV39H2 across the Cancer Genome Atlas (TCGA) cohort to investigate their expression, prognostic relevance, associations with the immune landscape, and interactions with nuclear lamina genes. Both enzymes were significantly overexpressed in multiple tumor types, with SUV39H2 showing particularly high expression in high-grade serous ovarian cancer (HGSOC), where elevated levels correlated with poor overall survival (HR = 3.27, p < 0.001). Immune infiltration analysis revealed that high SUV39H2 expression was inversely associated with tumor-infiltrating lymphocytes, indicating reduced immune infiltration. Correlation studies demonstrated strong positive associations between SUV39H1/H2 and Lamin B genes (LMNB1, LMNB2), suggesting an association with nuclear lamina-linked heterochromatin. Conversely, Lamin A (LMNA) exhibited weak or negative correlation with SUV39 enzymes. Functional validation in A2780 ovarian cancer cells demonstrated that pharmacological inhibition of SUV39H2 by Chaetocin resulted in the upregulation of Lamin A, suggesting that SUV39H1/H2 inhibition is associated with Lamin A regulation. Collectively, our findings uncover a previously underappreciated association between SUV39H2, chromatin-lamina interactions, and immune evasion in ovarian cancer, highlighting SUV39H2 as a potential chromatin-associated biomarker and regulator of nuclear organization and providing a rationale for targeting SUV39H2 in therapeutic epigenetic interventions. - Source: PubMed
Publication date: 2026/04/09
Kundu SubhadipAkhtar Abdur RahmaanKumar ArunSharma Ashok