Ask about this productRelated genes to: LMNB1 antibody
- Gene:
- LMNB1 NIH gene
- Name:
- lamin B1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-28
- Date modifiied:
- 2014-11-19
Related products to: LMNB1 antibody
Related articles to: LMNB1 antibody
- Liposarcoma (LPS) is a common soft tissue sarcoma; however, its molecular pathogenesis and immune cell infiltration remain poorly understood. This study investigated potential driver genes and pathways in LPS and characterized immune cell infiltration patterns to identify potential markers for targeted therapy. Differentially expressed genes (DEGs) in LPS were analyzed by GO and KEGG pathway enrichment analysis. A protein-protein interaction network was constructed using the STRING database and visualized with Cytoscape. mRNA expression of genes with high |logFC| values was verified by RT-qPCR. Immune cell subsets were quantified using CIBERSORT. GO and KEGG analysis revealed significant functional clusters and pathways, and most verified genes were consistent with the bioinformatics analysis. Survival analysis showed that high expression of TYMS, KIF20A, BUB1B, LMNB1, RRM2, ZWINT, and RACGAP1 was significantly associated with poor overall survival and poor disease-free survival (DFS). High levels of TMSB15A, TPX2, PKM2, and PTTG1 were significantly associated with poor DFS alone. CIBERSORT analysis identified a significantly higher fraction of resting mast cells (MCs) in LPS tissues compared to normal fatty tissues (P < 0.05). TOP2A, IL-6, PCNA, CDK1, JUN, MYC, CCNB1, EGFR, ACACB, and BIRC5 were identified as potential diagnostic biomarkers of LPS, providing strong evidence for hub gene studies. Immune cell infiltration analysis further suggested that resting MCs may play a potential role in LPS development, although further experimental validation is warranted. Collectively, these findings clarify the molecular basis of LPS and provide a foundation for future research into its treatment. - Source: PubMed
Publication date: 2026/09/11
Liu ChunxiaoWang YanhuaLiu QiuxiaZhang Sha - Cerebral small vessel disease (CSVD) describes a range of neurological diseases affecting the small arteries, veins, and capillaries which supply the white matter and deep grey matter structures of the brain. They are the most common form of cerebrovascular disease, accounting for almost half of vascular dementia cases and approximately 20% of stroke incidence globally. Genetic testing is a routine diagnostic tool for monogenic CSVDs; however, less than 20% of patients have a causal variant in a known gene. Genetic testing for these disorders focuses on single nucleotide variants and short insertions or deletions, with larger genomic variation often unexplored as a cause of disease. In this study we performed whole-exome sequencing (WES) on 111 patients suspected of familial CSVD that had previously tested negative for pathogenic variants in seven known CSVD genes (NOTCH3, HTRA1, COL4A1, COL4A2, TREX1, GLA, and FOXC1). Bioinformatic analysis of WES data, multiplex ligation-dependent probe amplification, quantitative real-time polymerase chain reaction assays, and Nanopore long-read sequencing were used to identify suspected copy number variants. This work identified four candidate CNVs across NOTCH3, LMNB1, and COL4A2 which are potential causes of CSVD and highlights the need for further investigation of more complex forms of genetic variation and their potential roles as causal of CSVD. - Source: PubMed
Publication date: 2026/08/27
Guyler Solomon KMaksemous NevenLea Rodney ASmith Robert ASutherland Heidi GGriffiths Lyn R - Ultraviolet B (UVB) radiation is a major environmental factor contributing to skin photoaging through excessive reactive oxygen species (ROS) generation, activation of stress-responsive signaling pathways, DNA damage, cellular senescence, and extracellular matrix (ECM) degradation. Mangiferin, a naturally occurring xanthone glucoside with potent antioxidant and anti-inflammatory properties, has attracted considerable interest as a potential photoprotective agent. The present study investigated the protective effects of mangiferin against UVB-induced photoaging in human dermal fibroblasts (HDFs). The effects of mangiferin on oxidative stress, RAGE/NF-κB/MAPK signaling, DNA damage, cellular senescence, and ECM degradation were evaluated. Mangiferin significantly suppressed UVB-induced ROS accumulation and attenuated activation of the RAGE/NF-κB/MAPK signaling cascade. Furthermore, mangiferin reduced γ-H2AX expression, indicating protection against UVB-mediated DNA damage, while decreasing p16, p21, and p53 expression and restoring LMNB1 levels. Mangiferin also inhibited MMP-2 and MMP-9 activities as well as collagenase, elastase, and hyaluronidase activities, suggesting preservation of ECM homeostasis. These findings demonstrate that mangiferin protects dermal fibroblasts against UVB-induced photoaging through suppression of oxidative stress, inhibition of RAGE/NF-κB/MAPK signaling, attenuation of DNA damage and cellular senescence, and preservation of ECM integrity, supporting its potential application in photoprotective and anti-photoaging dermocosmetic formulations. - Source: PubMed
Publication date: 2026/07/25
Kurt-Celep İnci - Senescence-associated secretory phenotype (SASP) signaling, along with key markers such as and , has not been systematically studied in circulating lymphocyte subsets in head and neck squamous cell carcinoma (HNSCC). This study aimed to evaluate SASP-related genes and senescence markers in peripheral CD4, CD8, and CD19 cells and assess their clinical relevance. Expression of , , , , /, and was measured by RT-qPCR in sorted lymphocytes from 58 HNSCC patients at baseline, 31 post-treatment, and 13 controls. Statistical analyses included nonparametric tests, correlation analyses, and survival models (Kaplan-Meier, Cox regression). In the results, was significantly upregulated in all lymphocyte subsets of HNSCC patients. , , and were elevated in CD4 T cells. A coordinated co-expression network involving , , , /, and was observed. Clinically, in CD8 T cells was associated with higher nodal stage and worse survival, while in CD19 B cells independently predicted survival. No differences were found between pre- and post-treatment samples. Circulating lymphocytes in HNSCC display coordinated expression of selected senescence-associated genes, with and as candidate prognostic biomarkers linked to tumor progression that warrant further validation. - Source: PubMed
Publication date: 2026/08/18
Ostrowska KamilaNiewinski PatrykPiotrowski IgorKubicka AgataOstapowicz JuliaKozikowska JuliaJazikowska AleksandraCzochór KarolinaMarchlewska JoannaProcyk DanutaLeporowska EwaSuchorska Wiktoria MYousefzadeh Matthew JMasternak Michal MGolusiński Wojciech - Nuclear lamina integrity is fundamental to cellular homeostasis across the lifespan , and its progressive deterioration is closely linked to human aging . Yet, the regulatory mechanism that govern this decline and how they might be counteracted in long-lived individuals remain poorly defined. Here, by combining whole-exome sequencing of Ashkenazi Jewish centenarians with GTEx transcriptomes, we identify ubiquitin E3 ligase UBE3C strongly associated with exceptional longevity and progressively declines with age across human tissues. UBE3C knockdown triggers premature senescence and destabilizes key nuclear lamina components Lamin B1 (LMNB1) and Lamin B receptor (LBR), while the longevity-associated UBE3C variant delays senescence and preserves LMNB1/LBR expression. Mechanistically, UBE3C interacts directly with LMNB1/LBR and modulates their abundance via selective autophagy. Notably, we uncover the ER- resident autophagy trigger CKAP4 bridges UBE3C and LMNB1. UBE3C loss enhances LMNB1-CKAP4 binding, linking nuclear lamina turnover to autophagy. Together, our findings establish UBE3C as a central guardian of nuclear lamina maintenance during senescence and offering novel insights into interventions against age-related nuclear lamina deterioration. - Source: PubMed
Publication date: 2026/08/06
Guan DiKim SeungsooOmar KarimHao YingHuang GordonHan HyeRimYang JipingHorwitz NaftaliDinh Phuong-AnhHwang JihyunYu HaiyuanSuh Yousin