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
- Glioblastoma (GBM) remains a lethal malignancy characterized by therapeutic resistance and recurrence. Emerging evidence suggests that senescent niches may shape tumor progression, support tumor stemness, and modulate immune engagement. We integrated transcriptomic data from the Glioma Longitudinal Analysis Consortium (GLASS; 118 primary and 113 recurrent IDH-wildtype GBM samples) with protein-level analysis from an independent cohort of 37 GBM patients (25 primary, 12 recurrent), including 6 matched primary-recurrent pairs. Senescence-, stemness-, and immune-related pathways were assessed using single-sample gene set enrichment analysis (ssGSEA), while immunohistochemistry quantified the expression of Lamin B1, Ki67, p53, SOX2, HLA-DRA, B2M, and CD56. Transcript-level validation was performed using matched-pair Wilcoxon testing in 101 GLASS pairs. Recurrent tumors demonstrated increased enrichment of senescence-associated transcriptional programs, including upregulated KAMMINGA_SENESCENCE and reduced TANG_SENESCENCE_TP53_TARGETS_DN scores. Lamin B1 and Ki67 protein levels were significantly lower in recurrent tumors (p = 0.004 and p = 0.016), while p53 expression increased overall (p = 0.001), suggestive of a senescence enrichment upon recurrence. In the matched analysis (6 pairs; 12 samples total), Lamin B1 and Ki67 generally trended lower at recurrence, although paired differences were not statistically significant. SOX2 expression remained broadly stable at the protein level but showed a modest decrease in RNA expression. Immune markers (HLA-DRA, B2M, CD56) exhibited minimal differences, although HLA-DRA increased significantly overall at recurrence (p = 0.025). Matched transcriptomic analysis in GLASS pairs supported recurrent-specific reductions in LMNB1, MKI67, and SOX2, with no consistent changes in TP53, HLA-DRA, B2M, or NCAM1. Recurrent IDH-wildtype GBM exhibits a transcriptional and protein expression shift towards a senescence-associated state with no concomitant changes in SOX2 and select immune markers. - Source: PubMed
Publication date: 2026/05/06
Al Shboul SofianAlrjoub MoathAl Karsaneh Ola AbuSurakhy MirvatAlhesa AhmadEl-Sadoni MohammadAl-Sheyab MaramAlsoud AnoudFriehat KholoudKhasawneh Ashraf IAbabneh Nidaa AAlotaibi Moureq RHupp TedSaleh Tareq - Homology-directed repair (HDR) enables precise genome editing; however, its application in mammalian cells is limited by low efficiency owing to competition from error-prone repair pathways and intrinsically restricted HDR activity. Existing HDR-enhancement strategies, including small-molecule treatments and marker-based selection, are constrained by cytotoxicity, genomic scarring, and inconsistent performance. Here, we present essential-gene-supported scarless HDR (ESS-HDR), a robust, drug- and marker-free platform that selectively enriches HDR-proficient cells. By leveraging essential-gene coediting, ESS-HDR enables precise and scarless genome modification with enhanced efficiency. CRISPR-Cas9 induces double-strand breaks at both the target locus and an essential gene, accompanied by two donor templates: one introducing the desired edit and the other restoring essential-gene function. Only cells that undergo accurate HDR at the essential locus survive, providing endogenous selection without exogenous markers. Single-cell clone analysis confirms that enrichment of HDR-proficient cells enhances editing at the target locus. Using ssODN donors carrying a 1 nucleotide substitution or a 10 nucleotide insertion, ESS-HDR increases HDR efficiencies by sevenfold to 16-fold in HEK293 cells and 41-fold in primary epidermal keratinocytes compared with conventional single-site HDR. With plasmid donors targeting , , or , ESS-HDR improves knock-in efficiencies by sixfold to 34-fold across HEK293, U2OS, and HeLa cells. ESS-HDR also outperforms chemical enhancers including RS-1, SCR7, nocodazole, and AZD7648. Together, these findings establish ESS-HDR as a broadly applicable strategy for efficient, scarless genome editing without external selection markers. - Source: PubMed
Publication date: 2026/05/15
Yeo Joo HyeKim Hyongbum HenryOh Sang HoLee Jinu - 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 - Aging is a long-term and complex process characterized by cellular changes, including cell cycle arrest, increased production of the senescence-associated secretory phenotype (SASP), and nuclear membrane disintegration. To accelerate the aging process, various animal models are made using chemical inducers, such as D-galactose (D-Gal). D-Gal has been extensively applied to induce aging in experimental animals; however, its effects on the gastrointestinal system, particularly the colon, remain underexplored. Observation of molecular aging markers will provide a valuable approach to assess these cellular changes. This study aimed to observe the expression of genes related to cell cycle arrest (p53 and Cdkn1a), SASP production (Il-6 and Il-1β), nuclear membrane disintegration (Lmnb1), as well as histological inflammation process in the colon of D-Gal-induced aging rat models. Twelve-week-old male Sprague-Dawley rats (n = 12) were divided into the control and D-Gal (100 mg/kg/day for 6 weeks) groups. The expression levels of aging-related genes (p53, Cdkn1a, Il-6, Il-1β, and Lmnb1) were assessed by reverse-transcription quantitative polymerase chain reaction. The D-Gal group exhibited inflammatory cell infiltration. Il-1β immunohistochemical score along with Il-1β expression was significantly elevated in D-Gal group (p < 0.01), suggesting SASP activation and pro-inflammatory signaling. No statistically significant differences were observed in the expression levels of p53, Il-6, Cdkn1a, or Lmnb1 expression. Molecular and histological results demonstrated that D-Gal administration induces colonic inflammation, characterized by increased Il-1β expression, which subsequently promotes potential cellular senescence. - Source: PubMed
Publication date: 2026/03/18
Azaria CherrySusilowati RinaSumiwi Yustina Andwi AriPurnomosari Dewajani - Precise control of keratinocyte proliferation and differentiation is critical for oral epithelial regeneration, yet the mechanobiological cues guiding these processes remain incompletely defined. Here, we systematically evaluated how electrospun polycaprolactone (PCL) scaffolds with defined fiber orientations (aligned vs. random) and diameters (600-800 nm, 1.2-1.7 µm, 2.0-2.5 µm) direct gingival keratinocyte fate. Using immortalized human gingival keratinocytes, we assessed cell and nuclear morphology, proliferation dynamics, differentiation marker expression, and the effects of basal keratin (KRT5/KRT14) knockdown. Quantitative morphological analysis revealed scaffold-dependent changes in cell shape: aligned medium-diameter fibers (with fiber diameters of 1.2-1.7 µm) induced pronounced cell and nuclear elongation, whereas random fibers (600-800 nm) promoted larger, more rounded cell and nuclear shapes. Time-resolved EdU assays indicated that aligned scaffolds supported sustained proliferation, whereas random scaffolds elicited a transient proliferative burst followed by a decline. Gene expression analysis (ddPCR) demonstrated that random scaffolds (especially 600-800 nm fibers) upregulated basal keratins (KRT5, KRT14) and early differentiation markers (KRT1, KRT10, KRT4, KRT13) relative to aligned scaffolds. At the protein level, differentiation markers involucrin (IVL) and filaggrin (FLG) were likewise elevated on random scaffolds, corroborating the mRNA findings. Functional KRT5/KRT14 knockdown experiments revealed scaffold-specific dependencies: cells on random scaffolds required these keratins for viability, whereas aligned cultures remained viable upon KRT5/14 loss. Furthermore, KRT5/14 depletion differentially altered downstream differentiation markers (IVL, KRT1) and mechanotransduction markers (LMNB1, YAP1) in a scaffold-dependent manner. Collectively, these findings establish fiber orientation and diameter as key design parameters for controlling keratinocyte fate. As a translational concept, layered scaffolds combining aligned and random fibers may enable spatially controlled proliferation and differentiation in engineered oral epithelia. - Source: PubMed
Publication date: 2026/02/05
Ramminger ImkeSteinberg ThorstenRolauffs BerndSelig MischaTomakidi Pascal