LMNB1 Antibody
- Known as:
- LMNB1 Antibody
- Catalog number:
- abx001562
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- LMNB1 Antibody
Related 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
- The endomembrane system plays a pivotal role in protein synthesis, trafficking, and degradation, and has been implicated in colorectal cancer (CRC) progression. Post-translational modifications (PTMs) regulate endomembrane-associated proteins, but a comprehensive understanding of how multiple PTMs collectively impact the endomembrane system in CRC remains limited. This study aimed to systematically map multi-PTM landscapes in CRC and uncover potential regulatory nodes within the endomembrane system. - Source: PubMed
Publication date: 2026/06/25
Du JieZhang WeiSong WencongZhang YujieHao ErjiaoLi TianyuanFeng MinZhu FengDai Yong - Lung squamous cell carcinoma (LUSC) remains one of the leading causes to global cancer mortality, yet effective molecular-targeted therapies are lacking. Dysregulation of cell cycle checkpoint genes is common in LUSC, but therapeutic inhibition of CDK4/6 has yielded disappointing clinical outcomes. Guanine nucleotide-binding protein-like 3-like protein (GNL3L), a conserved nucleolar GTPase and G2/M checkpoint regulator, has been implicated in several malignancies, though its role in LUSC remains undefined. - Source: PubMed
Publication date: 2026/06/26
Hu HongWang YueLi HangChen HaiqingShao LonglongDing XushengLi YuanWang Jie - Cellular senescence is increasingly recognized as a hallmark of Chronic Obstructive Pulmonary Disease (COPD), with higher levels in lung fibroblasts from COPD patients. Upon senescence, both hypomethylation and hypermethylation have been described, but not in COPD-derived fibroblasts yet. This study investigated whether altered DNA methylation can be a driver of fibroblasts senescence in COPD. Genome wide gene expression and DNA methylation data was generated from primary lung fibroblasts of 11 COPD stage IV patients and 10 matched controls. Gene expression of six well-known senescence genes was compared between COPD and control. COPD-associated senescence genes were correlated with their related CpG sites in an expression quantitative trait methylation (eQTM) analysis. Methylation levels of significant eQTMs were compared between COPD and control fibroblasts. A causal relationship between altered DNA methylation and senescence was validated in 5-Aza-2'-deoxycytidine (5-Aza-2'-dC)-treated primary lung fibroblasts. Gene expression of , , and was higher, while expression was lower in COPD-derived fibroblasts compared to control. A total of 19 eQTMs were found for the COPD-associated senescence genes , , and . Among these, seven CpG sites (four for and three for ) exhibited differential methylation between COPD and control. Treatment with 5-Aza-2'-dC led to global demethylation and increased senescence and importantly, confirmed the association between senescence and hypomethylation of the COPD-associated CpG site cg04924375. Altered DNA methylation is linked to fibroblast senescence in COPD and seven CpG sites are identified as potential epigenetic regulators of the senescence genes and . - Source: PubMed
Publication date: 2026/07/08
Lyu Yinde Vries MaaikeBanchero MartinGuryev VictorTimens Wimvan den Berge MaartenSarno FedericaBrandsma Corry-AnkeWoldhuis Roy R - Adult-onset autosomal dominant leukodystrophy (ADLD) is an ultra-rare inherited white matter disorder caused by variants in the gene. Here, we report a case of ADLD and characterize its typical magnetic resonance imaging (MRI) features, with the aim of facilitating its clinical recognition and differential diagnosis. - Source: PubMed
Publication date: 2026/06/03
Wang Yu-XinDu TongYang Chun-LinZhang MinDuan Rui-Sheng - Lamin B1 is a structural component of the nuclear lamina that participates in genome organization and transcriptional control. During adaptive immune responses, B lymphocytes in germinal centers (GCs) undergo clonal expansion and programmed DNA damage at immunoglobulin loci, while simultaneously downregulating Lamin B1. Likewise, Lamin B1 downregulation has been observed in GC-derived lymphomas and myeloid malignancies, yet the functional consequences of Lamin B1 loss during B cell development remain poorly understood. Here, we used in vivo and in vitro B cell models of conditional hypomorphic Lamin B1 expression, which showed elevated DNA damage and disrupted transcriptional profiles. Using sBLISS (in situ labeling and sequencing of double-strand breaks), we identified nonrandom double-strand break hotspots in both mouse and human GC B cells depleted of Lamin B1. These breaks are preferentially located near transcriptional start sites (TSSs) and regulatory elements that control translation and mRNA fate, suggesting Lamin B1 has a role in protecting regulatory genomic regions. Moreover, low LMNB1 expression is associated with poor clinical outcomes in patients with diffuse large B-cell lymphoma (DLBCL). Together, this study reveals a crucial role for Lamin B1 in preserving genomic stability in B cells, underscoring its impact on the pathogenesis of B cell-derived malignancies. - Source: PubMed
Publication date: 2026/06/07
Filipsky FilipChapman Katarina BBloehdorn JohannesMaiques OscarLee AbigailClear AndrewWang JunGribben JohnHausmann MichaelCremer ChristophBraun AndrejsSallan Marta CKlymenko Tanya