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Last update 08 May 2025

LMNB1

Last update 08 May 2025

Basic Info

Synonyms

lamin B1, Lamin-B1, LMN2

+ [2]

Introduction

Lamins are intermediate filament proteins that assemble into a filamentous meshwork, and which constitute the major components of the nuclear lamina, a fibrous layer on the nucleoplasmic side of the inner nuclear membrane (PubMed:28716252, PubMed:32910914). Lamins provide a framework for the nuclear envelope, bridging the nuclear envelope and chromatin, thereby playing an important role in nuclear assembly, chromatin organization, nuclear membrane and telomere dynamics (PubMed:28716252, PubMed:32910914). The structural integrity of the lamina is strictly controlled by the cell cycle, as seen by the disintegration and formation of the nuclear envelope in prophase and telophase, respectively (PubMed:28716252, PubMed:32910914).

Drugs associated with LMNB1

nL-LMNB1-001

Target

LMNB1

Mechanism

LMNB1 modulators

Active Org.

n-Lorem Foundation

Originator Org.

n-Lorem Foundation

Active Indication

Leukodystrophy, Demyelinating, Adult-Onset, Autosomal Dominant

Inactive Indication-

Drug Highest PhasePhase 1/2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with LMNB1

NCT06816498

/ Enrolling by invitationPhase 1/2IIT

An Open-label, Single-center, Single-participant Study of an Experimental Antisense Oligonucleotide Treatment for a Patient with LMNB1 Mutation Associated Autosomal Dominant Leukodystrophy (ADLD)

This research project entails delivery of a personalized antisense oligonucleotide (ASO) drug designed for a single participant with Autosomal Dominant Leukodystrophy (ADLD) due to LMNB1 mutation

Start Date01 Feb 2025

Sponsor / Collaborator

n-Lorem Foundation

[+1]

100 Clinical Results associated with LMNB1

100 Translational Medicine associated with LMNB1

0 Patents (Medical) associated with LMNB1

792

Literatures (Medical) associated with LMNB1

31 Dec 2025·Animal Cells and Systems

Lamin B1 regulates RNA splicing factor expression by modulating the spatial positioning and chromatin interactions of the ETS1 gene locus

Article

Author: Kim, Chul-Hong ; Kim, Jinho ; Jo, Ah-Ra ; Kim, Ji-Young ; Park, Yuna ; Kim, Jung-Woong ; Hwangbo, Yujeong ; Shin, Geun-Seup ; An, Mi-Jin ; Lee, Hyun-Min

Lamin B1, a crucial component of the nuclear lamina, plays a pivotal role in chromatin organization and transcriptional regulation in eukaryotic cells. While recent studies have highlighted the connection between Lamin B1 and RNA splicing regulation, the precise molecular mechanisms remain elusive. In this study, we demonstrate that Lamin B1 depletion leads to a global reduction in splicing factor expression, as evidenced by analysis of multiple RNA-seq datasets. Motif analysis suggests that members of the ETS transcription factor family likely bind to the promoter regions of these splicing factors. Further analysis using transcription factor databases and ChIP-seq data identified ETS1 as a key regulator of splicing factor expression. Hi-C sequencing revealed that the loss of Lamin B1 disrupts inter-LAD chromatin interactions near the ETS1 gene locus, resulting in its downregulation. These findings suggest that Lamin B1 indirectly regulates RNA splicing by sustaining proper ETS1 expression, uncovering a novel link between nuclear architecture, gene regulation, and RNA splicing.

01 Sep 2025·Comparative Biochemistry and Physiology Part D: Genomics and Proteomics

Biochemical indices, histological observations and transcriptome sequencing reveal the response mechanism of largemouth bass (Micropterus salmoides) to transport stress

Article

Author: Qiang, Jun ; Wang, Qing Chun ; Hua, Jixiang ; Duan, Xue Jun ; Tao, Yi Fan

In this study, transport conditions were simulated to investigate changes in intestinal tissue structure, oxidative stress, apoptosis and transcriptome levels during transport stress of largemouth bass (Micropterus salmoides). The results showed that the serum cortisol and lactic acid levels in largemouth bass significantly increased with increasing transport time, and the glucose content peaked after 8 h of transport. After 8 h and 12 h, the Reactive oxygen species, superoxide dismutase, malondialdehyde, and lipid peroxide contents in the intestine were significantly higher than those in the control group and the stressed group at 4 h. Additionally, more of the mucous membrane of intestinal tissue was exfoliated, resulting in edema, and the intestinal villi height and density significantly decreased. The differentially expressed genes were further analyzed after 0 h, 8 h, and 12 h of transport stress. There were significant differences in genes associated with the p53 signaling pathway (igfbp1a, ccnb1, cdk1, and igfbp6b) and apoptosis (bcl2l11, parp3, pik3r1, fadd, aifm1, and lmnb1). Combined with the increasing amount of apoptotic cells after stress, these results indicated that transport stress had a substantial effect on intestinal cell apoptosis. The intestinal antioxidant activity and tissue structure of the stressed groups recovered to the pre-stress level after 7 d of recovery from 8 h of transport; however, these parameters did not return to pre-stress levels after 7 d of recovery from 12 h of transport. This finding further demonstrated that long-term transport stress induced apoptosis and tissue damage in the largemouth bass intestine through p53 signaling.

01 Jun 2025·Current Cancer Drug Targets

LMNB1/CDKN1A Signaling Regulates the Cell Cycle and Promotes Hepatocellular Carcinoma Progression

Article

Author: Liu, Zhaochen ; Bao, Liang ; Gao, Dute ; Dang, Xiaowei ; Qiu, Jiange ; Wang, Yunchao ; Li, Suxin ; jiang, Binghua ; Guo, Huahu

Background:Hepatocellular carcinoma (HCC) is one of the most aggressive malignancies in the world. Lamin B1 (LMNB1) is a key component of the nuclear skeleton structure. Recent studies have found that LMNB1 is overexpressed in tumor tissues and is associated with the prognosis of patients. However, the underlying mechanism remains unclear in HCC.Objective:This study aims to explore the clinical significance and molecular mechanisms of LMNB1 in HCC.Methods:The expression level of LMNB1 and its clinical values were analyzed with public databases, and the level of LMNB1 in HCC tissues and adjacent normal tissues was confirmed by qRT-PCR and IHC. Functional assays were conducted to explore the impact of LMNB1 knockdown on cell proliferation both in vivo and in vitro. Additionally, Genes and Genomes enrichment analysis, recovery analysis, and ChIP assays were employed to investigate its underlying molecular mechanisms. Finally, we carried out an analysis of the relationship between LMNB1 and immune cell infiltration in HCC.Results:LMNB1 was found to be overexpressed in HCC and correlated with the pathological stage and unfavorable prognosis. Functional assays demonstrated that LMNB1 promotes HCC proliferation both in vitro and in vivo. Further analysis revealed that LMNB1 promotes the progression of HCC by regulating CDKN1A expression. Furthermore, the infiltration of immune cells in HCC tissues suggests a potential correlation between immune infiltration cell markers and the expression of LMNB1.Conclusions:LMNB1 emerged as a promising therapeutic target and prognostic biomarker for HCC, with its expression showing a correlation with several immune infiltration cell markers.

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