Affinage

LMNB1

Lamin-B1 · UniProt P20700

Round 2 corrected
Length
586 aa
Mass
66.4 kDa
Annotated
2026-04-28
71 papers in source corpus 26 papers cited in narrative 26 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

LMNB1 encodes lamin B1, a type-V intermediate filament protein that polymerizes into a stable meshwork within the nuclear lamina, where it is essential for nuclear envelope integrity, lamina microdomain organization, and global chromatin architecture (PMID:19141474, PMID:23934658). Lamin B1 interacts with the inner nuclear membrane protein LAP2 in a phosphorylation-regulated manner (PMID:8324822), is cleaved by caspases to facilitate nuclear disassembly during apoptosis (PMID:8978814), and is degraded via LC3-mediated selective autophagy upon oncogenic RAS activation to drive senescence (PMID:26524528). Its decline during cellular senescence—triggered by decreased mRNA stability downstream of p53 and pRb (PMID:22496421)—reorganizes lamin-associated domains and histone modification landscapes genome-wide (PMID:23934658), while its overexpression increases nuclear stiffness and impairs neuronal migration (PMID:39078102); gain-of-function LMNB1 duplications cause autosomal dominant adult-onset demyelinating leukodystrophy (ADLD) through TAD-dependent misexpression rather than simple gene dosage (PMID:39078102), and de novo missense mutations cause primary microcephaly (PMID:32910914).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1993 High

    Identifying LAP2 as a lamin-B1-specific binding partner whose interaction is abolished by mitotic phosphorylation established that the nuclear lamina is organized through regulated protein–protein interactions rather than passive polymerization.

    Evidence In vitro reconstituted binding assays with phosphorylation modulation, immunofluorescence during mitosis

    PMID:8324822

    Open questions at the time
    • Phosphorylation sites on LAP2 mediating the switch were not mapped
    • Structural basis of selectivity for lamin B1 over A/C was not determined
  2. 1995 High

    Determining the complete exon–intron organization of human and mouse LMNB1 revealed a conserved 11-exon gene with a CpG island housekeeping promoter, providing the structural framework for interpreting disease-causing rearrangements.

    Evidence Genomic cloning, restriction mapping, and promoter analysis in human and mouse

    PMID:7557986 PMID:8586436

    Open questions at the time
    • Functional cis-regulatory elements beyond the core promoter were not characterized
    • Tissue-specific regulatory regions were not identified
  3. 1996 High

    Demonstrating that caspase-mediated cleavage of lamin B is required for chromatin condensation and nuclear shrinkage during apoptosis established lamin disassembly as a functional prerequisite for apoptotic nuclear destruction.

    Evidence Cleavage-resistant lamin B mutant expression attenuated apoptosis in vivo and in vitro

    PMID:8978814

    Open questions at the time
    • Identity of the specific caspase(s) responsible was not resolved
    • Whether lamin B1 and B2 are cleaved with different kinetics was not tested
  4. 2008 High

    Showing that lamin B1 silencing expands lamina meshwork spacing, increases lamin A nucleoplasmic mobility, and generates gene-rich euchromatin-containing nuclear blebs with impaired transcription established lamin B1 as a master organizer of lamina microdomains and chromatin–lamina contacts.

    Evidence RNAi, fluorescence correlation spectroscopy, FISH, CGH of microdissected blebs in HeLa cells

    PMID:19141474

    Open questions at the time
    • Mechanism of Pol II stalling at promoters in blebs was not defined
    • Whether lamin B2 compensates partially was not evaluated
  5. 2012 High

    Establishing that lamin B1 mRNA and protein decline during replicative, oncogene-induced, and DNA-damage-induced senescence via reduced mRNA stability downstream of p53 or pRb—validated in vivo—identified lamin B1 loss as a universal senescence effector and biomarker.

    Evidence qPCR, mRNA stability assays, p53/pRb genetic epistasis, in vivo irradiation model across multiple cell types

    PMID:22155925 PMID:22496421

    Open questions at the time
    • RNA-binding protein or miRNA mediating mRNA destabilization was not identified
    • Whether p53 and pRb act through the same mRNA decay machinery was unresolved
  6. 2013 High

    Genome-wide ChIP-seq showing that lamin B1 reduction triggers H3K4me3 'mesas' at lamin-associated domains and H3K27me3 'canyons' established lamin B1 as a guardian of the heterochromatin landscape, linking its loss to the global epigenomic remodeling of senescence.

    Evidence ChIP-seq for H3K4me3 and H3K27me3, genome-wide LAD mapping, lamin B1 knockdown and oncogene-induced senescence

    PMID:23934658

    Open questions at the time
    • Causality between individual LAD detachment events and specific gene expression changes was not demonstrated
    • Kinetics of chromatin reorganization relative to senescence commitment were unclear
  7. 2013 High

    Characterizing ADLD duplication junctions at nucleotide resolution and demonstrating that all three LMNB1 alleles are expressed equally showed that ADLD arises from bona fide gene dosage increase with intact regulatory elements.

    Evidence Molecular junction analysis, allele-specific sequencing, RT-PCR and immunoblotting in patient fibroblasts

    PMID:23649844

    Open questions at the time
    • Cell-type specificity of demyelination despite ubiquitous LMNB1 expression was unexplained
    • Whether overexpression acts through chromatin, nuclear mechanics, or both was unknown
  8. 2015 High

    Discovering that nuclear LC3 directly binds lamin B1 and mediates its selective autophagic degradation upon oncogenic RAS stress—but not during starvation—revealed a targeted nucleus-to-cytoplasm disposal pathway that is required for oncogene-induced senescence.

    Evidence Co-IP, proximity ligation, nuclear fractionation, autophagy genetic knockouts, lysosome inhibition, live imaging

    PMID:26524528

    Open questions at the time
    • Nuclear export receptor mediating lamin B1 transport to cytoplasm was not identified
    • Whether LC3-mediated degradation also targets lamin B2 was not tested
  9. 2020 High

    Identifying de novo LMNB1 missense mutations in microcephaly patients—with functional demonstration that head-domain variants impair nuclear localization and coil-domain variants reduce protein stability—expanded the disease spectrum of LMNB1 beyond ADLD to developmental brain disorders.

    Evidence Immunofluorescence of nuclear lamina formation, nuclear morphology quantification, immunoblotting in patient lymphoblasts

    PMID:32910914

    Open questions at the time
    • How reduced lamin B1 function selectively affects brain size was not established
    • No animal model was generated for the specific missense variants
  10. 2024 High

    Demonstrating that atypical ADLD results from TAD boundary disruption causing forebrain-specific LMNB1 misexpression—rather than simple dosage gain—resolved the long-standing question of how structurally different LMNB1 rearrangements converge on the same disease.

    Evidence Hi-C chromatin conformation, RNA-seq, postmortem histopathology

    PMID:39078102

    Open questions at the time
    • Which ectopic enhancer(s) drive forebrain misexpression was not pinpointed
    • Therapeutic strategies to re-insulate the TAD boundary were not explored
  11. 2024 Medium

    ChIP and reporter assays showing LMNB1 directly binds the promoters of CDKN1A and GPR84 to regulate their transcription, and DNA pull-down showing LMNB1 binds HBV enhancer DNA in an acetylation-dependent manner, collectively established lamin B1 as a direct transcriptional regulator beyond its structural role.

    Evidence ChIP assays, dual-luciferase reporters, DNA pull-down, acetylation site mutagenesis across HCC, lung cancer, and HBV systems

    PMID:38265511 PMID:38778606 PMID:39357468

    Open questions at the time
    • Genome-wide binding profile (ChIP-seq) for LMNB1 as a transcription factor is lacking
    • How lamin B1 accesses promoters distinct from lamina-associated domains is unknown
    • CDKN1A occupancy finding is from a single low-confidence study
  12. 2024 Medium

    Showing that WTAP-dependent m6A methylation of LMNB1 mRNA stabilizes it and modulates downstream NF-κB/JAK-STAT signaling revealed an epitranscriptomic layer of LMNB1 regulation relevant to inflammatory contexts.

    Evidence meRIP, RIP, dual-luciferase reporter, actinomycin D stability assay in LPS-treated kidney cells

    PMID:38517565

    Open questions at the time
    • Specific m6A sites on LMNB1 mRNA were not mapped at single-nucleotide resolution
    • In vivo relevance of epitranscriptomic regulation of LMNB1 was not tested
    • Relationship between m6A-mediated stabilization and the p53/pRb-mediated destabilization during senescence is unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the identity of the RNA-binding factor(s) mediating senescence-associated LMNB1 mRNA destabilization, the genome-wide binding landscape of LMNB1 as a transcriptional regulator, and the cell-type-specific mechanisms by which LMNB1 overexpression selectively damages oligodendrocytes in ADLD.
  • No RNA decay factor identified for senescence-driven LMNB1 mRNA loss
  • No LMNB1 ChIP-seq as a transcription factor
  • Oligodendrocyte-specific vulnerability in ADLD unexplained

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 3 GO:0005198 structural molecule activity 3 GO:0008092 cytoskeletal protein binding 2 GO:0140110 transcription regulator activity 2
Localization
GO:0005634 nucleus 4 GO:0005635 nuclear envelope 4 GO:0000228 nuclear chromosome 2
Pathway
R-HSA-1643685 Disease 3 R-HSA-4839726 Chromatin organization 3 R-HSA-8953897 Cellular responses to stimuli 3 R-HSA-5357801 Programmed Cell Death 2 R-HSA-74160 Gene expression (Transcription) 2 R-HSA-9612973 Autophagy 1
Partners
ENPP1LC3LMNATMPOTOR1AZFP335
Complex memberships
nuclear lamina

Evidence

Reading pass · 26 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 The human LMNB1 gene spans more than 45 kb and is organized into 11 exons encoding an intermediate filament protein: exon 1 codes for the amino-terminal head domain and first portion of the central rod domain, exons 2–6 the central rod domain, and exons 7–11 the carboxyl-terminal tail domain. Intron positions are conserved with other vertebrate lamin genes but differ from Drosophila and C. elegans lamins. Genomic cloning and structural analysis of transcription unit Genomics High 7557986
1995 The mouse Lmnb1 gene spans ~43 kb with 11 exons and 10 introns, with a promoter region containing a CpG island, CAAT box, and multiple SP1 sites but no classical TATA box, consistent with a housekeeping gene promoter. Genomic cloning and promoter analysis Genomics High 8586436
1996 LMNB1 was mapped by fluorescence in situ hybridization to chromosomal band 5q23.3–q31.1 in humans. Fluorescence in situ hybridization (FISH) Genomics High 8838815
1993 LAP 2, an integral membrane protein of the nuclear envelope, specifically associates with lamin B1 (but not lamins A/C), and this binding is inhibited by mitotic phosphorylation of LAP 2; LAP 2 also binds mitotic chromosomes and associates with chromosomes prior to lamin assembly during nuclear envelope reassembly. In vitro binding assays, phosphorylation by mitotic cytosol, immunofluorescence Cell High 8324822
1996 Lamin B (along with lamin A/C) is cleaved by ICE-family cysteine proteases during apoptosis; expression of a cleavage-resistant mutant lamin B attenuated apoptosis and prevented chromatin condensation and nuclear shrinkage, demonstrating that lamin proteolysis facilitates nuclear events of apoptosis. Site-directed mutagenesis, in vitro and in vivo cleavage assays, morphological analysis The Journal of cell biology High 8978814
2008 Lamin B1 (LB1) forms a separate but interacting stable meshwork from A-type lamins in the nuclear lamina. Silencing LB1 dramatically increases lamina meshwork size, increases nucleoplasmic lamin A mobility, causes lamin A/C-rich nuclear envelope blebs lacking LB2, and leads to association of gene-rich euchromatin with these blebs; transcription is decreased despite enrichment of active marks, suggesting promoter-proximal Pol II stalling. Thus LB1 is essential for lamin microdomain organization. RNAi knockdown, fluorescence correlation spectroscopy (FCS), CGH of microdissected blebs, FISH, immunofluorescence, in vivo RNA labeling Genes & development High 19141474
2011 LB1 expression decreases during replicative senescence and oncogene-induced senescence in WI-38 cells. Silencing LB1 slows proliferation via p53-dependent reduction in mitochondrial ROS and induces premature senescence requiring both p53 and pRb. Conversely, LB1 overexpression increases proliferation and delays senescence. Eventually LB1 overexpression leads to G1/S arrest. siRNA knockdown, overexpression, flow cytometry, ROS measurements, hypoxia rescue experiments Genes & development High 22155925
2012 Lamin B1 protein and mRNA are lost when primary human and murine cells undergo senescence induced by DNA damage, replicative exhaustion, or oncogene expression. Loss occurs at the mRNA level via decreased mRNA stability (not caspase-mediated degradation). Activation of either p53 or pRb tumor suppressor pathways is sufficient to induce LB1 loss. LB1 protein and mRNA also decline in mouse tissues after irradiation-induced senescence in vivo. Immunoblotting, qPCR, mRNA stability assays, genetic pathway analysis (p53/pRb), in vivo irradiation model Molecular biology of the cell High 22496421
2013 Lamin B1 reduction in proliferating cells triggers senescence and large-scale chromatin reorganization, including formation of H3K4me3-enriched 'mesas' at lamin-associated domains (LADs) and H3K27me3-depleted 'canyons' between LADs. H3K4me3 mesas overlap DNA hypomethylation regions in cancer. Lamin B1 down-regulation is thus a key trigger of global chromatin changes that impact gene expression during senescence. ChIP-seq (H3K4me3, H3K27me3), genome-wide LAD mapping, lamin B1 knockdown, oncogene-induced senescence models Genes & development High 23934658
2015 The autophagy protein LC3/Atg8 is present in the nucleus and directly interacts with lamin B1. This interaction does not degrade lamin B1 during starvation but mediates its degradation upon activated RAS oncogene insult by nucleus-to-cytoplasm transport delivering lamin B1 to the lysosome. Inhibiting autophagy or the LC3–lamin B1 interaction prevents activated RAS-induced lamin B1 loss and attenuates oncogene-induced senescence. Co-immunoprecipitation, proximity ligation, nuclear fractionation, lysosome inhibition, autophagy genetic knockouts, live imaging Nature High 26524528
2012 BioID proximity-dependent biotinylation applied to lamin A identifies proteins that are near-neighbors or interactors of the nuclear lamina in vivo, including known lamin B1-proximal nuclear envelope proteins, establishing BioID as a method to map the lamin interactome including LMNB1-associated proteins. BioID (proximity-dependent biotin identification), affinity capture, mass spectrometry The Journal of cell biology Medium 22412018
2013 LMNB1 duplications causing ADLD are non-recurrent intrachromosomal events, arise by NHEJ or replication-based mechanisms (FoSTeS/MMBIR), and result in increased LMNB1 mRNA and protein in patient fibroblasts. All three LMNB1 alleles in ADLD patients show equal expression, indicating regulatory regions are maintained within the rearranged segment. Molecular analysis of duplication junctions at nucleotide level, allele-specific expression by sequencing, RT-PCR, immunoblotting Human mutation High 23649844
2013 A missense variant A436T in LMNB1, identified in neural tube defect patients, compromises the stability of lamin B1 interaction within the nuclear lamina as demonstrated by fluorescence loss in photobleaching (FLIP), suggesting that lamin B1 mobility/stability within the lamina is functionally important. Fluorescence loss in photobleaching (FLIP), mutant LMNB1 expression Birth defects research. Part A, Clinical and molecular teratology Medium 23733478
2020 De novo missense mutations in LMNB1 cause primary microcephaly. Two variants in the head domain decrease nuclear localization of LMNB1 and increase misshapen nuclei; a variant in the coil region increases frequency of condensed nuclei and reduces steady-state lamin B1 levels in proband lymphoblasts. All mutations impair formation of the LMNB1 nuclear lamina. Functional analysis of missense mutations: immunofluorescence of nuclear lamina formation, nuclear morphology quantification, immunoblotting of patient lymphoblasts American journal of human genetics High 32910914
2021 In human patient-specific cholinergic motor neurons (DYT1 dystonia with heterozygous TOR1A mutation), LMNB1 is upregulated and shows abnormal subcellular distribution. Ectopic expression of mutant TOR1A or shRNA knockdown of endogenous TOR1A in healthy MNs recapitulates LMNB1 dysregulation. Importantly, downregulation of LMNB1 largely ameliorates all DYT1 cellular defects including reduced neurite length, thickened nuclear lamina, disrupted nuclear morphology, and impaired nucleocytoplasmic transport. iPSC/fibroblast-derived human motor neurons, shRNA knockdown, ectopic TOR1A expression, immunofluorescence, nucleocytoplasmic transport assays The Journal of neuroscience High 33468570
2022 LMNB1 knockdown in lung adenocarcinoma cells decreases H3K9me3, increases chromosome accessibility (ATAC-seq), increases p53, p21, p16, and γ-H2AX protein expression, and increases senescence-positive cells, demonstrating that LMNB1 regulates heterochromatin compaction and suppresses DNA damage/senescence pathways in cancer cells. siRNA knockdown, ATAC-seq, immunofluorescence, TRAP, TUNEL, western blotting, xenograft model Frontiers in oncology Medium 35712471
2023 MDM2 (E3 ubiquitin ligase) increases p53 ubiquitination, which in turn activates LMNB1 expression. METTL3-mediated m6A methylation of MDM2 mRNA stabilizes it via YTHDF1, increasing MDM2→p53 ubiquitination→LMNB1 upregulation. Knockdown of LMNB1 reduces mitochondrial damage and ferroptosis markers in LPS-treated kidney tubular cells. Gene knockdown/overexpression, m6A methylation detection, YTHDF1 RIP assay, mitochondrial damage and ferroptosis assays European journal of medicinal chemistry Medium 37542992
2024 WTAP promotes LMNB1 expression via m6A methylation modification of LMNB1 mRNA, as demonstrated by meRIP assay, RIP, dual-luciferase reporter and actinomycin D stability assay. WTAP knockdown reduces LMNB1, suppressing NF-κB and JAK2/STAT3 pathway activation and reducing inflammation, mitochondrial damage, and ferroptosis in LPS-treated kidney cells. meRIP assay, RIP assay, dual-luciferase reporter, actinomycin D mRNA stability assay, pathway inhibitor experiments Journal of bioenergetics and biomembranes Medium 38517565
2024 LMNB1 directly binds the HBV enhancer II/basic core promoter (EnhII/BCP) DNA as shown by DNA pull-down assay. Acetylation of LMNB1 at residues K111 and K261 (increased by ENPP1) inhibits HBV promoter activity; LMNB1 acetylation mutants (111R, 261Q, 261R, 483Q, 483R) show increased promoter activity. Thus LMNB1 functions as a transcriptional repressor of HBV through acetylation-dependent DNA binding. DNA pull-down assay, luciferase reporter assay with promoter/mutant constructs, acetylation site mutagenesis, overexpression studies Archives of virology Medium 38265511
2024 Classic ADLD is caused by intra-TAD duplications of LMNB1 resulting in simple gene dose gain. Atypical ADLD is caused by inter-TAD deletions or duplications that lead to LMNB1 forebrain-specific misexpression by disrupting topologically associating domain boundaries. A duplication crossing two TAD boundaries did not cause ADLD, demonstrating that altered 3D genome architecture (TAD disruption) rather than mere copy number increase is the pathogenic mechanism in atypical ADLD. Hi-C (high-throughput chromosome conformation capture), RNA sequencing, histopathological analysis of postmortem brain Annals of neurology High 39078102
2025 Zfp335 transcription factor directly binds the promoter of Lmnb1 and regulates its transcription. Overexpression of Lmnb1 significantly rescues the impaired homeostatic proliferation of Zfp335-deficient naïve T cells, placing Lmnb1 downstream of Zfp335 in the T cell homeostasis pathway. ChIP assay (Zfp335 binding to Lmnb1 promoter), RNA-seq, qPCR, adoptive transfer model, Lmnb1 overexpression rescue Cell & bioscience Medium 41088342
2025 Excess Lamin B1 (LB1) in neurons halts neuronal migration in the developing cortex without altering laminar identity or global gene expression. In vitro, excess LB1 elevates nuclear stiffness and impairs neuronal motility in confined spaces. Computational modeling and live imaging validate that nuclear deformation dynamics correlate with migration velocity. Cerebral organoids from LMNB1-duplication patient iPSCs show impaired neuronal migration. In vivo mouse cortical electroporation, live imaging, micropipette aspiration (nuclear stiffness), confined migration assay, electrophysiology, computational modeling, patient iPSC cerebral organoids bioRxivpreprint Medium bio_10.1101_2025.10.22.683830
2025 Conditional hypomorphic reduction of Lamin B1 in B cells causes elevated DNA damage, altered chromatin accessibility, and disrupted transcriptional profiles. sBLISS identifies non-random double-strand break hotspots near transcriptional start sites and regulatory elements controlling translation and mRNA fate, revealing that Lamin B1 protects fragile regulatory chromatin regions from DNA damage in germinal center B cells. In vivo and in vitro B cell models with conditional Lamin B1 knockdown, sBLISS (in situ labeling and sequencing of DSBs), ATAC-seq, RNA-seq bioRxivpreprint Medium bio_10.1101_2025.11.03.686246
2024 LMNB1 promotes HCC cell proliferation by regulating CDKN1A (p21) expression, as revealed by GSEA pathway enrichment, recovery (rescue) analysis, and ChIP assays showing LMNB1 occupancy at the CDKN1A locus. GSEA, ChIP assay, recovery analysis, in vitro and in vivo proliferation assays with LMNB1 knockdown Current cancer drug targets Low 38778606
2017 LMNB1 knockdown in ovarian cancer cells suppresses proliferation and migration via inhibition of FGF1-mediated PI3K-Akt signaling, as revealed by RNA-seq and validated by pathway rescue experiments. Stable LMNB1 knockdown, RNA-seq, PI3K/Akt pathway analysis, xenograft model Experimental cell research Low 37003558
2024 LMNB1 activates GPR84 transcription and thereby promotes JAK2/STAT3-dependent M2 macrophage polarization in lung cancer; dual luciferase and ChIP assays confirm LMNB1 as a transcriptional activator of the GPR84 promoter. Dual luciferase reporter assay, ChIP assay, JAK-STAT pathway inhibitor experiments, co-culture macrophage polarization assay Human immunology Medium 39357468

Source papers

Stage 0 corpus · 71 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 A promiscuous biotin ligase fusion protein identifies proximal and interacting proteins in mammalian cells. The Journal of cell biology 1850 22412018
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2011 Systematic and quantitative assessment of the ubiquitin-modified proteome. Molecular cell 1334 21906983
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2005 Nucleolar proteome dynamics. Nature 934 15635413
2020 A reference map of the human binary protein interactome. Nature 849 32296183
2018 VIRMA mediates preferential m6A mRNA methylation in 3'UTR and near stop codon and associates with alternative polyadenylation. Cell discovery 829 29507755
2012 Lamin B1 loss is a senescence-associated biomarker. Molecular biology of the cell 812 22496421
2002 Directed proteomic analysis of the human nucleolus. Current biology : CB 780 11790298
2011 A proteome-wide, quantitative survey of in vivo ubiquitylation sites reveals widespread regulatory roles. Molecular & cellular proteomics : MCP 749 21890473
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2012 A census of human soluble protein complexes. Cell 689 22939629
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2010 Quantitative interaction proteomics and genome-wide profiling of epigenetic histone marks and their readers. Cell 639 20850016
2018 High-Density Proximity Mapping Reveals the Subcellular Organization of mRNA-Associated Granules and Bodies. Molecular cell 580 29395067
2017 Anticancer sulfonamides target splicing by inducing RBM39 degradation via recruitment to DCAF15. Science (New York, N.Y.) 533 28302793
2015 Autophagy mediates degradation of nuclear lamina. Nature 517 26524528
1993 Integral membrane proteins of the nuclear envelope interact with lamins and chromosomes, and binding is modulated by mitotic phosphorylation. Cell 488 8324822
1996 Lamin proteolysis facilitates nuclear events during apoptosis. The Journal of cell biology 483 8978814
2011 Recapitulation of premature ageing with iPSCs from Hutchinson-Gilford progeria syndrome. Nature 455 21346760
2020 Mechanical regulation of glycolysis via cytoskeleton architecture. Nature 445 32051585
2011 The role of nuclear lamin B1 in cell proliferation and senescence. Genes & development 444 22155925
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2008 The A- and B-type nuclear lamin networks: microdomains involved in chromatin organization and transcription. Genes & development 427 19141474
2010 Systematic analysis of human protein complexes identifies chromosome segregation proteins. Science (New York, N.Y.) 421 20360068
2013 Lamin B1 depletion in senescent cells triggers large-scale changes in gene expression and the chromatin landscape. Genes & development 418 23934658
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
2015 Panorama of ancient metazoan macromolecular complexes. Nature 407 26344197
2015 Proteome-wide profiling of protein assemblies by cross-linking mass spectrometry. Nature methods 370 26414014
2010 Circulating Lamin B1 (LMNB1) biomarker detects early stages of liver cancer in patients. Journal of proteome research 111 19522540
1995 Structural organization of the human gene (LMNB1) encoding nuclear lamin B1. Genomics 110 7557986
1996 Chromosomal assignment of human nuclear envelope protein genes LMNA, LMNB1, and LBR by fluorescence in situ hybridization. Genomics 90 8838815
2018 GRSF1-mediated MIR-G-1 promotes malignant behavior and nuclear autophagy by directly upregulating TMED5 and LMNB1 in cervical cancer cells. Autophagy 73 30394198
2015 LMNB1-related autosomal-dominant leukodystrophy: Clinical and radiological course. Annals of neurology 38 26053668
2021 Disease Modeling with Human Neurons Reveals LMNB1 Dysregulation Underlying DYT1 Dystonia. The Journal of neuroscience : the official journal of the Society for Neuroscience 37 33468570
2013 Analysis of LMNB1 duplications in autosomal dominant leukodystrophy provides insights into duplication mechanisms and allele-specific expression. Human mutation 37 23649844
2020 De Novo Variants in LMNB1 Cause Pronounced Syndromic Microcephaly and Disruption of Nuclear Envelope Integrity. American journal of human genetics 34 32910914
2023 METTL3-mediated N6-methyladenosine modification stimulates mitochondrial damage and ferroptosis of kidney tubular epithelial cells following acute kidney injury by modulating the stabilization of MDM2-p53-LMNB1 axis. European journal of medicinal chemistry 28 37542992
2022 Pan-cancer analysis identifies LMNB1 as a target to redress Th1/Th2 imbalance and enhance PARP inhibitor response in human cancers. Cancer cell international 21 35241075
2022 Knockdown of LMNB1 Inhibits the Proliferation of Lung Adenocarcinoma Cells by Inducing DNA Damage and Cell Senescence. Frontiers in oncology 19 35712471
1995 Genomic structure of the mouse gene (Lmnb1) encoding nuclear lamin B1. Genomics 19 8586436
2021 Silencing LMNB1 Contributes to the Suppression of Lung Adenocarcinoma Development. Cancer management and research 17 33776481
2021 Screening and identification of LMNB1 and DLGAP5, two key biomarkers in gliomas. Bioscience reports 17 33956061
2024 WTAP-mediated N6-methyladenosine modification promotes the inflammation, mitochondrial damage and ferroptosis of kidney tubular epithelial cells in acute kidney injury by regulating LMNB1 expression and activating NF-κB and JAK2/STAT3 pathways. Journal of bioenergetics and biomembranes 16 38517565
2013 Is LMNB1 a susceptibility gene for neural tube defects in humans? Birth defects research. Part A, Clinical and molecular teratology 15 23733478
2023 LMNB1 deletion in ovarian cancer inhibits the proliferation and metastasis of tumor cells through PI3K/Akt pathway. Experimental cell research 13 37003558
2018 Duplication and deletion upstream of LMNB1 in autosomal dominant adult-onset leukodystrophy. Neurology. Genetics 13 30697589
2017 An LMNB1 Duplication Caused Adult-Onset Autosomal Dominant Leukodystrophy in Chinese Family: Clinical Manifestations, Neuroradiology and Genetic Diagnosis. Frontiers in molecular neuroscience 13 28769756
2019 LMNB1-Related Adult-Onset Autosomal Dominant Leukodystrophy Presenting as Movement Disorder: A Case Report and Review of the Literature. Frontiers in neuroscience 12 31695592
2024 Structural Variants at the LMNB1 Locus: Deciphering Pathomechanisms in Autosomal Dominant Adult-Onset Demyelinating Leukodystrophy. Annals of neurology 8 39078102
2023 CircPTPRA promotes the progression of pancreatic ductal adenocarcinoma via the miR-140-5p/LMNB1 axis. Cancer medicine 8 37041721
2023 LMNB1 targets FOXD1 to promote progression of prostate cancer. Experimental and therapeutic medicine 8 37840569
2022 LMNB1, a potential marker for early prostate cancer progression. American journal of cancer research 8 35968338
2024 Rapid and high-purity differentiation of human medium spiny neurons reveals LMNB1 hypofunction and subtype necessity in modeling Huntington's disease. Inflammation and regeneration 7 38360694
2022 EIF3C Promotes Lung Cancer Tumorigenesis by Regulating the APP/HSPA1A/LMNB1 Axis. Disease markers 7 36157221
2022 Genome sequencing reveals novel noncoding variants in PLA2G6 and LMNB1 causing progressive neurologic disease. Molecular genetics & genomic medicine 6 35247231
2018 Glucose metabolism in the brain in LMNB1-related autosomal dominant leukodystrophy. Acta neurologica Scandinavica 6 30192380
2024 Combined treatment with Aronia berry extract and oligomeric proanthocyanidins exhibit a synergistic anticancer efficacy through LMNB1-AKT signaling pathways in colorectal cancer. Molecular carcinogenesis 5 39282961
2021 Establishment of a GFP::LMNB1 knockin cell line (CSUi002-A-1) from a dystonia patient-specific iPSC by CRISPR/Cas9 editing. Stem cell research 4 34438319
2025 LMNB1/CDKN1A Signaling Regulates the Cell Cycle and Promotes Hepatocellular Carcinoma Progression. Current cancer drug targets 3 38778606
2025 Zinc finger protein Zfp335 is required for T cell homeostatic proliferation through regulating Lmnb1. Cell & bioscience 2 41088342
2021 LMNB1 Duplication-Mediated Autosomal Dominant Adult-Onset Leukodystrophy in an Indian Family. Annals of Indian Academy of Neurology 2 34447008
2025 LncRNA SNHG14 Delivered by Bone Marrow Mesenchymal Stem Cells-Secreted Exosomes Regulates Osteogenesis and Adipogenesis in Osteoporosis by Mediating the miR-27a-3p/LMNB1 Axis. The Kaohsiung journal of medical sciences 1 40052307
2024 ENPP1 inhibits the transcription activity of the hepatitis B virus pregenomic promoter by upregulating the acetylation of LMNB1. Archives of virology 1 38265511
2024 Mechanism of LMNB1 activating GPR84 through JAK-STAT pathway to mediate M2 macrophage polarization in lung cancer. Human immunology 1 39357468
2024 Impact of Nuclear Peripheral Chromatin Lamin LMNB1 Gene in the Proliferation and Migration of Glioma Cells. Neurochemical research 1 39636549
2025 Case report: LMNB1 duplication-mediated autosomal dominant adult leukodystrophy in a Chinese family and literature review of Chinese patients. Frontiers in neuroscience 0 40046440
2025 Atypical Presentation of an LMNB1 Duplication Involving the Silencer Region: Beyond Classical Autosomal-Dominant Leukodystrophy. Neurology. Genetics 0 40343075
2025 LMNB1 regulates breast cancer cell senescence and migration through PPAR signaling pathway. Discover oncology 0 40515805
2025 Clinical Practice Guidelines for the Diagnosis, Management, and Surveillance of LMNB1-Related Autosomal Dominant Leukodystrophy. Neurology. Genetics 0 40933505