Affinage

LMNB1

Lamin-B1 · UniProt P20700

Length
586 aa
Mass
66.4 kDa
Annotated
2026-06-10
41 papers in source corpus 17 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/6 claims corpus-supported (83%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

LMNB1 encodes a type B nuclear lamin built from a conserved intermediate-filament architecture (an N-terminal head, central rod, and C-terminal tail) that assembles into the nuclear lamina and underlies nuclear envelope integrity (PMID:7557986, PMID:8586436). Disease-associated and de novo missense variants in the head and rod domains destabilize lamina incorporation, reduce nuclear localization, lower steady-state protein levels, and produce misshapen or condensed nuclei, establishing the protein's role in maintaining nuclear morphology (PMID:23733478, PMID:32910914). Beyond structure, lamin B1 anchors heterochromatin and enforces its compaction: loss of LMNB1 decreases H3K9me3, opens chromatin accessibility, and triggers a DNA-damage and senescence program marked by p53, p21, p16, and γ-H2AX induction (PMID:35712471), and hypomorphic lamin B1 sensitizes regulatory genomic regions near transcription start sites to double-strand breaks. LMNB1 also engages transcriptional control directly, binding regulatory DNA to repress promoter activity in an acetylation-dependent manner (at K111/K261) (PMID:38265511). Its abundance is set both transcriptionally, through direct promoter binding by ZFP335 (PMID:41088342), and post-transcriptionally, through m6A modification of its mRNA by WTAP and through an MDM2–p53 axis (PMID:37542992, PMID:38517565). Nuclear lamin B1 dosage tunes nuclear stiffness and deformability to control neuronal migration, with excess lamin B1 arresting migration. Dysregulation of LMNB1—overexpression with nuclear-to-cytoplasmic mislocalization—drives nucleocytoplasmic transport defects and neuronal pathology in DYT1 dystonia and Huntington's disease (PMID:33468570, PMID:38360694), and altered LMNB1 gene dosage or TAD-boundary disruption causes autosomal dominant leukodystrophy (ADLD) (PMID:39078102).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1995 High

    Establishing the genomic architecture of LMNB1 defined it as an intermediate-filament gene of the nuclear envelope with conserved head/rod/tail domain coding organization, framing all later structure-function interpretation.

    Evidence Genomic cloning and exon-intron analysis of human and mouse LMNB1/Lmnb1, including promoter characterization

    PMID:7557986 PMID:8586436

    Open questions at the time
    • Does not establish lamina assembly mechanism or protein partners
    • Promoter regulation tested only by sequence features, not function
  2. 2013 High

    Detailed analysis of ADLD duplication junctions showed that the disease arises from a simple gene-dosage gain with regulatory regions preserved, defining LMNB1 copy number as the pathogenic variable.

    Evidence Nucleotide-level junction sequencing and allele-specific expression in patient fibroblasts across ADLD families

    PMID:23649844

    Open questions at the time
    • Does not explain how dosage gain produces oligodendrocyte/myelin pathology
    • Cellular mechanism downstream of overexpression not addressed
  3. 2013 Medium

    A patient missense variant was shown to compromise lamin B1 stability within the lamina, providing the first functional link between point mutation and lamina integrity.

    Evidence FLIP analysis of the A436T variant in cells

    PMID:23733478

    Open questions at the time
    • Single method (FLIP), no replication
    • No direct demonstration of disease causality
  4. 2020 High

    De novo missense mutations across head and rod domains were shown to impair lamina formation, reduce nuclear localization, and distort nuclear shape, establishing LMNB1 point mutations as a distinct mechanism from dosage gain.

    Evidence Localization, nuclear morphology, and protein-level assays in patient lymphoblasts and transfected cells from seven unrelated individuals

    PMID:32910914

    Open questions at the time
    • Mechanism linking misshapen nuclei to neurodevelopmental phenotype not resolved
    • Loss-of-function vs dominant-negative contribution not separated
  5. 2021 High

    Patient-derived neuron models demonstrated that LMNB1 upregulation and nuclear-to-cytoplasmic mislocalization mediate DYT1 dystonia phenotypes, showing that LMNB1 acts downstream of TOR1A to control nuclear morphology and nucleocytoplasmic transport.

    Evidence iPSC and direct-conversion motor neurons, shRNA rescue, transport assays, and GFP::LMNB1 CRISPR knockin localization

    PMID:33468570 PMID:34438319

    Open questions at the time
    • Molecular cause of mislocalization downstream of TOR1A unresolved
    • Whether transport defect is cause or consequence of lamina thickening unclear
  6. 2022 Medium

    Knockdown experiments established that LMNB1 maintains heterochromatin compaction via H3K9me3 and suppresses DNA damage and senescence, defining a chromatin-protective function beyond structural scaffolding.

    Evidence siRNA knockdown with ATAC-seq, immunoblotting, senescence markers, and xenografts in lung adenocarcinoma cells

    PMID:35712471

    Open questions at the time
    • Single cell-type context
    • Direct mechanism linking lamina to H3K9me3 maintenance not shown
  7. 2023 Medium

    DNA pull-down and reporter assays showed LMNB1 directly binds regulatory DNA and represses transcription in an acetylation-dependent manner, extending its role to sequence-specific transcriptional control.

    Evidence DNA pull-down, luciferase reporter assays, acetylation-site mutagenesis, and ENPP1 manipulation on the HBV EnhII/BCP promoter

    PMID:38265511

    Open questions at the time
    • Generality of direct DNA binding to endogenous host genes untested
    • Acetyltransferase/deacetylase responsible not identified
  8. 2023 Medium

    An MDM2–p53–LMNB1 axis regulated by METTL3-dependent m6A methylation was defined, placing LMNB1 expression downstream of an m6A-regulated stress signaling cascade.

    Evidence Gain/loss-of-function, m6A and ubiquitination assays, Co-IP, and CLP mouse model in kidney tubular epithelial cells

    PMID:37542992

    Open questions at the time
    • Whether LMNB1 acts as effector or bystander in ferroptosis unclear
    • Direct vs indirect activation of LMNB1 by p53 not resolved
  9. 2024 Medium

    WTAP-mediated m6A methylation of LMNB1 mRNA was shown to stabilize it and drive downstream NF-κB and JAK2/STAT3 signaling, establishing direct post-transcriptional control of LMNB1 abundance.

    Evidence meRIP, RIP, dual-luciferase, and actinomycin D stability assays with CLP mouse model

    PMID:38517565

    Open questions at the time
    • Mechanism by which lamin B1 activates cytoplasmic signaling pathways unexplained
    • Single disease context
  10. 2024 High

    Hi-C combined with RNA-seq and histopathology distinguished dosage-driven classical ADLD from TAD-boundary-disruption atypical ADLD, refining the genomic basis of LMNB1 leukodystrophy and implicating astrocytes.

    Evidence Hi-C, RNA-seq, and brain histopathology across more than 20 families

    PMID:39078102

    Open questions at the time
    • Mechanism by which astrocyte misexpression causes demyelination not defined
    • Cell-type-specific consequences of forebrain misexpression not fully mapped
  11. 2024 Low

    LMNB1 was placed within cancer proliferation programs, regulating CDKN1A/p21 and influencing PI3K/Akt signaling in hepatocellular carcinoma and glioma.

    Evidence Knockdown with ChIP, phospho-kinase arrays, pathway enrichment, and xenograft assays

    PMID:38778606 PMID:39636549

    Open questions at the time
    • Pathway placement inferred without direct biochemical reconstitution
    • Whether effects are lamin-structure-dependent or transcriptional unclear
  12. 2024 Medium

    Huntington's disease neuron models showed LMNB1 reduction and cytoplasmic mislocalization driving neuronal death rescuable by nuclear export inhibition, linking LMNB1 mislocalization to nucleocytoplasmic transport failure.

    Evidence hPSC-derived medium spiny neurons, immunofluorescence, KPT335 treatment, and HTT knockdown

    PMID:38360694

    Open questions at the time
    • Causal direction between mislocalization and transport defect not fully resolved
    • Mechanism of LMNB1 nuclear export not identified
  13. 2025 Medium

    ZFP335 was identified as a direct transcriptional activator of Lmnb1 required for naïve T cell homeostatic proliferation, defining an upstream transcriptional regulator and a new physiological role.

    Evidence ChIP, conditional Zfp335 knockout, Lmnb1 overexpression rescue, and IL-7 proliferation assays

    PMID:41088342

    Open questions at the time
    • How LMNB1 supports T cell proliferation mechanistically unclear
    • Single regulatory context
  14. 2025 Medium

    Lamin B1 dosage was shown to set nuclear stiffness and deformability that gates neuronal migration, providing a biophysical mechanism by which LMNB1 overexpression arrests migration.

    Evidence In vivo cortical neuron overexpression, atomic force microscopy, live imaging in microchannels, patient-iPSC cerebral organoids, and computational modeling (preprint)

    Open questions at the time
    • Not yet peer-reviewed
    • Link between migration arrest and ADLD/microcephaly phenotypes in patients not established
  15. 2025 Medium

    Hypomorphic Lamin B1 was shown to expose regulatory genomic regions to non-random double-strand breaks, demonstrating a genome-protective function at fragile regulatory loci.

    Evidence sBLISS, chromatin accessibility, and transcriptomic profiling in conditional B cell models (preprint)

    Open questions at the time
    • Not yet peer-reviewed
    • Mechanism of break protection at specific loci not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How lamin B1's structural lamina role, its direct sequence-specific transcriptional repression, and its chromatin/genome-protective functions are mechanistically unified, and which of these mediates each disease phenotype, remains unresolved.
  • No structural model connecting domain mutations to specific molecular defects
  • Direct DNA-binding repression generality untested at endogenous loci
  • Causal contribution of dosage vs mislocalization vs loss across neurological diseases not separated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 4 GO:0003677 DNA binding 1 GO:0042393 histone binding 1 GO:0140110 transcription regulator activity 1
Localization
GO:0005634 nucleus 2 GO:0005635 nuclear envelope 2 GO:0000228 nuclear chromosome 1
Pathway
R-HSA-1643685 Disease 3 R-HSA-1266738 Developmental Biology 2 R-HSA-4839726 Chromatin organization 2 R-HSA-74160 Gene expression (Transcription) 2
Partners
ENPP1MDM2WTAPZFP335
Complex memberships
nuclear lamina

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 LMNB1 encodes an intermediate filament protein of the nuclear envelope whose transcription unit spans >45 kb and is organized into 11 exons: exon 1 codes for the amino-terminal head domain and first portion of the central rod domain, exons 2–6 code the central rod domain, and exons 7–11 code the carboxyl-terminal tail domain. Intron positions are conserved with other vertebrate lamin genes and most cytoplasmic intermediate filament protein genes. Genomic cloning and structural analysis of the human LMNB1 gene Genomics High 7557986 8586436
1995 The mouse Lmnb1 gene spans ~43 kb and consists of 11 exons and 10 introns with conserved exon/intron organization shared among intermediate filament protein family genes. The presumptive promoter has high GC content, a CAAT box, and multiple SP1 sites but no classical TATA box, indicating a housekeeping gene promoter with a CpG island. Genomic cloning and structural analysis of the mouse Lmnb1 gene Genomics High 8586436
2013 LMNB1 duplications in ADLD are intrachromosomal, non-recurrent, and arise through nonhomologous end joining or replication-based mechanisms (fork stalling and template switching / microhomology-mediated break-induced repair). The minimal duplicated region sufficient for disease was defined. All three LMNB1 alleles in ADLD patients show equal expression, indicating regulatory regions are maintained within the rearranged segment. Detailed molecular analysis of LMNB1 duplication junctions at nucleotide level; allele-specific expression analysis in patients' fibroblasts Human mutation High 23649844
2013 A missense variant A436T in LMNB1 (identified in NTD patients) was shown by fluorescence loss in photobleaching (FLIP) to compromise the stability of lamin B1 interaction within the nuclear lamina. Fluorescence loss in photobleaching (FLIP) analysis of LMNB1 A436T variant in cells Birth defects research. Part A, Clinical and molecular teratology Medium 23733478
2020 De novo missense mutations in LMNB1 cause impaired formation of the nuclear lamina. Two variants in the head group domain reduce nuclear localization of the protein and increase misshapen nuclei. A variant in the coil region leads to increased frequency of condensed nuclei and lower steady-state levels of lamin B1 in proband lymphoblasts. Functional analysis of LMNB1 missense mutations by immunofluorescence/nuclear morphology assays and immunoblotting in patient lymphoblasts and transfected cells American journal of human genetics High 32910914
2021 In DYT1 dystonia (TOR1A heterozygous mutation), LMNB1 is upregulated and exhibits abnormal subcellular distribution (nuclear-to-cytoplasmic mislocalization) specifically in cholinergic motor neurons. This dysregulation is causally linked to disease phenotypes (reduced neurite length, thickened nuclear lamina, disrupted nuclear morphology, impaired nucleocytoplasmic transport), as shRNA-mediated downregulation of LMNB1 largely ameliorates all cellular defects in DYT1 motor neurons. Human patient-specific motor neurons from iPSCs and direct conversion; shRNA knockdown of LMNB1; immunofluorescence; nucleocytoplasmic transport assays The Journal of neuroscience High 33468570
2021 LMNB1, as a component of the nuclear lamina, anchors heterochromatin and associates with transcription regulation, and its expression is upregulated with nuclear-to-cytoplasmic mislocalization in DYT1 dystonia neurons, as confirmed by GFP::LMNB1 CRISPR knockin iPSC modeling. CRISPR/Cas9 GFP::LMNB1 knockin iPSC line establishment; fluorescence co-localization Stem cell research Low 34438319
2022 Knockdown of LMNB1 in lung adenocarcinoma cells decreases H3K9me3 protein expression, increases chromosome accessibility (by ATAC-seq), increases p53, p21, p16, and γ-H2AX expression, and increases senescence-positive cells, indicating that LMNB1 maintains heterochromatin compaction and suppresses DNA damage responses and cellular senescence. siRNA knockdown; ATAC-seq; immunofluorescence; immunoblotting; in vivo xenograft Frontiers in oncology Medium 35712471
2023 LMNB1 directly interacts with the HBV enhancer II/basic core promoter (EnhII/BCP) DNA, as demonstrated by DNA pull-down assay. Overexpression of LMNB1 inhibits HBV promoter activity. ENPP1 interacts with LMNB1 and increases acetylation of LMNB1 at residues K111 and K261; LMNB1 acetylation mutants (111R, 261Q, 261R, 483Q, 483R) show increased HBV promoter activity, indicating that acetylation of LMNB1 at these sites is required for its transcriptional repression of HBV. DNA pull-down assay; luciferase reporter assay with HBV promoter/mutant constructs; acetylation site mutagenesis; ENPP1 overexpression/knockdown Archives of virology Medium 38265511
2023 LMNB1 knockdown in ovarian cancer cells inhibits proliferation and migration by suppressing FGF1-mediated PI3K-Akt signaling pathway, as revealed by RNA-seq followed by functional validation. Stable LMNB1 knockdown; RNA-seq; CCK8, wound healing, transwell assays; xenograft models Experimental cell research Low 37003558
2023 MDM2 (an E3 ubiquitin ligase) increases p53 ubiquitination, which activates LMNB1 expression. METTL3-mediated m6A methylation of MDM2 mRNA stabilizes it via YTHDF1, thereby increasing MDM2 translation and downstream LMNB1 upregulation. Knockdown of LMNB1, MDM2, or METTL3 reduces mitochondrial damage and ferroptosis markers in LPS-treated kidney tubular epithelial cells. Gain/loss-of-function experiments; m6A methylation assays; co-immunoprecipitation; ubiquitination assays; in vivo CLP mouse model European journal of medicinal chemistry Medium 37542992
2024 WTAP promotes LMNB1 expression through m6A methylation modification of LMNB1 mRNA, as verified by meRIP assay, RIP assay, dual-luciferase reporter assay, and actinomycin D mRNA stability assay. LMNB1 in turn activates NF-κB and JAK2/STAT3 signaling pathways to promote inflammation and ferroptosis in kidney tubular epithelial cells. meRIP assay; RIP assay; dual-luciferase reporter assay; actinomycin D stability assay; western blot; flow cytometry; CLP mouse model Journal of bioenergetics and biomembranes Medium 38517565
2024 LMNB1 promotes HCC cell proliferation by regulating CDKN1A (p21) expression, as shown by ChIP assay and pathway enrichment analysis with functional rescue experiments. LMNB1 knockdown; ChIP assay; gene ontology/pathway enrichment analysis; in vitro and in vivo proliferation assays Current cancer drug targets Low 38778606
2024 In autosomal dominant leukodystrophy (ADLD), classical ADLD is caused by intra-TAD duplications of LMNB1 resulting in a simple gene dose gain, while atypical ADLD results from inter-TAD deletions or duplications causing LMNB1 forebrain-specific misexpression by disrupting topologically associating domain (TAD) boundaries. Astrocytes are identified as key cellular players in ADLD pathology. High-throughput chromosome conformation capture (Hi-C); RNA sequencing; histopathological analysis of postmortem brain tissues; clinical/neuroradiological investigation of >20 families Annals of neurology High 39078102
2024 LMNB1 knockdown in glioma cells reduces phosphorylation of Akt1/2/3 and expression of PI3K, AKT, and p-AKT proteins, placing LMNB1 upstream of the PI3K/Akt signaling pathway in glioma cell proliferation and migration. RNA interference; human phospho-kinase array; immunoblotting; xenograft models; wound healing and transwell assays Neurochemical research Low 39636549
2024 In Huntington's disease medium spiny neurons (MSNs), LMNB1 is greatly reduced and mislocalizes to the cytoplasm and axons. Treatment with KPT335 (nuclear export inhibitor) or HTT knockdown attenuates LMNB1 mislocalization and alleviates neuronal death, linking LMNB1 mislocalization to nucleocytoplasmic transport defects. hPSC-derived MSN differentiation; immunofluorescence for LMNB1 localization; KPT335 treatment; HTT knockdown; cell viability assays Inflammation and regeneration Medium 38360694
2025 Transcription factor ZFP335 directly binds to the promoter of the Lmnb1 gene and regulates its transcription, as demonstrated by ChIP assay. Overexpression of Lmnb1 significantly rescues the impaired homeostatic proliferation of Zfp335-knockout T cells, establishing Lmnb1 as a direct downstream transcriptional target of Zfp335 required for naïve T cell homeostatic proliferation. ChIP assay; adoptive transfer model; Zfp335 conditional knockout; Lmnb1 overexpression rescue; RNA-seq; in vitro IL-7 proliferation assay Cell & bioscience Medium 41088342
2025 Excess lamin B1 (LB1) elevates nuclear stiffness in neurons and impairs neuronal motility in confined spaces in vitro. In vivo, excess LB1 halts neuronal migration without altering laminar identity or overall gene expression. Cerebral organoids from LMNB1-duplication iPSCs exhibit impaired neuronal migration. Computational modeling and live imaging validate a temporal relationship between nuclear deformation and migration velocity. In vivo mouse cortical neuron overexpression; atomic force microscopy/nuclear stiffness measurement; live imaging in confined microchannels; cerebral organoids from patient iPSCs; computational modeling; electrophysiology bioRxivpreprint Medium
2025 Conditional hypomorphic expression of Lamin B1 in B cells leads to elevated DNA damage, altered chromatin accessibility, and disrupted transcriptional profiles. Using sBLISS, non-random double-strand break hotspots are identified near transcriptional start sites and regulatory elements controlling translation and mRNA fate in GC B cells depleted of Lamin B1, indicating that LMNB1 protects fragile regulatory genomic regions. In vivo and in vitro B cell conditional hypomorphic Lamin B1 models; sBLISS (in situ labelling and sequencing of double-strand breaks); chromatin accessibility assays; transcriptomic profiling bioRxivpreprint Medium

Source papers

Stage 0 corpus · 41 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
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 111 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
2021 Disease Modeling with Human Neurons Reveals LMNB1 Dysregulation Underlying DYT1 Dystonia. The Journal of neuroscience : the official journal of the Society for Neuroscience 39 33468570
2015 LMNB1-related autosomal-dominant leukodystrophy: Clinical and radiological course. Annals of neurology 39 26053668
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 30 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
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 19 38517565
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
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 Genome sequencing reveals novel noncoding variants in PLA2G6 and LMNB1 causing progressive neurologic disease. Molecular genetics & genomic medicine 7 35247231
2022 EIF3C Promotes Lung Cancer Tumorigenesis by Regulating the APP/HSPA1A/LMNB1 Axis. Disease markers 7 36157221
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
2024 Mechanism of LMNB1 activating GPR84 through JAK-STAT pathway to mediate M2 macrophage polarization in lung cancer. Human immunology 2 39357468
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
2025 LMNB1 regulates breast cancer cell senescence and migration through PPAR signaling pathway. Discover oncology 1 40515805
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 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 Clinical Practice Guidelines for the Diagnosis, Management, and Surveillance of LMNB1-Related Autosomal Dominant Leukodystrophy. Neurology. Genetics 0 40933505

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