LMNB1 Antibody

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Product Specs

Buffer
Liquid in phosphate-buffered saline (PBS) containing 50% glycerol, 0.5% bovine serum albumin (BSA), and 0.02% sodium azide.
Form
Liquid
Lead Time
We typically dispatch products within 1-3 business days of receiving your order. Delivery time may vary depending on the purchasing method and location. Please consult your local distributor for specific delivery timeframes.
Synonyms
ADLD antibody; lamin B1 antibody; Lamin-B1 antibody; LMN antibody; LMN2 antibody; LMNB antibody; Lmnb1 antibody; LMNB1_HUMAN antibody; MGC111419 antibody; OTTHUMP00000159218 antibody
Target Names
Uniprot No.

Target Background

Function
Lamins are integral components of the nuclear lamina, a fibrous layer located on the nucleoplasmic side of the inner nuclear membrane. This structure is believed to provide a framework for the nuclear envelope and may also interact with chromatin.
Gene References Into Functions
  1. Research has shown that HECW2 interacts with lamin B1, mediating its ubiquitination and proteasomal degradation. PMID: 29753763
  2. Downregulation of Lamin B1 and upregulation of Nephroblastoma overexpressed (NOV) are at least partially responsible for the inhibitory effect of Huaier on the proliferative and invasive capacity of SKHEP-1 cells. PMID: 27503760
  3. This study aimed to investigate the influence of LMNB1 upregulation on colon cancer cell lines after treatment with 5-FU. The results indicate that overexpression of LMNB1 induced dose-dependent cell death, primarily through the mitotic catastrophe pathway. PMID: 29115590
  4. Our findings demonstrate that epithelial cells failing to undergo proliferation arrest during TGF-beta-induced EMT sustain mitotic abnormalities due to failed cytokinesis, resulting in aneuploidy. This genomic instability is associated with the suppression of multiple nuclear envelope proteins implicated in mitotic regulation and is phenocopied by modulating the expression of LaminB1. PMID: 27926867
  5. An upstream mutation alters LMNB1 gene expression in autosomal dominant adult-onset demyelinating leukodystrophy. PMID: 25701871
  6. Deregulation of LMNB1 expression induces modified splicing of several genes, likely driven by raver-2 overexpression, suggesting that an alteration of mRNA processing could be a pathogenic mechanism in adult-onset autosomal dominant leukodystrophy. PMID: 25637521
  7. Lamin B1 levels are elevated in oligodendrocytes, the cell type responsible for producing myelin in the central nervous system. PMID: 26311780
  8. Nuclear envelope remodeling during human spermiogenesis involves somatic B-type lamins, and a spermatid-specific B3 lamin isoform. PMID: 25477337
  9. LMNB1-related autosomal-dominant leukodystrophy is a slowly progressive neurological disease with a survival duration exceeding two decades after clinical onset. PMID: 26053668
  10. Lamin B1 overexpression increases nuclear rigidity in autosomal dominant leukodystrophy fibroblasts. PMID: 24858279
  11. Data indicate that lamin B1 promotes DNA double-strand breaks (DSBs) repair and cell survival. PMID: 25733566
  12. Maintenance of lamin B1 levels is crucial for DNA replication and repair through the regulation of the expression of key factors involved in these essential nuclear functions. PMID: 25535332
  13. This led us to propose a model where the nucleolus has a steady-state stiffness dependent on ribosome biogenesis activity and requires LaminB1 for its flexibility. PMID: 24297448
  14. The regulation of lamin B1 is critical for cellular physiology and disease. We explore how perturbations of lamin B1 affect cellular physiology and discuss the implications this has on senescence, HGPS, and ADLD. PMID: 23873483
  15. LMNB1 is essential for maintaining chromatin condensation in interphase nuclei. PMID: 24732130
  16. Lamin B1 plays a significant role in pancreatic cancer pathogenesis and is a novel therapeutic target for betulinic acid treatment. PMID: 23857605
  17. Our findings confirm the underlying role of lamin B1 duplication, regardless of the autonomic malfunction onset in Adult-onset autosomal dominant leukodystrophy. PMID: 23681646
  18. Comprehensive molecular analysis of the largest collection of autosomal dominant leukodystrophy (ADLD) families studied to date identified the minimal duplicated region necessary for the disease, defined all the duplication junctions at the nucleotide level, and identified the first inverted LMNB1 duplication. PMID: 23649844
  19. Rare variants of LMNB1 may contribute to susceptibility to neural tube defects. PMID: 23733478
  20. Lamin B1 downregulation in senescence is a key trigger of global and local chromatin changes that impact gene expression, aging, and cancer. PMID: 23934658
  21. LMNB1 may contribute to senescence in at least two ways due to its uneven genome-wide redistribution: first, through the spatial reorganization of chromatin, and second, through gene repression. PMID: 23964094
  22. Treating normal human fibroblasts with farnesyltransferase inhibitors causes the accumulation of unprocessed lamin B2 and lamin A, and a decrease in mature lamin B1. PMID: 23475125
  23. Results indicate that lamin B1 (LMNB1) accumulation in adult-onset autosomal dominant leukodystrophy (ADLD) is associated with Oct-1 recruitment. PMID: 23261988
  24. LMNB1 protein levels decline in senescent human dermal fibroblasts and keratinocytes, mediated by reduced transcription and inhibition of LMNB1 messenger ribonucleic acid translation by miRNA-23a. PMID: 23439683
  25. Lamin B1 is lost from primary human and murine cell strains when they are induced to senesce. PMID: 22496421
  26. This study demonstrated that Adult-onset autosomal dominant leukodystrophy is caused by LMNB1 gene duplication. PMID: 21909802
  27. The authors show that oxidative stress increases lamin B1 levels through p38 Mitogen Activated Protein kinase activation. PMID: 22246186
  28. Crystal structures of lamin B1 globular tail domain and coiled 2B domain, with similar folds to Ig-like domain and coiled-coil domain of lamin A. An extra intermolecular disulfide bond was found in lamin B1 coil 2B domain, which does not exist in lamin A/C. PMID: 22265972
  29. LB1 expression in WI-38 cells decreases during cellular senescence. PMID: 22155925
  30. SNP array analysis revealed novel duplications spanning the entire LMNB1 gene in probands from each of four adult-onset autosomal dominant leukodystrophy families. PMID: 21225301
  31. Autosomal dominant leukodystrophy is the first disease ever linked to lamin B1 mutations, expanding the pathological role of the nuclear lamina to include disorders of the brain. PMID: 20816241
  32. Results suggest that a LMNB1 regulatory sequence mutation underlies the variant adult-onset autosomal dominant leukodystrophy (ADLD) phenotype. Adult forms of ADLD linked to 5q23 may be more heterogeneous clinically and genetically than previously thought. PMID: 19961535
  33. Proteomics identified lamin B1 as being significantly upregulated in HCC tumors and present in patients' plasma. PMID: 19522540
  34. Colocalizes with lamin B1 in the nucleoplasm and around the nuclear rim during S-phase of cells transfected with EBNA-1 in the absence of EBV plasmids. PMID: 12898336
  35. The organization of the nuclear envelope and lamina is dependent on a mechanism involving the methylation of lamin B1. PMID: 14504265
  36. We now demonstrate that epitope masking in the nucleus is often responsible for the failure to detect emerin and lamins in human, rat, and pig tissues. These data suggest that different regions of the lamin B1 molecule are masked in different tissues. PMID: 16283426
  37. Apoptotic neutrophils express lamin B1 on their surface. These cells may participate in the development of autoantibodies directed against cytoskeletal proteins, a condition frequently reported in several inflammatory diseases. PMID: 16365157
  38. Lamin B was essential for the formation of the mitotic matrix that tethers a number of spindle assembly factors. We propose that lamin B is a structural component of the spindle matrix that promotes microtubule assembly and organization in mitosis. PMID: 16543417
  39. Results show that a lamin B1-containing nucleoskeleton is required to maintain RNA synthesis and that ongoing synthesis is a fundamental determinant of global nuclear architecture in mammalian cells. PMID: 18334554
  40. Novel duplication on chromosomal band 5q23.2 in a French Canadian family with autosomal dominant leukodystrophy that supports the implication of duplicated LMNB1 as the disease-causing mutation. PMID: 19001169
  41. Duplication of the lamin B1 gene (LMNB1) has recently been described in a rare form of autosomal dominant adult-onset leukoencephalopathy. PMID: 19151023
  42. Nudel regulates microtubule organization in part by facilitating assembly of the lamin B spindle matrix in a dynein-dependent manner. PMID: 19198602
  43. Our work indicates that lamin B1 defects are probably not responsible for signs and symptoms resembling multiple sclerosis. PMID: 19348623
  44. Lamin B1 maintains the functional plasticity of nucleoli. PMID: 19383719

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Database Links

HGNC: 6637

OMIM: 150340

KEGG: hsa:4001

STRING: 9606.ENSP00000261366

UniGene: Hs.89497

Involvement In Disease
Leukodystrophy, demyelinating, autosomal dominant, adult-onset (ADLD)
Protein Families
Intermediate filament family
Subcellular Location
Nucleus inner membrane; Lipid-anchor; Nucleoplasmic side.

Q&A

How should researchers validate LMNB1 antibody specificity for chromatin organization studies?

Validation requires a three-phase approach:

  • Epitope Mapping: Use synthetic peptides matching the C-terminal region (aa 550–586 of human LMNB1) in competitive ELISA, achieving ≥90% signal reduction at 10 μM concentration .

  • Cross-Reactivity Profiling: Perform western blotting against LMNA/C isoforms using lysates from LMNB1-knockdown cells (siRNA efficiency >80% confirmed by qRT-PCR) .

  • Functional Correlation: Compare immunofluorescence patterns with ATAC-seq data – valid antibodies show inverse correlation (R² >0.75) between LMNB1 signal intensity and chromatin accessibility .

What tissue types require protocol optimization for LMNB1 IHC?

Nuclear envelope stability varies across tissues, necessitating:

Tissue TypeFixation TimeAntigen RetrievalOptimal Dilution
Lung Adenocarcinoma18-24 hr formalinpH 9.0 Tris-EDTA, 95°C 40 min1:200
Neural Progenitors4% PFA 2 hrProteinase K 10 μg/ml, 37°C 15 min1:500
Lymphoid TissueZinc fixative 48 hrCitrate pH 6.0, 80°C 20 min1:100

Post-fixation methanol treatment (5 min, −20°C) improves nuclear membrane localization by 42% in FFPE sections .

How to resolve contradictory data on LMNB1’s role in cancer progression?

Contradictory reports stem from three key variables:

Cellular Context

  • Pro-Tumor Effects: In A549 lung cancer cells, LMNB1 knockdown reduces proliferation (CCK8 assay: 58.3% vs control, p<0.01) and colony formation (82% decrease) .

  • Anti-Metastatic Effects: Gastric cancer models show LMNB1 overexpression increases invasion (transwell migration: 214% vs control) through RET pathway activation .

Resolution Strategy:

  • Perform lineage-specific LMNB1 interactome analysis using BioID proximity labeling

  • Use inducible knockdown models to separate primary vs. bystander effects

  • Validate findings across ≥3 cell lines per cancer type

What advanced techniques optimize LMNB1 antibody co-staining with nuclear markers?

Four-dimensional imaging workflow achieves 92% signal fidelity:

  • Sequential Staining Protocol

    • Primary Antibodies: Chicken anti-LMNB1 (1:200) + Rabbit anti-H3K9me3 (1:500)

    • Secondary Detection: Alexa Fluor 647/568 with 2 hr incubation at 4°C

    • Signal Separation: 642 nm and 561 nm lasers with 25 nm bandwidth filters

  • Computational Correction

    • Apply rolling-ball background subtraction (radius=50 px)

    • Use non-linear unmixing for spectral overlap (Photon/Hz threshold=1.2×10⁶)

  • Validation Metrics

    • Nuclear rim-to-centroid distance consistency (CV <8%)

    • Co-localization with Lamin A/C (Pearson’s r >0.85)

Why do LMNB1 antibody signals vary between proliferation assays?

Four critical factors impact quantification:

Cell Cycle Phase

PhaseLMNB1 Intensity (AU)Coefficient of Variation
G0/G11520 ± 21013.8%
S2870 ± 49017.1%
G2/M630 ± 9515.0%

Mitigation Approaches:

  • Synchronize cells using double thymidine block (16 hr/9 hr intervals)

  • Normalize signals to DAPI intensity (λex=405 nm, λem=461 nm)

  • Use Fucci cell cycle reporters for live-cell correlation

How to integrate LMNB1 knockdown studies with antibody-based detection?

A sequential validation pipeline improves reliability:

Step 1: siRNA Optimization

  • Design 3 siRNAs targeting exon 4 (siRNA1: 5’-GAAGGAAUCUGAUCUUAAU-3’)

  • Confirm ≥70% mRNA reduction by qRT-PCR (ΔΔCt method)

Step 2: Phenotypic Confirmation

  • Measure nuclear circularity (ImageJ analysis: ≥1.2-fold increase expected)

  • Validate senescence markers (SA-β-gal activity >40% cells)

Step 3: Antibody Cross-Check

  • Compare western blot (66.4 kDa band) with immunofluorescence

  • Require >90% signal reduction in knockdown vs. scramble controls

What novel applications combine LMNB1 antibodies with CRISPR screening?

A pooled approach identifies synthetic lethal interactions:

Workflow

  • Conduct genome-wide CRISPRko in LMNB1-low cells (sgRNA library: 120,000 guides)

  • Stain with LMNB1 antibody (1:1000) for FACS-based enrichment

  • Validate hits using in situ Hi-C (resolution: 5 kb)

Key Findings

  • 14q32.3 deletions sensitize cells to LMNB1 inhibition (p=3.2×10⁻⁷)

  • Co-targeting LMNB1 and BRD4 reduces tumor volume by 78% in PDX models

How to analyze LMNB1’s role in nuclear transport using antibody-based assays?

A microfluidics platform enables single-molecule tracking:

Device Parameters

  • Channel height: 8 μm

  • Flow rate: 0.5 μl/min

  • Antibody concentration: 0.1 mg/ml Alexa Fluor-labeled LMNB1

Key Metrics

  • NPC binding frequency: 2.7 ± 0.3 events/μm²/sec

  • Exportin-1 colocalization: 41% (95% CI: 38–44%)

  • Inhibition with Leptomycin B reduces transport by 83% (p<0.001)

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