HCSGD entry for LMNB1


1. General information

Official gene symbolLMNB1
Entrez ID4001
Gene full namelamin B1
Other gene symbolsADLD LMN LMN2 LMNB
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0005198Structural molecule activityIEAmolecular_function
GO:0005635Nuclear envelopeIEA TAScellular_component
GO:0005637Nuclear inner membraneIEAcellular_component
GO:0005638Lamin filamentIEAcellular_component
GO:0005654NucleoplasmIEA TAScellular_component
GO:0006915Apoptotic processTASbiological_process
GO:0006921Cellular component disassembly involved in execution phase of apoptosisTASbiological_process
GO:0043274Phospholipase bindingIEAmolecular_function
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.98879364390.00001004520.99999024730.0069833333

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Down-2.5132701213
GSE13712_SHEARDown-0.4174441119
GSE13712_STATICDown-0.1770814437
GSE19018Down-0.7638278804
GSE19899_A1Down-2.9404355937
GSE19899_A2Down-4.7098091073
PubMed_21979375_A1Down-3.1101610245
PubMed_21979375_A2Down-7.0753576618
GSE35957Down-2.8489558253
GSE36640Down-5.6885157049
GSE54402Down-0.9767291967
GSE9593Down-1.5908709983
GSE43922Down-1.6328950104
GSE24585Down-0.1836461354
GSE37065Down-0.3003484468
GSE28863_A1Down-0.1436976140
GSE28863_A2Up0.7467983253
GSE28863_A3Down-0.0870039195
GSE28863_A4Up0.1703820819
GSE48662Down-1.1231778501

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

    • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-373-3pMIMAT0000726MIRT002510Microarray//Microarray;OtherFunctional MTI (Weak)15685193
hsa-miR-124-3pMIMAT0000422MIRT002571Proteomics;MicroarrayFunctional MTI (Weak)18668037
hsa-miR-124-3pMIMAT0000422MIRT002571MicroarrayFunctional MTI (Weak)15685193
hsa-miR-128-3pMIMAT0000424MIRT022094SequencingFunctional MTI (Weak)20371350
hsa-miR-1MIMAT0000416MIRT023965ProteomicsFunctional MTI (Weak)18668040
hsa-miR-215-5pMIMAT0000272MIRT024320MicroarrayFunctional MTI (Weak)19074876
hsa-miR-192-5pMIMAT0000222MIRT026682MicroarrayFunctional MTI (Weak)19074876
hsa-miR-101-3pMIMAT0000099MIRT027335SequencingFunctional MTI (Weak)20371350
hsa-miR-26b-5pMIMAT0000083MIRT029849MicroarrayFunctional MTI (Weak)19088304
hsa-miR-193b-3pMIMAT0002819MIRT041285CLASHFunctional MTI (Weak)23622248
hsa-miR-484MIMAT0002174MIRT042270CLASHFunctional MTI (Weak)23622248
hsa-miR-320aMIMAT0000510MIRT044805CLASHFunctional MTI (Weak)23622248
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    • mirRecord

MicroRNA name

mirBase ID

Target site number

MiRNA mature ID

Test method inter

MiRNA regulation site

Reporter target site

Pubmed ID

hsa-miR-373-3pMIMAT0000726NAhsa-miR-37315685193
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6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 15 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

26654219We reveal that the autophagy protein LC3/Atg8 directly interacts with the nuclear lamina protein LMNB1 (lamin B1), and binds to LMN/lamin-associated chromatin domains (LADs)
26354777These include the activation of autophagy, a catabolic process operating in the cytoplasm and downregulation of lamin B1, a component of the nuclear lamina
26354777We discovered that cells entering BRAF(V600E)- or H-RAS(G12V)-induced senescence downregulate not only lamin B1 but also lamin A, as well as several other nuclear envelope (NE) proteins, resulting in an altered NE morphology
26354777Depletion of LMNB1 or LMNA/C was sufficient to recapitulate some OIS features, including cell cycle exit and downregulation of NE proteins
27350809Introduction of telomerase gene function in HGPS cells reversed such aging phenotypes along with upregulation of lamin B1 and downregulation of progerin, which is a hallmark of young cells
24861957Here, we summarize and review recent findings shedding light on SAHF composition and formation via spatial repositioning of chromatin, with a specific focus on the role of lamin B1 for this process
24380701In humans duplication of the LMNB1 gene (encoding lamin B1) causes an adult onset neurodegenerative disorder, termed autosomal dominant leukodystrophy, whilst very recently, LMNB1 has been implicated as a susceptibility gene in neural tube defects
23964094Redistribution of the Lamin B1 genomic binding profile affects rearrangement of heterochromatic domains and SAHF formation during senescence
23964094Studying a key component of the nuclear lamina lamin B1 (LMNB1), we report dynamic alterations in its genomic profile and their implications for SAHF formation and gene regulation during senescence
23964094Genome-wide mapping reveals that LMNB1 is depleted during senescence, preferentially from the central regions of lamina-associated domains (LADs), which are enriched for Lys9 trimethylation on histone H3 (H3K9me3)
23964094LMNB1 knockdown facilitates the spatial relocalization of perinuclear H3K9me3-positive heterochromatin, thus promoting SAHF formation, which could be inhibited by ectopic LMNB1 expression
23964094Furthermore, despite the global reduction in LMNB1 protein levels, LMNB1 binding increases during senescence in a small subset of gene-rich regions where H3K27me3 also increases and gene expression becomes repressed
23964094These results suggest that 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
23934658Lamin B1 depletion in senescent cells triggers large-scale changes in gene expression and the chromatin landscape
23934658While chromatin regulation and lamin B1 down-regulation have been implicated as senescence effectors, functional interactions between them are poorly understood
23934658Lamin B1 reduction in proliferating cells triggers senescence and formation of mesas and canyons
23934658Our data illustrate profound chromatin reorganization during senescence and suggest that lamin B1 down-regulation in senescence is a key trigger of global and local chromatin changes that impact gene expression, aging, and cancer
23873483Duplication of the LMNB1 locus, leading to elevated levels of lamin B1, causes adult-onset autosomal dominant leukodystrophy (ADLD), a rare genetic disease that leads to demyelination in the central nervous system (CNS)
23873483How do elevated levels of lamin B1 cause disease and why is the CNS particularly susceptible to lamin B1 fluctuations
23849162WRN-mutated fibroblasts showed oxidative stress, increased lamin B1 expression, nuclear dysmorphies and premature senescence
23849162Increased expression of lamin B1 with altered lamina architecture observed in WRN-mutated fibroblasts could contribute to premature cellular senescence
23816621In senescent cells, lamin A/C-negative, but strongly gamma-H2AX-positive and H3K27me3-positive, cytoplasmic chromatin fragments (CCFs) budded off nuclei, and this was associated with lamin B1 down-regulation and the loss of nuclear envelope integrity
23475125Disruption of lamin B1 and lamin B2 processing and localization by farnesyltransferase inhibitors
23475125Lamin A and the B-type lamins, lamin B1 and lamin B2, are translated as pre-proteins that are modified at a carboxyl terminal CAAX motif by farnesylation, proteolysis and carboxymethylation
23475125Lamin B1 and lamin B2 play important roles in cell proliferation and organ development, but little is known about the role of farnesylation in their functions
23475125Treating normal human fibroblasts with farnesyltransferase inhibitors causes the accumulation of unprocessed lamin B2 and lamin A and a decrease in mature lamin B1
23357361Since beta-asarone induced lamin B1 expression, a model is proposed in which beta-asarone inhibits colorectal cancer by inducing senescence through lamin B1
22496421Lamin B1 loss is a senescence-associated biomarker
22496421We show here than lamin B1 is lost from primary human and murine cell strains when they are induced to senesce by DNA damage, replicative exhaustion, or oncogene expression
22496421However, activation of either the p53 or pRB tumor suppressor pathway was sufficient to induce lamin B1 loss
22496421Lamin B1 declined at the mRNA level via a decrease in mRNA stability rather than by the caspase-mediated degradation seen during apoptosis
22496421Last, lamin B1 protein and mRNA declined in mouse tissue after senescence was induced by irradiation
22496421Our findings suggest that lamin B1 loss can serve as biomarker of senescence both in culture and in vivo
22155925Nuclear lamin B1 (LB1) is a major structural component of the nucleus that appears to be involved in the regulation of many nuclear functions
19522540Circulating Lamin B1 (LMNB1) biomarker detects early stages of liver cancer in patients
19522540LMNB1 functions in nuclear envelope lamina and possesses a transcriptional coregulatory activity having an important role in DNA replication, cellular aging, and stress responses
19522540Clinically, the expression level of lamin B1 correlated positively with tumor stages, tumor sizes, and number of nodules
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