ReviewCells2018
Consequences of Lamin B1 and Lamin B Receptor Downregulation in Senescence.
Review in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 92 citations in OpenAlex.
- Extracellular Vesicle Protein Panel Enables Early Lung Cancer Detection in a Large Clinical Cohort.Journal of extracellular vesicles · 2025Trial
- Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026Review
- Cellular senescence of renal tubular epithelial cells in diabetic kidney disease: emerging mechanisms and targeted interventions.Frontiers in cell and developmental biology · 2026Review
- Fragmentation of nucleoli in senescent cancer cells is associated with increased levels of polyadenylated transcripts derived from noncoding regions of rDNA units.European biophysics journal : EBJ · 2025Article
- cTAGE5/MEA6 Regulates LBR Localization to Maintain Nuclear Envelope Integrity and Safeguard Against Aging.Aging cell · 2025Article
- Interrogating the regulatory epigenome of cellular senescence.Cellular and molecular life sciences : CMLS · 2025Review
- Role of Cellular Senescence in Parkinson's Disease: Potential for Disease-Modification Through Senotherapy.Biomedicines · 2025Review
- Mechanotransduction for therapeutic approaches: Cellular aging and rejuvenation.APL bioengineering · 2025Review
- Spatio-Temporal Characterization of Cellular Senescence Hallmarks in Experimental Ischemic Stroke.International journal of molecular sciences · 2025Article
- Cytogenetic bands and sharp peaks of Alu underlie large-scale segmental regulation of nuclear genome architecture.Nucleus (Austin, Tex.) · 2024Article
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- Altered expression and localization of nuclear envelope proteins in a prostate cancer cell system.Molecular biology reports · 2024Article
- Nuclear reassembly defects after mitosis trigger apoptotic and p53-dependent safeguard mechanisms in Drosophila.PLoS biology · 2024Article
- Cellular Senescence in Acute Liver Injury: What Happens to the Young Liver?Aging and disease · 2024Review
- Molecular Basis of Neuronal and Microglial States in the Aging Brain and Impact on Cerebral Blood Vessels.International journal of molecular sciences · 2024Review
- Loss of miR-101-3p in melanoma stabilizes genomic integrity, leading to cell death prevention.Cellular & molecular biology letters · 2024Article
- Differences in Alu vs L1-rich chromosome bands underpin architectural reorganization of the inactive-X chromosome and SAHFs.bioRxiv : the preprint server for biology · 2024Article
- PURPL and NEAT1 Long Non-Coding RNAs Are Modulated in Vascular Smooth Muscle Cell Replicative Senescence.Biomedicines · 2023Article
- Reliable Hallmarks and Biomarkers of Senescent Lymphocytes.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anchoring of heterochromatin to the nuclear envelope appears to be an important process ensuring the spatial organization of the chromatin structure and genome function in eukaryotic nuclei. Proteins of the inner nuclear membrane (INM) mediating these interactions are able to recognize lamina-associated heterochromatin domains (termed LAD) and simultaneously bind either lamin A/C or lamin B1. One of these proteins is the lamin B receptor (LBR) that binds lamin B1 and tethers heterochromatin to the INM in embryonic and undifferentiated cells. It is replaced by lamin A/C with specific lamin A/C binding proteins at the beginning of cell differentiation and in differentiated cells. Our functional experiments in cancer cell lines show that heterochromatin in cancer cells is tethered to the INM by LBR, which is downregulated together with lamin B1 at the onset of cell transition to senescence. The downregulation of these proteins in senescent cells leads to the detachment of centromeric repetitive sequences from INM, their relocation to the nucleoplasm, and distension. In cells, the expression of LBR and LB1 is highly coordinated as evidenced by the reduction of both proteins in LBR shRNA lines. The loss of the constitutive heterochromatin structure containing LADs results in changes in chromatin architecture and genome function and can be the reason for the permanent loss of cell proliferation in senescence.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.