ReviewJournal of biosciences2011
Lamins, laminopathies and disease mechanisms: possible role for proteasomal degradation of key regulatory proteins.
Review in Journal of biosciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
11 citing papers in PubMed, 25 citations in OpenAlex.
- Dynamic Post-translational Modifications of Nuclear Lamins in Cellular Function and Pathophysiology.Sub-cellular biochemistry · 2025Review
- Chromatin and Cancer: Implications of Disrupted Chromatin Organization in Tumorigenesis and Its Diversification.Cancers · 2023Review
- Post-Translational Modification of Lamins: Mechanisms and Functions.Frontiers in cell and developmental biology · 2022Review
- Recent advances in understanding nuclear size and shape.Nucleus (Austin, Tex.) · 2016Review
- Use of Xenopus cell-free extracts to study size regulation of subcellular structures.The International journal of developmental biology · 2016Review
- Sustained accumulation of prelamin A and depletion of lamin A/C both cause oxidative stress and mitochondrial dysfunction but induce different cell fates.Nucleus (Austin, Tex.) · 2015Article
- Breaking down protein degradation mechanisms in cardiac muscle.Trends in molecular medicine · 2013Review
- Review
- Lamin A/C haploinsufficiency modulates the differentiation potential of mouse embryonic stem cells.PloS one · 2013Article
- Lamin misexpression upregulates three distinct ubiquitin ligase systems that degrade ATR kinase in HeLa cells.Molecular and cellular biochemistry · 2012Article
- Ubiquitin ligase RNF123 mediates degradation of heterochromatin protein 1α and β in lamin A/C knock-down cells.PloS one · 2012Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lamins are major structural proteins of the nucleus and are essential for nuclear integrity and organization of nuclear functions. Mutations in the human lamin genes lead to highly degenerative genetic diseases that affect a number of different tissues such as muscle, adipose or neuronal tissues, or cause premature ageing syndromes. New findings on the role of lamins in cellular signalling pathways, as well as in ubiquitin-mediated proteasomal degradation, have given important insights into possible mechanisms of pathogenesis.
Indexed as
Identifiers
What OpenQuestion holds
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.