ArticleJournal of cell science2018
Nucleoplasmic lamins define growth-regulating functions of lamina-associated polypeptide 2α in progeria cells.
Article in Journal of cell science, 2018. 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
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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.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Radiation symptoms resemble laminopathies and the physical underlying cause may sit at the lamin A C-terminus.Molecular medicine (Cambridge, Mass.) · 2025Article
- Dexamethasone induces p21FEBS open bio · 2023Article
- Activation of endoplasmic reticulum stress in premature aging via the inner nuclear membrane protein SUN2.Cell reports · 2023Article
- Nuclear mechanosignaling in striated muscle diseases.Frontiers in physiology · 2023Review
- Cytoplasmic keratins couple with and maintain nuclear envelope integrity in colonic epithelial cells.Molecular biology of the cell · 2022Article
- Mechanical Pressure Driving Proteoglycan Expression in Mammographic Density: a Self-perpetuating Cycle?Journal of mammary gland biology and neoplasia · 2021Review
- A hub-and-spoke nuclear lamina architecture in trypanosomes.Journal of cell science · 2021Article
- The nucleoplasmic interactions among Lamin A/C-pRB-LAP2α-E2F1 are modulated by dexamethasone.Scientific reports · 2021Article
- Knockdown of LAP2α inhibits osteogenic differentiation of human adipose-derived stem cells by activating NF-κB.Stem cell research & therapy · 2020Article
- The Cutting Edge: The Role of mTOR Signaling in Laminopathies.International journal of molecular sciences · 2019Review
- Hutchinson-Gilford Progeria Syndrome-Current Status and Prospects for Gene Therapy Treatment.Cells · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
A-type lamins are components of the peripheral nuclear lamina but also localize in the nuclear interior in a complex with lamina-associated polypeptide (LAP) 2α. Loss of LAP2α and nucleoplasmic lamins in wild-type cells increases cell proliferation, but in cells expressing progerin (a mutant lamin A that causes Hutchinson-Gilford progeria syndrome), low LAP2α levels result in proliferation defects. Here, the aim was to understand the molecular mechanism governing how relative levels of LAP2α, progerin and nucleoplasmic lamins affect cell proliferation. Cells from progeria patients and inducible progerin-expressing cells expressing low levels of progerin proliferate faster than wild-type or lamin A-expressing control cells, and ectopic expression of LAP2α impairs proliferation. In contrast, cells expressing high levels of progerin and lacking lamins in the nuclear interior proliferate more slowly, and ectopic LAP2α expression enhances proliferation. However, simultaneous expression of LAP2α and wild-type lamin A or an assembly-deficient lamin A mutant restored the nucleoplasmic lamin A pool in these cells and abolished the growth-promoting effect of LAP2α. Our data show that LAP2α promotes or inhibits proliferation of progeria cells depending on the level of A-type lamins in the nuclear interior.This article has an associated First Person interview with the first author of the paper.
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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.