ArticleCell cycle (Georgetown, Tex.)2014
The aggregation and inheritance of damaged proteins determines cell fate during mitosis.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- Vimentin protects differentiating stem cells from stress.Scientific reports · 2020Article
- Asymmetric cell division and replicative aging: a new perspective from the spindle poles.Current genetics · 2020Review
- Modelling stem cell ageing: a multi-compartment continuum approach.Royal Society open science · 2020Article
- Replacement of microglia in the aged brain reverses cognitive, synaptic, and neuronal deficits in mice.Aging cell · 2018Article
- Long Term Aggresome Accumulation Leads to DNA Damage, p53-dependent Cell Cycle Arrest, and Steric Interference in Mitosis.The Journal of biological chemistry · 2015Article
- Imperfect asymmetry: The mechanism governing asymmetric partitioning of damaged cellular components during mitosis.Bioarchitecture · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Recent evidence suggests that proliferating cells polarize damaged proteins during mitosis to protect one cell from aging, and that the structural conformation of damaged proteins mediates their toxicity. We report that the growth, resistance to stress, and differentiation characteristics of a cancer cell line (PC12) with an inducible Huntingtin (Htt) fused to enhanced green fluorescent protein (GFP) are dependent on the conformation of Htt. Cell progeny containing inclusion bodies have a longer cell cycle and increased resistance to stress than those with diffuse Htt. Using live imaging, we demonstrate that asymmetric division resulting from a cell containing a single inclusion body produces sister cells with different fates. The cell that receives the inclusion body has decreased proliferation and increased differentiation compared with its sister cell without Htt. This is the first report that reveals a functional consequence of the asymmetric division of damaged proteins in mammalian cells, and we suggest that this is a result of inclusion body-induced proteasome impairment.
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Registered trials
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