Lamin A-Dependent Nuclear Defects in Human Aging
By Paola Scaffidi, Tom Misteli. Science, 2006
1,194 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/ed8db8a02925bbcdf69af9d4a71174b965c78e9c
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In Molecular Biology
- Linda Partridge
- Manuel Serrano
- L. Studer
- Guido Kroemer
- C. López‐Otín
- J. Tyler
- M. Blasco
- Fred H. Gage
Citations in the corpus
- Skin anti-aging strategies (2012, background): “These factors lead together to cumulative structural and physiological alterations and progressive changes in each skin layer as well as changes in skin appearance, especially, on the sun-exposed skin areas.(2-12) In contrast to thin and atrophic, finely wrinkled and dry intrinsically aged skin, pre”
- The hallmarks of aging. (2013, background): “Alterations of the nuclear lamina and production of an aberrant prelamin A isoform called progerin have also been detected during normal human aging (Ragnauth et al., 2010; Scaffidi and Misteli, 2006).”
- Directly Reprogrammed Human Neurons Retain Aging-Associated Transcriptomic Signatures and Reveal Age-Related Nucleocytoplasmic Defects (2015, positive): “nuclear stiffness and severely altered nuclear architecture, leading to a body-wide phenotype of premature aging (Hennekam, 2006; Scaffidi and Misteli, 2006).”
- Epigenetics and aging (2016, background): “Although some of the defects observed in premature aging patients have also been observed in aged individuals (39), it is still debatable whether the findings are equally applicable to physiological aging.”
- Human iPSC-based Modeling of Late-Onset Disease via Progerin-induced Aging (2013, positive): “However, the age-associated signature could be dependent on progerin expression (Scaffidi and Misteli, 2006), and the absence of an age-related phenotype in iPSCs may simply reflect the fact that pluripotent cells do not express A-type lamins including progerin (Constantinescu et al., 2006).”
- Aging Hematopoietic Stem Cells Decline in Function and Exhibit Epigenetic Dysregulation (2007, background): “For instance, lamin A declined with age and is linked to normal human aging [42] and Hutchinson-Gilford progeria [43] (Table 1).”
- Nuclear lamins: major factors in the structural organization and function of the nucleus and chromatin. (2008, positive): “Of great interest is the possibility that the altered lamins expressed in progeria patients may be involved not only in premature aging, but also in normal aging, as LA 50/progerin has been found in a small number of cells in cultures obtained from healthy individuals, especially in those from older”