Mutant nuclear lamin A leads to progressive alterations of epigenetic control in premature aging.

By D. Shumaker, T. Dechat, Alexander Kohlmaier, S. Adam, Matthew R. Bozovsky, M. Erdos, M. Eriksson, A. Goldman, S. Khuon, F. S. Collins and 2 more. Proceedings of the National Academy of Sciences of the United States of America, 2006

761 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b2cecc15781610734e2031e2e09c1e05038425c2

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Citations in the corpus

The hallmarks of aging. (2013, background): “Cells from patients and mice with progeroid syndromes exhibit DNA methylation patterns and histone modifications that largely recapitulate those found in normal aging (Osorio et al., 2010; Shumaker et al., 2006).”
A promiscuous biotin ligase fusion protein identifies proximal and interacting proteins in mammalian cells (2012, background): “In these cells, myc-BirA*LaA localizes predominantly to the nuclear envelope, similar to both endogenous LaA and LaA harboring an N-terminal GFP tag, a modi cation that does not appear to alter the function of LaA (Broers et al., 1999; Shumaker et al., 2006).”
Beyond the sequence: cellular organization of genome function. (2007, neutral): “Interestingly, a hallmark of at least one of the lamin A-mediated genetic diseases is the dramatic change in histone-modiﬁcation patterns and the almost complete loss of heterochromatin (Scafﬁdi and Misteli, 2005; Shumaker et al., 2006).”
Epigenetics and aging (2016, background): “The same study also revealed an increase in the level of H4 K20me3, which serves as a signature epigenetic mark of constitutive heterochromatin, demonstrating a shift in the epigenetic landscape in HGPS patients (40).”
Nuclear lamins: major factors in the structural organization and function of the nucleus and chromatin. (2008, neutral): “The reduction in H3K27me3 is probably the direct result of the significant decrease in the expression of the histone methyltransferase (HMT), enhancer of zeste homolog (EZH2), that has been reported in HGPS fibroblasts (Shumaker et al. 2006).”
Next-Generation Genomics: an Integrative Approach (2010, neutral): “Nuclear-membrane-attached loci are typically marked by H3K9 methylation, and this modification is decreased in the laminin-associated diseases Hutchinson–Gilford progeria syndrome and facioscapulohumeral dystroph”