The DOI matches its Crossref record; 111 of the 111 references it cites were found in a registry or an index.
Werner and Hutchinson–Gilford progeria syndromes: mechanistic basis of human progeroid diseases
Abstract
Progeroid syndromes have been the focus of intense research in part because they might provide a window into the pathology of normal ageing. Werner syndrome and Hutchinson-Gilford progeria syndrome are two of the best characterized human progeroid diseases. Mutated genes that are associated with these syndromes have been identified, mouse models of disease have been developed, and molecular studies have implicated decreased cell proliferation and altered DNA-damage responses as common causal mechanisms in the pathogenesis of both diseases.
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In the citing paper
“The aberrantly processed protein produced is called progerin, a truncated form of lamin A with a hydrophobic farnesylated C-terminal 105–112.”
From Xeroderma Pigmentosa Group A (XPA), Nucleotide Excision Repair and Regulation by ATR in Response to Ultraviolet Irradiation (2017) · cites this paper as [107]
In the citing paper
“Hutchison-Gilford progeria syndrome (HGPS) patients suffer from a variety of laminopathy ailments due to a sporadic deficiency in the proteolytic processing of the precursor form of lamin A into the mature protein.”
From Xeroderma Pigmentosa Group A (XPA), Nucleotide Excision Repair and Regulation by ATR in Response to Ultraviolet Irradiation (2017) · cites this paper as [107]
In the citing paper
“Interestingly, HGPS and RD are laminopathy-based diseases; they arise not from mutated DNA metabolism genes but from mutations causing altered processing/maturation of lamin A, an intermediate-filament protein component of the nuclear lamina [6,11-16].”
From Genomic instability and DNA damage responses in progeria arising from defective maturation of prelamin A (2009) · cites this paper as [6]
In the citing paper
“Progerin and FC-prelamin A, the mutant forms of lamin A in HGPS and RD cells, respectively (Figure 1; [6,11-16]), are known to disrupt normal nuclear structure including the perinucleolar lamin A/C granules containing the replicative proteins PCNA and polymerase δ [33].”
From Genomic instability and DNA damage responses in progeria arising from defective maturation of prelamin A (2009) · cites this paper as [6]
In the citing paper
“Nonetheless, changes in chromatin state have been strongly implicated in ageing by progeroid syndromes, which disrupt the nuclear lamina and its associated regulation of heterochromatin structure142,143.”
From Measuring biological age using omics data (2022) · cites this paper as [142]
In the citing paper
“Werner syndrome (WS) is a premature aging disorder caused by WRN protein deficiency.”
From A Werner syndrome stem cell model unveils heterochromatin alterations as a driver of human aging (2015) · cites this paper as [1]
Citations
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“Therefore, the pathogenesis of WS might reflect the progressive accumulation of mutant or senescent cells that have lost cell-specific functions, as well as trophic or regulatory interactions with adjacent epithelial or stromal cell”
BackgroundRecurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome
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Metadata
- Authors
- Kudlow, B. A., Kennedy, B. K., & Monnat, R. J.
- Affiliations
- University of Washington (US)
- Corresponding author
- Kennedy, Brian K.
- Monnat, Raymond J.
- Venue
- Nature Reviews Molecular Cell Biology
- Published
- 2007-05
- Volume
- 8
- Issue
- 5
- Pages
- 394-404
- ISSN
- 1471-0072 (ISSN-L)
- 1471-0080
- OpenAlex
- W2163819508
- Cited by
- 304
- References
- 110
- Citations by year
- 2026: 10 · 2025: 8 · 2024: 12 · 2023: 12 · 2022: 17 · 2021: 11 · 2020: 14 · 2019: 13 · 2018: 18 · 2017: 12 · 2016: 17 · 2015: 14 · 2014: 10 · 2013: 14 · 2012: 14
- FWCI
- 2.28
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Molecular Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- Werner syndrome, Hutchinson-Gilford progeria syndrome, progeroid syndromes, premature aging, DNA damage response, cell proliferation, mouse models of human disease, genetic mutations, normal aging
- MeSH terms
- Werner Syndrome Helicase, Aging, Animals, Disease Models, Animal, DNA Damage, Exodeoxyribonucleases, Humans, Models, Biological, Phenotype, Progeria, Protein Processing, Post-Translational, Werner Syndrome, Lamin Type A, RecQ Helicases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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