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The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.

Progeria: A Paradigm for Translational Medicine

Gordon, Leslie B., Rothman, Frank G., López-Otín, Carlos, Misteli, Tom·2014·Cell
DOI 10.1016/j.cell.2013.12.028PMC PMC6318797
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Crossref · 10.1016/j.cell.2013.12.028

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  • Alterations of the nuclear lamina and production of progerin are characteristics of normal human aging, and lamin B1 levels decline during cellular senescence.

    “Alterations of the nuclear lamina and production of an aberrant prelamin A isoform called progerin are also characteristics of normal human aging, and lamin B1 levels decline during cellular senescence 25 .”

    From Hallmarks of aging: An expanding universe (2023) · cites this paper as [25]

    The section “What Progeria May or May Not Teach Us about Normal Aging” states that progerin is produced in normally aging individuals and discusses cellular defects associated with aging. The “Nuclear Morphology and Function” section describes nuclear-lamina changes in HGPS cells, but does not establish those specific changes as characteristics of normal aging. No passage found reports that lamin B1 levels decline during cellular senescence. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Loss of ZMPSTE24 abolishes normal proteolytic maturation of prelamin A and causes a progeroid syndrome in mice, phenocopying humans with loss-of-function ZMPSTE24 mutations.

    “Loss of the protease ZMPSTE24 abolishes the normal proteolytic maturation of prelamin A and causes a progeroid syndrome in mice, phenocopying that observed in humans with loss-of-function mutations of ZMPSTE24 25 .”

    From Hallmarks of aging: An expanding universe (2023) · cites this paper as [25]

    “A Short History of HGPS” identifies ZMPSTE24 as the enzyme that cleaves prelamin A during normal maturation. “What Progeria May or May Not Teach Us about Normal Aging” describes a progeroid mouse model lacking ZMPSTE24 that recapitulates some HGPS phenotypes. The copy does not establish the more specific comparison with humans carrying loss-of-function ZMPSTE24 mutations; its account of HGPS instead identifies an LMNA mutation. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

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Research works printed but not linked: 66

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Metadata

Authors
Gordon, L. B., Rothman, F. G., López-Otín, C., & Misteli, T.
Venue
Cell
Publisher
Elsevier BV
Published
2014-01
Volume
156
Issue
3
Pages
400-407
ISSN
0092-8674
DOI
10.1016/j.cell.2013.12.028
PMC
PMC6318797
Cited by
278
References
7
Language
en
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