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Long lifetime and tissue-specific accumulation of lamin A/C in Hutchinson-Gilford progeria syndrome. [PDF]

open access: yesJ Cell Biol
Hasper J   +5 more
europepmc   +1 more source

Coronary and carotid artery dysfunction and KV7 overexpression in a mouse model of Hutchinson-Gilford progeria syndrome. [PDF]

open access: yesGeroscience
Macías Á   +7 more
europepmc   +1 more source
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Telomere length in Hutchinson-Gilford Progeria Syndrome

Mechanisms of Ageing and Development, 2009
Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare premature aging disorder caused by mutations in the gene LMNA, which encodes the nuclear matrix protein lamin A. Previous research has shown that the average telomere length in fibroblasts from HGPS patients is shorter than in age-matched controls. How mutations in lamin A lead to shortened telomere
Michelle L, Decker   +3 more
openaire   +4 more sources

Hutchinson–Gilford progeria syndrome

Clinical Genetics, 2004
Hutchinson–Gilford progeria syndrome (HGPS) is an extremely rare genetic disorder that causes premature, rapid aging shortly after birth. Recently, de novo point mutations in the Lmna gene have been found in individuals with HGPS. Lmna encodes lamin A and C, the A‐type lamins, which are an important structural component of the nuclear envelope.
R L, Pollex, R A, Hegele
openaire   +3 more sources

Lethal neonatal Hutchinson‐Gilford progeria syndrome

American Journal of Medical Genetics, 1999
We report on a 35-week gestation female fetus with Hutchinson-Gilford progeria (HGP). This patient, who is the first reported with neonatal HGP in the English literature but is the fourth, counting three previous French cases, supports the existence of a more severe prenatal form of progeria. She died 7 hours after birth and presented with intrauterine
J I, Rodríguez   +3 more
openaire   +2 more sources

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