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Progeri
> Publikationer
Publikationer av Progeri
Néstor-Guillermo progeria syndrome: a novel premature aging condition with early onset and chronic development caused by BANF1 mutations.
https://www.ncbi.nlm.nih.gov/pubmed/21932319
av Juan
Forskare
Exome sequencing and functional analysis identifies BANF1 mutation as the cause of a hereditary progeroid syndrome.
https://www.ncbi.nlm.nih.gov/pubmed/21549337
av Juan
Forskare
Aging and chronic DNA damage response activate a regulatory pathway involving miR-29 and p53.
https://www.ncbi.nlm.nih.gov/pubmed/21522133
av Juan
Forskare
Type B mandibuloacral dysplasia with congenital myopathy due to homozygous ZMPSTE24 missense mutation.
https://www.ncbi.nlm.nih.gov/pubmed/21267004
av Juan
Forskare
Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice.
https://www.ncbi.nlm.nih.gov/pubmed/21113150
av Juan
Forskare
Combined treatment with statins and aminobisphosphonates extends longevity in a mouse model of human premature aging.
https://www.ncbi.nlm.nih.gov/pubmed/18587406
av Juan
Forskare
Premature aging in mice activates a systemic metabolic response involving autophagy induction.
https://www.ncbi.nlm.nih.gov/pubmed/18443001
av Juan
Forskare
Nuclear envelope defects cause stem cell dysfunction in premature-aging mice.
https://www.ncbi.nlm.nih.gov/pubmed/18378773
av Juan
Forskare
Human progeroid syndromes, aging and cancer: new genetic and epigenetic insights into old questions.
https://www.ncbi.nlm.nih.gov/pubmed/17131053
av Juan
Forskare
From immature lamin to premature aging: molecular pathways and therapeutic opportunities.
https://www.ncbi.nlm.nih.gov/pubmed/16258283
av Juan
Forskare
Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation.
https://www.ncbi.nlm.nih.gov/pubmed/16079796
av Juan
Forskare
Genomic instability in laminopathy-based premature aging.
https://www.ncbi.nlm.nih.gov/pubmed/15980864
av Juan
Forskare
Loss of ZMPSTE24 (FACE-1) causes autosomal recessive restrictive dermopathy and accumulation of Lamin A precursors.
https://www.ncbi.nlm.nih.gov/pubmed/15843403
av Juan
Forskare
Defective prelamin A processing and muscular and adipocyte alterations in Zmpste24 metalloproteinase-deficient mice.
https://www.ncbi.nlm.nih.gov/pubmed/11923874
av Juan
Forskare