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Progerie > Veröffentlichungen

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
von Juan
Forscher

Exome sequencing and functional analysis identifies BANF1 mutation as the cause of a hereditary progeroid syndrome.

https://www.ncbi.nlm.nih.gov/pubmed/21549337
von Juan
Forscher

Aging and chronic DNA damage response activate a regulatory pathway involving miR-29 and p53.

https://www.ncbi.nlm.nih.gov/pubmed/21522133
von Juan
Forscher

Type B mandibuloacral dysplasia with congenital myopathy due to homozygous ZMPSTE24 missense mutation.

https://www.ncbi.nlm.nih.gov/pubmed/21267004
von Juan
Forscher

Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice.

https://www.ncbi.nlm.nih.gov/pubmed/21113150
von Juan
Forscher

Combined treatment with statins and aminobisphosphonates extends longevity in a mouse model of human premature aging.

https://www.ncbi.nlm.nih.gov/pubmed/18587406
von Juan
Forscher

Premature aging in mice activates a systemic metabolic response involving autophagy induction.

https://www.ncbi.nlm.nih.gov/pubmed/18443001
von Juan
Forscher

Nuclear envelope defects cause stem cell dysfunction in premature-aging mice.

https://www.ncbi.nlm.nih.gov/pubmed/18378773
von Juan
Forscher

Human progeroid syndromes, aging and cancer: new genetic and epigenetic insights into old questions.

https://www.ncbi.nlm.nih.gov/pubmed/17131053
von Juan
Forscher

From immature lamin to premature aging: molecular pathways and therapeutic opportunities.

https://www.ncbi.nlm.nih.gov/pubmed/16258283
von Juan
Forscher

Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation.

https://www.ncbi.nlm.nih.gov/pubmed/16079796
von Juan
Forscher

Genomic instability in laminopathy-based premature aging.

https://www.ncbi.nlm.nih.gov/pubmed/15980864
von Juan
Forscher

Loss of ZMPSTE24 (FACE-1) causes autosomal recessive restrictive dermopathy and accumulation of Lamin A precursors.

https://www.ncbi.nlm.nih.gov/pubmed/15843403
von Juan
Forscher

Defective prelamin A processing and muscular and adipocyte alterations in Zmpste24 metalloproteinase-deficient mice.

https://www.ncbi.nlm.nih.gov/pubmed/11923874
von Juan
Forscher