Welcome to the Leibniz Institute on Aging (FLI)
The Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) is the first national research institute in Germany focusing on biomedical research on human aging, a multifactorial process controlled by environmental and genetic factors.
This website will provide you with an insight into our institute, the research we do and the faces behind FLI's science activities. We wish you an exciting and entertaining voyage of discovery into the world of aging research at FLI.
Since 2004, our mission has been to delineate basic molecular mechanisms that underlie the aging process in humans and its consequences for the development of aging-related cell and tissue dysfunction and diseases. Research at the FLI will provide a knowledge basis for the development of therapies aiming to facilitate healthy aging by prolonging organismal functions and disease prevention in the elderly.
In order to better correspond to this research focus, the institute was re-named from Leibniz Institute for Age Research to the Leibniz Institute on Aging in 2015.
recent high impact publications
- OmoMYC blunts promoter invasion by oncogenic MYC to inhibit gene expression characteristic of MYC-dependent tumors.
Jung LA, Gebhardt A, Koelmel W, Ade CP, Walz S, Kuper J, von Eyss B, Letschert S, Redel C, d'Artista L, Biankin A, Zender L, Sauer M, Wolf E, Evan G, Kisker C, Eilers M
Oncogene 2017 (epub ahead of print) published during change of institution
- The tumour suppressor CYLD regulates the p53 DNA damage response.
Fernández-Majada V, Welz PS, Ermolaeva MA, Schell M, Adam A, Dietlein F, Komander D, Büttner R, Thomas RK, Schumacher B, Pasparakis M
Nat Commun 2016, 7, 12508 published during change of institution
- Rictor/mTORC2 deficiency enhances keratinocyte stress tolerance via mitohormesis.
Tassone B, Saoncella S, Neri F, Ala U, Brusa D, Magnuson MA, Provero P, Oliviero S, Riganti C, Calautti E
Cell Death Differ 2017 (epub ahead of print) published during change of institution
- Intragenic DNA methylation prevents spurious transcription initiation.
Neri F, Rapelli S, Krepelova A, Incarnato D, Parlato C, Basile G, Maldotti M, Anselmi F, Oliviero S
Nature 2017 (epub ahead of print)
- Citron Kinase Deficiency Leads to Chromosomal Instability and TP53-Sensitive Microcephaly.
Bianchi FT, Tocco C, Pallavicini G, Liu Y, Vernì F, Merigliano C, Bonaccorsi S, El-Assawy N, Priano L, Gai M, Berto GE, Chiotto AMA, Sgrò F, Caramello A, Tasca L, Ala U, Neri F, Oliviero S, Mauro A, Geley S, Gatti M, Di Cunto F
Cell Rep 2017, 18(7), 1674-86 published during change of institution
- MicroRNA miR-29 controls a compensatory response to limit neuronal iron accumulation during adult life and aging.
Ripa R, Dolfi L, Terrigno M, Pandolfini L, Savino A, Arcucci V, Groth M, Terzibasi Tozzini E, Baumgart M, Cellerino A
BMC Biol 2017, 15(1), 9