People of Beyond the exome
Assistant Prof. Dr. rer. nat. Ferah Yildirim
Department of Psychiatry and Psychotherapy
Charité-Universitätsmedizin Berlin
Charitéplatz 1,
D-10117 Berlin, Germany
Phone: +49 (0)30 450539193
FAX: +49 (0)30 4507539920
Email: ferah.yildirim@charite.de
Homepage: www.ferahyildirimlab.com
Ferah Yildirim is an assistant professor for Neuropsychiatry at the Department of Psychiatry and Psychotherapy in the Mitte Campus of Charité University Hospital Berlin and a Principal Investigator at the Einstein Center for Neurosciences Berlin. She received a BSc in Medical Biology from Cerrahpasa Medical School at Istanbul University, followed by a MSc and PhD in Medical Neurosciences from Charité University Hospital Berlin. She received her post-doctoral training at Massachusetts Institute of Technology. From the earliest stages, her scientific career has been dedicated to understanding the dysregulation of gene expression and the role of epigenetics in central nervous system diseases, for the ultimate goal of developing effective treatments for patients. Her graduate work, in Ulrich Dirnagl’s lab at Charité Berlin, demonstrated therapeutic effects of histone deacetylase inhibitors in cell and mouse models of ischemic brain disease, elucidating an epigenetic mechanism leading to protection of neurons from ischemic injury. During her postdoctoral work in the labs of Ernest Fraenkel and David Housman at MIT, she and her colleagues have reported the first description of a neuron-specific chromatin signature underlying the vulnerability of neuronal genes to Huntingtin mutation resulting in their dysregulation in Huntington’s disease. Since November 2014, her group at Charité Berlin applies a combination of genome-wide DNA sequencing technologies with mechanistic and functional approaches to neuropsychiatric disease models to identify key epigenetic/transcriptional regulatory events that are responsible for aberrant gene expression in disease. Her lab has extensive experience in using next generation DNA sequencing techniques such as chromatin immunoprecipitation followed by sequencing (ChIP-seq) for histone marks and transcription factors, reduced representation bisulfite sequencing (RRBS) and RNA sequencing (RNA-seq) to study human disease. In collaboration with Christian Rosenmund, she has recently established single-cell RNA-seq method in her lab enabling them to measure cell-type-specific transcription and to link specific transcriptional modules to certain neuronal functions. In other studies, her lab evaluates therapeutic potentials of recently-developed, specific chromatin-targeting agents in models of neuropsychiatric conditions. She is currently concentrating on transferring her lab’s approaches to study other human conditions including muscle disease and alcohol addiction through established collaborations with Uwe Ohler, Markus Schuelke and Andreas Heinz.
Publications (selection)
HD iPSC Consortium. Developmental alterations in Huntington's disease neural cells and pharmacological rescue in cells and mice. Nat Neurosci 2017;20:648-660
Schweizer S, Harms C, Lerch H, Flynn J, Hecht J, Yildirim F, Meisel A, Märschenz S. Inhibition of histone methyltransferases SUV39H1 and G9a leads to neuroprotection in an in vitro model of cerebral ischemia. J Cereb Blood Flow Metab 2015;35:1640-7
Vashishtha M*, Ng CW*, Yildirim F*, Gipson TA, Kratter IH, Bodai L, Song W, Lau A, Labadorf A, Vogel-Ciernia A, Troncosco J, Ross CA, Bates GP, Krainc D, Sadri-Vakili G, Finkbeiner S, Marsh JL, Housman DE, Fraenkel E, Thompson LM. Targeting H3K4 trimethylation in Huntington disease. Proc Natl Acad Sci USA 2013;110:E3027-36. | * equal contribution
Ng CW, Yildirim F, Yap YS, Dalin S, Matthews BJ, Velez PJ, Labadorf A, Housman DE, Fraenkel E. Extensive changes in DNA methylation are associated with expression of mutant huntingtin. Proc Natl Acad Sci USA 2013;110:2354-9.
Yildirim F, Gertz K, Kronenberg G, Harms C, Fink KB, Meisel A, Endres M. Inhibition of histone deacetylation protects wildtype but not gelsolin-deficient mice from ischemic brain injury. Exp Neurol 2008;210:531-542.