Prof. Dr. Frank Kaiser

Sektion für Funktionelle Genetik
am Institut für Humangenetik
Universität zu Lübeck
Ratzeburger Allee 160
23538 Lübeck
Tel.: +49 451 5002623
Fax: +49 451 5004861



Curriculum vitae

Frank Kaiser studied biology at the Ruhr-University Bochum. He completed his diploma thesis in 1999 at the Department of Molecular Genetics at the Institute of Microbiology in Bochum. In his doctorate (2000-2003) and subsequent postdoctoral studies (2003-2006) at the Institute of Human Genetics in Essen (Prof. Dr. Horsthemke), he performed functional analysis of the transcription factor TRPS1. In 2006, he moved to the Institute of Human Genetics in Lübeck (Prof. Dr. Gillessen-Kaesbach), became head of the research laboratory and established a junior research group with the focus on cohesinopathies. In 2013, he was appointed W2 Professor for Functional Genetics and since 2014 he has been head of the newly established Functional Genetics Section at the Institute of Human Genetics in Lübeck. Since 2016, Frank Kaiser has been W3 Professor of Functional Genetics / Human Genetics. In addition to genetic and functional analyzes in the field of cohesinopathies, the research of his research group focusses on molecular mechanisms in the area of genetic disorders and hereditary diseases. Frank Kaiser is a member (Principal Investigator) at the German Center for Cardiovascular Research (DZHK), coordinator of the E-Rare network TARGET-CdLS and co-coordinator of the DFG research group FOR2488 ‘ProtectMove’, which was initiated in 2016.

Important publications

Watrin E, Kaiser FJ, Wendt KS. (2016) Gene regulation and chromatin organization: relevance of cohesin mutations to human disease. Curr Opin Genet Dev. 37:59-66.

Parenti I, Gervasini C, Pozojevic J, Graul-Neumann L, Azzollini J, Braunholz D, Watrin E, Wendt KS, Cereda A, Cittaro D, Gillessen-Kaesbach G, Lazarevic D, Mariani M, Russo S, Werner R, Krawitz P, Larizza L, Selicorni A, Kaiser FJ.(2016). Broadening of cohesinopathies: exome sequencing identifies mutations in ANKRD11 in two patients with Cornelia de Lange-overlapping phenotype. Clin Genet. 89(1):74-81.

Braunholz D, Obieglo C, Parenti I, Pozojevic J, Eckhold J, Reiz B, Braenne I, Wendt KS, Watrin E, Vodopiutz J, Rieder H, Gillessen-Kaesbach G, Kaiser FJ. (2015) Hidden mutations in Cornelia de Lange syndrome limitations of sanger sequencing in molecular diagnostics. Hum Mutat. 36(1):26-9.

Kaiser FJ, Ansari M, Braunholz D, …, Gillessen-Kaesbach G, Ramos FJ, Jackson LG, Shirahige K, Pie J. Christianson DW, Krantz ID, FitzPatrick DR, Deardorff MA. (2014). Loss of Function HDAC8 Mutations Cause a Phenotypic Spectrum of Cornelia de Lange Syndrome-like Features, Ocular Hypertelorism, Large Fontanelle and X-linked Inheritance . Hum Mol Genet. 23(11):2888-900.

Deardorff MA*, Bando M*, Nakato R*, Watrin E*, Itoh T, Minamino M, Saitoh K, Komata M, Katou Y, Clark D, Cole KE, De Baere E, Decroos C, Ernst S, Francey L, Gyftodimou Y, Hirashima K, Hullings M, Ishikawa Y, Kaur M, Kiyono T, Lombardi PM, Mortier GR, Nozaki N, Petersen MB, Seimiya H, Siu VM, Suzuki Y, Takagaki K, Tyshchenko N, Wilde JJ, Willems PJ, Gillessen-Kaesbach G, Christianson DW, Kaiser FJ, Jackson LG, Hirota T, Krantz ID, Shirahige K. (2012). HDAC8 mutations in Cornelia de Lange Syndrome affect the cohesin acetylation cycle. Nature 489(7415):313-7.

Deardorff MA, Wilde JJ, Albrecht M, Dickinson E, Tennstedt S, Braunholz D, Mönnich M, Yan Y, Xu W, Gil-Rodríguez MC, Clark D, Hakonarson H, Halbach S, Michelis LD, Rampuria A, Rossier E, Spranger S, Van Maldergem L, Lynch SA, Gillessen-Kaesbach G, Ludecke HJ, Ramsay RG, McKay MJ, Krantz ID, Xu H, Horsfield JA, Kaiser FJ. (2012). RAD21 Mutations Cause a Human Cohesinopathy. Am J Hum Genet. 90(6):1014-27.