C
Christopher Boehlke
Researcher at University of Freiburg
Publications - 32
Citations - 2254
Christopher Boehlke is an academic researcher from University of Freiburg. The author has contributed to research in topics: Cilium & Palliative care. The author has an hindex of 19, co-authored 30 publications receiving 2019 citations. Previous affiliations of Christopher Boehlke include University Medical Center Freiburg.
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Journal ArticleDOI
TRPP2 and TRPV4 form a polymodal sensory channel complex
Michael Köttgen,Björn Buchholz,Miguel A. Garcia-Gonzalez,Fruzsina Kotsis,Xiao-Hua Fu,Mara Doerken,Christopher Boehlke,Daniel Steffl,Robert Tauber,Tomasz Wegierski,Roland Nitschke,Makoto Suzuki,Albrecht Kramer-Zucker,Gregory G. Germino,Terry Watnick,Jean Prenen,Bernd Nilius,E. Wolfgang Kuehn,Gerd Walz +18 more
TL;DR: It is found that TRPV4, like TRPP2, is an essential component of the ciliary mechanosensor, and the concept that defective ciliary flow sensing constitutes the fundamental mechanism of cystogenesis is challenged.
Journal ArticleDOI
Primary cilia regulate mTORC1 activity and cell size through Lkb1
Christopher Boehlke,Fruzsina Kotsis,Vishal Patel,Simone Braeg,Henriette Voelker,Saskia Bredt,Theresa Beyer,Heike Janusch,Christoph Hamann,Markus Gödel,Klaus Müller,Martin Herbst,Miriam Hornung,Mara Doerken,Michael Köttgen,Roland Nitschke,Peter Igarashi,Gerd Walz,E. Wolfgang Kuehn +18 more
TL;DR: It is shown that ablation of cilia in transgenic mice results in enlarged cells when compared with control animals, and the cilium-basal body compartment is identified as a spatially restricted activation site for Lkb1 signalling.
Primary cilia regulate mTORC1 activity and cell size through Lkb1. Nature - Cell Biology
Christopher Boehlke,Fruzsina Kotsis,E. Wolfgang Kuehn,Vishal Patel,Simone Braeg,Henriette Voelker,Saskia Bredt,Theresa Beyer,Heike Janusch,Christoph Hamann,Markus Gödel,Klaus Müller,Martin Herbst,Miriam Hornung,Mara Doerken,Michael Köttgen,Roland Nitschke,Peter Igarashi,Gerd Walz +18 more
Abstract: The mTOR pathway is the central regulator of cell size. External signals from growth factors and nutrients converge on the mTORC1 multi-protein complex to modulate downstream targets, but how the different inputs are integrated and translated into specific cellular responses is incompletely understood. Deregulation of the mTOR pathway occurs in polycystic kidney disease (PKD), where cilia (filiform sensory organelles) fail to sense urine flow because of inherited mutations in ciliary proteins. We therefore investigated if cilia have a role in mTOR regulation. Here, we show that ablation of cilia in transgenic mice results in enlarged cells when compared with control animals. In vitro analysis demonstrated that bending of the cilia by flow is required for mTOR downregulation and cell-size control. Surprisingly, regulation of cell size by cilia is independent of flow-induced calcium transients, or Akt. However, the tumour-suppressor protein Lkb1 localises in the cilium, and flow results in increased AMPK phosphorylation at the basal body. Conversely, knockdown of Lkb1 prevents normal cell-size regulation under flow conditions. Our results demonstrate that the cilium regulates mTOR signalling and cell size, and identify the cilium-basal body compartment as a spatially restricted activation site for Lkb1 signalling.
Journal ArticleDOI
Inhibition of mTORC1 by Astrin and Stress Granules Prevents Apoptosis in Cancer Cells
Kathrin Thedieck,Birgit Holzwarth,Mirja Tamara Prentzell,Christopher Boehlke,Kathrin Kläsener,Kathrin Kläsener,Stefanie Ruf,Annika G Sonntag,Lars Maerz,Sushma Nagaraja Grellscheid,Elisabeth Kremmer,Roland Nitschke,E. Wolfgang Kuehn,Johan W. Jonker,Albert K. Groen,Michael Reth,Michael Reth,Michael N. Hall,Ralf Baumeister +18 more
TL;DR: In this paper, the authors identify astrin as an essential negative mTORC1 regulator in the cellular stress response and show that in cancer cells, apoptosis suppression during stress depends on the presence of the raptor to stress granules (SGs).
Journal ArticleDOI
ANKS6 is a central component of a nephronophthisis module linking NEK8 to INVS and NPHP3
Sylvia Hoff,Jan Halbritter,Daniel Epting,Valeska Frank,Thanh-Minh T. Nguyen,Jeroen van Reeuwijk,Christopher Boehlke,Christoph Schell,Takayuki Yasunaga,Martin Helmstädter,Miriam Mergen,Emilie Filhol,Emilie Filhol,Karsten Boldt,Nicola Horn,Marius Ueffing,Marius Ueffing,Edgar A. Otto,Tobias Eisenberger,Mariet W. Elting,Joanna A.E. van Wijk,Detlef Bockenhauer,Neil J. Sebire,Søren Rittig,Mogens Vyberg,Troels Ring,Martin Pohl,Lars Pape,Thomas J. Neuhaus,Neveen A. Soliman Elshakhs,Sarah J. Koon,Peter C. Harris,Florian Grahammer,Tobias B. Huber,E. Wolfgang Kuehn,Albrecht Kramer-Zucker,Hanno J. Bolz,Ronald Roepman,Sophie Saunier,Sophie Saunier,Gerd Walz,Friedhelm Hildebrandt,Friedhelm Hildebrandt,Carsten Bergmann,Soeren S. Lienkamp +44 more
TL;DR: It is shown that ANKS6 localizes to the proximal cilium and confirmed its role in renal development through knockdown experiments in zebrafish and Xenopus laevis, and network analyses uncovered additional putative NPHP proteins and placed AN KS6 at the center of this N PHP module, explaining the overlapping disease manifestation caused by mutation in ANKS 6, NEK8, INVS or NPHp3.