The Atypical Cyclin-Dependent Kinase 5 (Cdk5) Guards Podocytes from Apoptosis in Glomerular Disease While Being Dispensable for Podocyte Development

Autor: Nicole Mangold, Jeffrey Pippin, David Unnersjoe-Jess, Sybille Koehler, Stuart Shankland, Sebastian Brähler, Bernhard Schermer, Thomas Benzing, Paul T. Brinkkoetter, Henning Hagmann

Publikováno v: Cells, Vol 10, Iss 9, p 2464 (2021)

Cyclin-dependent kinase 5 (Cdk5) is expressed in terminally differentiated cells, where it drives development, morphogenesis, and survival. Temporal and spatial kinase activity is regulated by specific activators of Cdk5, dependent on the cell type a

Externí odkaz: https://doaj.org/article/a54a1550dd394d05bc239bd08365d0cf

The podocytes’ inflammatory responses in experimental GN are independent of canonical MYD88-dependent toll-like receptor signaling

Autor: Thomas Schömig, Paul Diefenhardt, Ingo Plagmann, Bastian Trinsch, Tim Merz, Giuliano Crispatzu, David Unnersjö-Jess, Jasper Nies, David Pütz, Claudio Sierra Gonzalez, Bernhard Schermer, Thomas Benzing, Paul Thomas Brinkkoetter, Sebastian Brähler

Publikováno v: Scientific Reports, Vol 14, Iss 1, Pp 1-12 (2024)

Abstract Podocytes form the kidney filtration barrier and continuously adjust to external stimuli to preserve their integrity even in the presence of inflammation. It was suggested that canonical toll-like receptor signaling, mediated by the adaptor

Externí odkaz: https://doaj.org/article/9876ddb5e0934f8d8f9d9a648f58c3d3

Genetic deficit of SK3 and IK1 channels disrupts the endothelium-derived hyperpolarizing factor vasodilator pathway and causes hypertension

Autor: Sebastian Brahler, Ralf Köhler, Stephanie E. Wölfle, Heike Wulff, Cor de Wit, Anuradha Kaistha, John P. Adelman, Joachim Hoyer, Brajesh P. Kaistha, Han Si, Chris T. Bond, Volker J. Schmidt, Ivica Grgic, Michael Kacik, Anna Lena Hasenau, Christoph Busch

Publikováno v: Brähler, S, Kaistha, A, Schmidt, V J, Wölfle, S E, Busch, C, Kaistha, B P, Kacik, M, Hasenau, A-L, Grgic, I, Si, H, Bond, C T, Adelman, J P, Wulff, H, de Wit, C, Hoyer, J & Köhler, R 2009, ' Genetic deficit of SK3 and IK1 channels disrupts the endothelium-derived hyperpolarizing factor vasodilator pathway and causes hypertension ', Circulation, vol. 119, no. 17, pp. 2323-32 . https://doi.org/10.1161/CIRCULATIONAHA.108.846634

Background— It has been proposed that activation of endothelial SK3 (K Ca 2.3) and IK1 (K Ca 3.1) K + channels plays a role in the arteriolar dilation attributed to an endothelium-derived hyperpolarizing factor (EDHF). However, our understanding of

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c65f59d8a41d70d4301b004d615aacc1
https://pubmed.ncbi.nlm.nih.gov/19380617

Inhibition of insulin/IGF‐1 receptor signaling protects from mitochondria‐mediated kidney failure

Autor: Christina Ising, Sybille Koehler, Sebastian Brähler, Carsten Merkwirth, Martin Höhne, Olivier R Baris, Henning Hagmann, Martin Kann, Francesca Fabretti, Claudia Dafinger, Wilhelm Bloch, Bernhard Schermer, Andreas Linkermann, Jens C Brüning, Christine E Kurschat, Roman‐Ulrich Müller, Rudolf J Wiesner, Thomas Langer, Thomas Benzing, Paul Thomas Brinkkoetter

Publikováno v: EMBO Molecular Medicine, Vol 7, Iss 3, Pp 275-287 (2015)

Abstract Mitochondrial dysfunction and alterations in energy metabolism have been implicated in a variety of human diseases. Mitochondrial fusion is essential for maintenance of mitochondrial function and requires the prohibitin ring complex subunit

Externí odkaz: https://doaj.org/article/aaed36cafd0a43ab8e7e6120f044f0e0