Decreased bone formation and increased osteoclastogenesis cause bone loss in mucolipidosis II

Autor: Katrin Kollmann, Jan Malte Pestka, Sonja Christin Kühn, Elisabeth Schöne, Michaela Schweizer, Kathrin Karkmann, Takanobu Otomo, Philip Catala‐Lehnen, Antonio Virgilio Failla, Robert Percy Marshall, Matthias Krause, Rene Santer, Michael Amling, Thomas Braulke, Thorsten Schinke

Publikováno v: EMBO Molecular Medicine, Vol 5, Iss 12, Pp 1871-1886 (2013)

Abstract Mucolipidosis type II (MLII) is a severe multi‐systemic genetic disorder caused by missorting of lysosomal proteins and the subsequent lysosomal storage of undegraded macromolecules. Although affected children develop disabling skeletal ab

Externí odkaz: https://doaj.org/article/0221b86517e749d69825ca9647adadc6

Sharpin Controls Osteogenic Differentiation of Mesenchymal Bone Marrow Cells

Autor: Andrea Mautner, Thorsten Schinke, Lara Duchstein, Robert P. Marshall, Philip Catala-Lehnen, Anke Jeschke, Michaela Schweizer, Michael Amling, Kristofer Wintges, Till Koehne, Benjamin Otto, Sabrina Sieber, Thomas Bickert, Andrea Kristina Horst, Hans-Juergen Kreienkamp

Publikováno v: The Journal of Immunology. 195:3675-3684

The cytosolic protein Sharpin is a component of the linear ubiquitin chain assembly complex, which regulates NF-κB signaling in response to specific ligands, such as TNF-α. Its inactivating mutation in chronic proliferative dermatitis mutation (Cpd

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e8f00045611045428cdee6e6ba10ad86
https://doi.org/10.4049/jimmunol.1402392

Telomerase-deficient mice exhibit bone loss owing to defects in osteoblasts and increased osteoclastogenesis by inflammatory microenvironment

Autor: Weimin Qiu, Michael Amling, Philip Catala-Lehnen, Nicholas Ditzel, Hamid Saeed, Moustapha Kassem, Basem M. Abdallah

Publikováno v: Saeed, H, Abdallah, B M, Ditzel, N, Catala-Lehnen, P, Qiu, W M, Amling, M & Kassem, M 2011, ' Telomerase-Deficient Mice Exhibit Bone Loss Owing to Defects in Osteoblasts and Increased Osteoclastogenesis by Inflammatory Microenvironment ', Journal of Bone and Mineral Research, vol. 26, no. 7, pp. 1494-1505 . https://doi.org/10.1002/jbmr.349

Telomere shortening owing to telomerase deficiency leads to accelerated senescence of human skeletal (mesenchymal) stem cells (MSCs) in vitro, whereas overexpression leads to telomere elongation, extended life span, and enhanced bone formation. To st

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::cf7407c8bf118ea87f61d68f6e2bf97a
https://doi.org/10.1002/jbmr.349

Increased trabecular bone formation in mice lacking the growth factor midkine

Autor: F. Timo Beil, Philip Catala-Lehnen, Thomas Streichert, Thorsten Schinke, Anke Baranowsky, Robert P. Marshall, Anita Ignatius, Vincent Kanbach, Michael Amling, Takashi Muramatsu, Wolfgang Lehmann, Claudia Neunaber

Publikováno v: Journal of Bone and Mineral Research. 25:1724-1735

Midkine (Mdk) and pleiotrophin (Ptn) comprise a family of heparin-binding growth factors known primarily for their effects on neuronal cells. Since transgenic mice overexpressing Ptn have been reported to display increased bone density, we have previ

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f009726d52e6746a50261a4a54fe6c1e
https://doi.org/10.1002/jbmr.75

The Protein Tyrosine Phosphatase Rptpζ Suppresses Osteosarcoma Development in Trp53-Heterozygous Mice

Autor: Peter Nollau, Sophia Buhs, Philip Catala-Lehnen, Michael Amling, Anke Jeschke, Helwe Gerull, Christina Baldauf, Vincent Kanbach, Daniel Baumhoer, Thorsten Schinke, Sheila Harroch

Publikováno v: PLoS ONE
PLoS ONE, Vol 10, Iss 9, p e0137745 (2015)

Osteosarcoma (OS), a highly aggressive primary bone tumor, belongs to the most common solid tumors in growing children. Since specific molecular targets for OS treatment remain to be identified, surgical resection combined with multimodal (neo-)adjuv

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3de502569941f82ba3fdf7373a05e199
https://pubmed.ncbi.nlm.nih.gov/26360410