Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.7/836
Título: Centrosomes and cilia in human disease
Autor: Bettencourt-Dias, Mónica
Hildebrandt, Friedhelm
Pellman, David
Woods, Geoff
Godinho, Susana A.
Palavras-chave: Aneuploidy
Cell Division
Centrosome
Chromosomal Instability
Cilia
Humans
Kidney Diseases, Cystic
Microcephaly
Mutation
Neoplasms
Signal Transduction
Spindle Apparatus
Data: Ago-2011
Editora: Elsevier
Citação: Mónica Bettencourt-Dias, Friedhelm Hildebrandt, David Pellman, Geoff Woods, Susana A. Godinho, Centrosomes and cilia in human disease, Trends in Genetics, Volume 27, Issue 8, 2011, Pages 307-315, ISSN 0168-9525, https://doi.org/10.1016/j.tig.2011.05.004. (http://www.sciencedirect.com/science/article/pii/S0168952511000655)
Resumo: Centrioles are microtubule-derived structures that are essential for the formation of centrosomes, cilia and flagella. The centrosome is the major microtubule organiser in animal cells, participating in a variety of processes, from cell polarisation to cell division, whereas cilia and flagella contribute to several mechanisms in eukaryotic cells, from motility to sensing. Although it was suggested more than a century ago that these microtubule-derived structures are involved in human disease, the molecular bases of this association have only recently been discovered. Surprisingly, there is very little overlap between the genes affected in the different diseases, suggesting that there are tissue-specific requirements for these microtubule-derived structures. Knowledge of these requirements and disease mechanisms has opened new avenues for therapeutical strategies. Here, we give an overview of recent developments in this field, focusing on cancer, diseases of brain development and ciliopathies.
Descrição: The deposited article is a post-print version (NIH-PA Author Manuscript) and has been submitted to peer review.
There is no public supplementary material available for this publication.
This publication hasn't any creative commons license associated.
Peer review: yes
URI: http://hdl.handle.net/10400.7/836
DOI: 10.1016/j.tig.2011.05.004
Versão do Editor: https://www.sciencedirect.com/science/article/pii/S0168952511000655?via%3Dihub
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