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  • 1
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    Proliferation of functional hair cells in vivo in the absence of the retinoblastoma protein (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: In mammals, hair cell loss causes irreversible hearing and balance impairment because hair cells are terminally differentiated and do not regenerate spontaneously. By profiling gene expression in developing mouse vestibular organs, we identified the retinoblastoma protein (pRb) as a candidate regulator of cell cycle exit in hair cells. Differentiated and functional mouse hair cells with a targeted deletion of Rb1 undergo mitosis, divide, and cycle, yet continue to become highly differentiated and functional. Moreover, acute loss of Rb1 in postnatal hair cells caused cell cycle reentry. Manipulation of the pRb pathway may ultimately lead to mammalian hair cell regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sage, Cyrille -- Huang, Mingqian -- Karimi, Kambiz -- Gutierrez, Gabriel -- Vollrath, Melissa A -- Zhang, Duan-Sun -- Garcia-Anoveros, Jaime -- Hinds, Philip W -- Corwin, Jeffrey T -- Corey, David P -- Chen, Zheng-Yi -- DC-00200/DC/NIDCD NIH HHS/ -- DC-04546/DC/NIDCD NIH HHS/ -- DC-AG20208/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 18;307(5712):1114-8. Epub 2005 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurology Service, MGH-HMS Center for Nervous System Repair, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653467" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Count ; Cell Cycle ; Cell Differentiation ; *Cell Proliferation ; Cell Shape ; Cochlea/cytology/embryology ; Female ; Gene Deletion ; Gene Expression Profiling ; Genes, Retinoblastoma ; Hair Cells, Auditory, Inner/*cytology/*physiology ; Mice ; Mice, Knockout ; Mitosis ; Oligonucleotide Array Sequence Analysis ; Pregnancy ; Pyridinium Compounds/metabolism ; Quaternary Ammonium Compounds/metabolism ; Regeneration ; Retinoblastoma Protein/genetics/*physiology ; Saccule and Utricle/embryology/metabolism ; Stem Cells/cytology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Structure of a force-conveying cadherin bond essential for inner-ear mechanotransduction (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-11-09
    Description: Hearing and balance use hair cells in the inner ear to transform mechanical stimuli into electrical signals. Mechanical force from sound waves or head movements is conveyed to hair-cell transduction channels by tip links, fine filaments formed by two atypical cadherins known as protocadherin 15 and cadherin 23 (refs 4, 5). These two proteins are involved in inherited deafness and feature long extracellular domains that interact tip-to-tip in a Ca(2+)-dependent manner. However, the molecular architecture of this complex is unknown. Here we combine crystallography, molecular dynamics simulations and binding experiments to characterize the protocadherin 15-cadherin 23 bond. We find a unique cadherin interaction mechanism, in which the two most amino-terminal cadherin repeats (extracellular cadherin repeats 1 and 2) of each protein interact to form an overlapped, antiparallel heterodimer. Simulations predict that this tip-link bond is mechanically strong enough to resist forces in hair cells. In addition, the complex is shown to become unstable in response to Ca(2+) removal owing to increased flexure of Ca(2+)-free cadherin repeats. Finally, we use structures and biochemical measurements to study the molecular mechanisms by which deafness mutations disrupt tip-link function. Overall, our results shed light on the molecular mechanics of hair-cell sensory transduction and on new interaction mechanisms for cadherins, a large protein family implicated in tissue and organ morphogenesis, neural connectivity and cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518760/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518760/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sotomayor, Marcos -- Weihofen, Wilhelm A -- Gaudet, Rachelle -- Corey, David P -- R01 DC002281/DC/NIDCD NIH HHS/ -- R01 DC02281/DC/NIDCD NIH HHS/ -- RC2GM093307/GM/NIGMS NIH HHS/ -- RR-15301/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Dec 6;492(7427):128-32. doi: 10.1038/nature11590. Epub 2012 Nov 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23135401" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cadherins/*chemistry/genetics/*metabolism ; Calcium/metabolism/pharmacology ; Chromatography, Gel ; Crystallography, X-Ray ; Deafness/genetics ; Ear, Inner/cytology/*physiology ; Mechanotransduction, Cellular/*physiology ; Mice ; Models, Molecular ; Molecular Dynamics Simulation ; Mutagenesis, Site-Directed ; Mutation/genetics ; Protein Binding/drug effects ; Protein Multimerization/drug effects ; Protein Precursors/*chemistry/genetics/*metabolism ; Repetitive Sequences, Amino Acid
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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