Neurofilament cytoskeleton disruption does not modify accumulation of trophic factor mRNA
Identifieur interne : 002727 ( Istex/Curation ); précédent : 002726; suivant : 002728Neurofilament cytoskeleton disruption does not modify accumulation of trophic factor mRNA
Auteurs : Patrick Robert [France] ; Alan C. Peterson [Canada] ; Joël Eyer [France]Source :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2001-06-01.
English descriptors
Abstract
Previously we described a transgenic mouse model in which neurofilaments are sequestered in neuronal cell bodies and withheld from the axonal compartment. This model and other transgenic models with disrupted neurofilaments are used widely to investigate the role of the neurofilament cytoskeleton in normal neurons and in inherited or acquired diseases. To interpret such studies, it is important to establish whether the maldistribution of neurofilaments has major secondary consequences on the cell biology of the affected neurons. Notably, multiple perturbations of the nervous system simultaneously affect both the neuronal cytoskeleton and neurotrophin expression. To determine whether the expression of neurotrophic factors or their receptors is perturbed by a primary disruption in neurofilaments, we compared the accumulated mRNA levels for ciliary neuroptrophic factor (CNTF), nerve growth factor, neurotrophin 3, and the α CNTF receptor in mature transgenic mice and their littermate controls. Consistently with the prolonged survival of neurons expressing atypical or abnormally distributed neurofilaments, no obvious changes were observed for any of the mRNA species examined. J. Neurosci. Res. 64:487–492, 2001. © 2001 Wiley‐Liss, Inc.
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DOI: 10.1002/jnr.1100
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Peterson</name><affiliation wicri:level="1"><mods:affiliation>Molecular Oncology Group, McGill University, Royal Victoria Hospital, Montreal, Quebec, Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Molecular Oncology Group, McGill University, Royal Victoria Hospital, Montreal, Quebec</wicri:regionArea></affiliation></author><author><name sortKey="Eyer, Joel" sort="Eyer, Joel" uniqKey="Eyer J" first="Joël" last="Eyer">Joël Eyer</name><affiliation wicri:level="1"><mods:affiliation>Laboratoire de Neurobiologie et Transgénèse, UPRES‐EA3143, INSERM E9928, Centre Hospitalier Universitaire, Angers, France</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Laboratoire de Neurobiologie et Transgénèse, UPRES‐EA3143, INSERM E9928, Centre Hospitalier Universitaire, Angers</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>INSERM Laboratoire de Neurobiologie et Transgénèse, UPRES‐EA3143, CHU, 49033 Angers, France</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM Laboratoire de Neurobiologie et Transgénèse, UPRES‐EA3143, CHU, 49033 Angers</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:1E5C311F6EDB5217BA9DD1244AECCE22D25DCBAE</idno><date when="2001" year="2001">2001</date><idno type="doi">10.1002/jnr.1100</idno><idno type="url">https://api-v5.istex.fr/document/1E5C311F6EDB5217BA9DD1244AECCE22D25DCBAE/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">002727</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002727</idno><idno type="wicri:Area/Istex/Curation">002727</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Neurofilament cytoskeleton disruption does not modify accumulation of trophic factor mRNA</title><author><name sortKey="Robert, Patrick" sort="Robert, Patrick" uniqKey="Robert P" first="Patrick" last="Robert">Patrick Robert</name><affiliation wicri:level="1"><mods:affiliation>Laboratoire de Neurobiologie et Transgénèse, UPRES‐EA3143, INSERM E9928, Centre Hospitalier Universitaire, Angers, France</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Laboratoire de Neurobiologie et Transgénèse, UPRES‐EA3143, INSERM E9928, Centre Hospitalier Universitaire, Angers</wicri:regionArea></affiliation></author><author><name sortKey="Peterson, Alan C" sort="Peterson, Alan C" uniqKey="Peterson A" first="Alan C." last="Peterson">Alan C. Peterson</name><affiliation wicri:level="1"><mods:affiliation>Molecular Oncology Group, McGill University, Royal Victoria Hospital, Montreal, Quebec, Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Molecular Oncology Group, McGill University, Royal Victoria Hospital, Montreal, Quebec</wicri:regionArea></affiliation></author><author><name sortKey="Eyer, Joel" sort="Eyer, Joel" uniqKey="Eyer J" first="Joël" last="Eyer">Joël Eyer</name><affiliation wicri:level="1"><mods:affiliation>Laboratoire de Neurobiologie et Transgénèse, UPRES‐EA3143, INSERM E9928, Centre Hospitalier Universitaire, Angers, France</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Laboratoire de Neurobiologie et Transgénèse, UPRES‐EA3143, INSERM E9928, Centre Hospitalier Universitaire, Angers</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>INSERM Laboratoire de Neurobiologie et Transgénèse, UPRES‐EA3143, CHU, 49033 Angers, France</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM Laboratoire de Neurobiologie et Transgénèse, UPRES‐EA3143, CHU, 49033 Angers</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neuroscience Research</title><title level="j" type="abbrev">J. Neurosci. Res.</title><idno type="ISSN">0360-4012</idno><idno type="eISSN">1097-4547</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-06-01">2001-06-01</date><biblScope unit="volume">64</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="487">487</biblScope><biblScope unit="page" to="492">492</biblScope></imprint><idno type="ISSN">0360-4012</idno></series><idno type="istex">1E5C311F6EDB5217BA9DD1244AECCE22D25DCBAE</idno><idno type="DOI">10.1002/jnr.1100</idno><idno type="ArticleID">JNR1100</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0360-4012</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>NFHLacZ transgenic mice</term><term>mRNA</term><term>microtubules</term><term>neurofilaments</term><term>neurotrophins</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Previously we described a transgenic mouse model in which neurofilaments are sequestered in neuronal cell bodies and withheld from the axonal compartment. This model and other transgenic models with disrupted neurofilaments are used widely to investigate the role of the neurofilament cytoskeleton in normal neurons and in inherited or acquired diseases. To interpret such studies, it is important to establish whether the maldistribution of neurofilaments has major secondary consequences on the cell biology of the affected neurons. Notably, multiple perturbations of the nervous system simultaneously affect both the neuronal cytoskeleton and neurotrophin expression. To determine whether the expression of neurotrophic factors or their receptors is perturbed by a primary disruption in neurofilaments, we compared the accumulated mRNA levels for ciliary neuroptrophic factor (CNTF), nerve growth factor, neurotrophin 3, and the α CNTF receptor in mature transgenic mice and their littermate controls. Consistently with the prolonged survival of neurons expressing atypical or abnormally distributed neurofilaments, no obvious changes were observed for any of the mRNA species examined. J. Neurosci. Res. 64:487–492, 2001. © 2001 Wiley‐Liss, Inc.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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