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Article: TAp73 knockout mice show morphological and functional nervous system defects associated with loss of p75 neurotrophin receptor

TitleTAp73 knockout mice show morphological and functional nervous system defects associated with loss of p75 neurotrophin receptor
Authors
Issue Date2013
Citation
Proceedings of the National Academy of Sciences of the United States of America, 2013, v. 110, n. 47, p. 18952-18957 How to Cite?
AbstractTotal and N-terminal isoform selective p73 knockout mice show a variety of central nervous system defects. Here we show that TAp73 is a transcriptional activator of p75 neurotrophin receptor (p75NTR) and that p75NTR mRNA and protein levels are strongly reduced in the central and peripheral nervous systems of p73 knockout mice. In parallel, primary cortical neurons from p73 knockout mice showed a reduction in neurite outgrowth and in nerve growth factor-mediated neuronal differentiation, together with reduced miniature excitatory postsynaptic current frequencies and behavioral defects. p73 null mice also have impairments in the peripheral nervous system with reduced thermal sensitivity, axon number, and myelin thickness. At least some of these morphological and functional impairments in p73 null cells can be rescued by p75NTR re-expression. Together, these data demonstrate that loss of p75NTR contributes to the neurological phenotype of p73 knockout mice.
Persistent Identifierhttp://hdl.handle.net/10722/292786
ISSN
2023 Impact Factor: 9.4
2023 SCImago Journal Rankings: 3.737
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNiklison-Chirou, Maria Victoria-
dc.contributor.authorSteinert, Joern R.-
dc.contributor.authorAgostini, Massimiliano-
dc.contributor.authorKnight, Richard A.-
dc.contributor.authorDinsdale, David-
dc.contributor.authorCattaneo, Antonio-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorMelino, Gerry-
dc.date.accessioned2020-11-17T14:57:13Z-
dc.date.available2020-11-17T14:57:13Z-
dc.date.issued2013-
dc.identifier.citationProceedings of the National Academy of Sciences of the United States of America, 2013, v. 110, n. 47, p. 18952-18957-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/292786-
dc.description.abstractTotal and N-terminal isoform selective p73 knockout mice show a variety of central nervous system defects. Here we show that TAp73 is a transcriptional activator of p75 neurotrophin receptor (p75NTR) and that p75NTR mRNA and protein levels are strongly reduced in the central and peripheral nervous systems of p73 knockout mice. In parallel, primary cortical neurons from p73 knockout mice showed a reduction in neurite outgrowth and in nerve growth factor-mediated neuronal differentiation, together with reduced miniature excitatory postsynaptic current frequencies and behavioral defects. p73 null mice also have impairments in the peripheral nervous system with reduced thermal sensitivity, axon number, and myelin thickness. At least some of these morphological and functional impairments in p73 null cells can be rescued by p75NTR re-expression. Together, these data demonstrate that loss of p75NTR contributes to the neurological phenotype of p73 knockout mice.-
dc.languageeng-
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of America-
dc.titleTAp73 knockout mice show morphological and functional nervous system defects associated with loss of p75 neurotrophin receptor-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.1221172110-
dc.identifier.pmid24190996-
dc.identifier.pmcidPMC3839698-
dc.identifier.scopuseid_2-s2.0-84888082989-
dc.identifier.volume110-
dc.identifier.issue47-
dc.identifier.spage18952-
dc.identifier.epage18957-
dc.identifier.eissn1091-6490-
dc.identifier.isiWOS:000327100600061-
dc.identifier.issnl0027-8424-

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