File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Tumor necrosis factor receptor-associated factor 6 (TRAF6) deficiency results in exencephaly and is required for apoptosis within the developing CNS

TitleTumor necrosis factor receptor-associated factor 6 (TRAF6) deficiency results in exencephaly and is required for apoptosis within the developing CNS
Authors
KeywordsThalamus
Neural tube closure
TUNEL
Gene targeting
Diencephalon
Programmed cell death
CNS
Issue Date2000
Citation
Journal of Neuroscience, 2000, v. 20, n. 19, p. 7384-7393 How to Cite?
AbstractTumor necrosis factor receptor-associated factors (TRAFs) are adaptor proteins important in mediating intracellular signaling. We report here that targeted deletion of traf6 greatly increases the frequency of failure of neural tube closure and exencephaly in traf6 (-/-) mice. The penetrance of this defect is influenced by genetic background. Neural tube fusion requires the coordination of several biological processes, including cell migration invoked by contact-dependent signaling, cell proliferation, and programmed cell death (PCD). To gain greater insight into the role of TRAF6 in these processes, neural development and migration within the CNS of traf6 (-/-) mice and controls were assessed through temporal examination of a number of immunohisto-chemical markers. In addition, relative levels of cellular proliferation and PCD were examined throughout embryonic development using bromodeoxyuridine (BrdU) and in situ terminal deoxynucleotidyl transferase-mediated dUTP biotinylated nick end labeling (TUNEL), respectively. The data suggest that loss of TRAF6 does not significantly alter the level of cellular proliferation or the pattern of neural differentiation per se, but rather regulates the level of PCD within specific regions of the developing CNS. Substantial reductions in TUNEL were observed within the ventral diencephalon and mesencephalon in exencephalic traf6 (-/-) embryos. Our results demonstrate a novel and prominent role for TRAF6 in the regional control of PCD within the developing CNS.
Persistent Identifierhttp://hdl.handle.net/10722/291533
ISSN
2023 Impact Factor: 4.4
2023 SCImago Journal Rankings: 2.321
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorLomaga, M. A.-
dc.contributor.authorHenderson, J. T.-
dc.contributor.authorElia, A. J.-
dc.contributor.authorRobertson, J.-
dc.contributor.authorNoyce, R. S.-
dc.contributor.authorYeh, W. C.-
dc.contributor.authorMak, T. W.-
dc.date.accessioned2020-11-17T14:54:34Z-
dc.date.available2020-11-17T14:54:34Z-
dc.date.issued2000-
dc.identifier.citationJournal of Neuroscience, 2000, v. 20, n. 19, p. 7384-7393-
dc.identifier.issn0270-6474-
dc.identifier.urihttp://hdl.handle.net/10722/291533-
dc.description.abstractTumor necrosis factor receptor-associated factors (TRAFs) are adaptor proteins important in mediating intracellular signaling. We report here that targeted deletion of traf6 greatly increases the frequency of failure of neural tube closure and exencephaly in traf6 (-/-) mice. The penetrance of this defect is influenced by genetic background. Neural tube fusion requires the coordination of several biological processes, including cell migration invoked by contact-dependent signaling, cell proliferation, and programmed cell death (PCD). To gain greater insight into the role of TRAF6 in these processes, neural development and migration within the CNS of traf6 (-/-) mice and controls were assessed through temporal examination of a number of immunohisto-chemical markers. In addition, relative levels of cellular proliferation and PCD were examined throughout embryonic development using bromodeoxyuridine (BrdU) and in situ terminal deoxynucleotidyl transferase-mediated dUTP biotinylated nick end labeling (TUNEL), respectively. The data suggest that loss of TRAF6 does not significantly alter the level of cellular proliferation or the pattern of neural differentiation per se, but rather regulates the level of PCD within specific regions of the developing CNS. Substantial reductions in TUNEL were observed within the ventral diencephalon and mesencephalon in exencephalic traf6 (-/-) embryos. Our results demonstrate a novel and prominent role for TRAF6 in the regional control of PCD within the developing CNS.-
dc.languageeng-
dc.relation.ispartofJournal of Neuroscience-
dc.subjectThalamus-
dc.subjectNeural tube closure-
dc.subjectTUNEL-
dc.subjectGene targeting-
dc.subjectDiencephalon-
dc.subjectProgrammed cell death-
dc.subjectCNS-
dc.titleTumor necrosis factor receptor-associated factor 6 (TRAF6) deficiency results in exencephaly and is required for apoptosis within the developing CNS-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1523/jneurosci.20-19-07384.2000-
dc.identifier.pmid11007897-
dc.identifier.pmcidPMC6772765-
dc.identifier.scopuseid_2-s2.0-0034307624-
dc.identifier.volume20-
dc.identifier.issue19-
dc.identifier.spage7384-
dc.identifier.epage7393-
dc.identifier.issnl0270-6474-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats