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The role of proneurotrophins in apoptotic signaling in rat brain neurons

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TypeOfResource
Text
TitleInfo (ID = T-1)
Title
The role of proneurotrophins in apoptotic signaling in rat brain neurons
SubTitle
PartName
PartNumber
NonSort
Identifier (displayLabel = ); (invalid = )
ETD_1783
Identifier (type = hdl)
http://hdl.rutgers.edu/1782.2/rucore10002600001.ETD.000051318
Language (objectPart = )
LanguageTerm (authority = ISO639-2); (type = code)
eng
Genre (authority = marcgt)
theses
Subject (ID = SBJ-1)
Name (authority = LC-NAF)
NamePart (type = )
Subject (ID = SBJ-2); (authority = RUETD)
Topic
Biology
Subject (ID = SBJ-3); (authority = ETD-LCSH)
Topic
Neurotrophic functions
Subject (ID = SBJ-4); (authority = ETD-LCSH)
Topic
Apoptosis
Subject (ID = SBJ-5); (authority = ETD-LCSH)
Topic
Neurons
Abstract
Proneurotrophins and mature neurotrophins can activate distinct signaling pathways and have opposing effects on cells: proneurotrophins induce apoptotic signaling via p75NTR while mature neurotrophins activate survival signaling by binding to Trk receptors. In the CNS, basal forebrain (BF) neurons express both p75NTR and Trk receptors. The work in this thesis demonstrates that proneurotrophins can induce loss of BF neurons through p75NTR, even in the presence of activated Trk receptors. Moreover, proNGF inhibits the phosphorylation of Akt induced by BDNF, suggesting that proNGF induces apoptotic signaling and simultaneously blocks survival signaling activated by BDNF. Phosphorylation of Akt can prevent proNGF-induced apoptosis, suggesting that regulation of Akt phosphorylation may be a critical point of interaction between survival and death signaling.
PTEN (phosphatase and tensin homologue deleted on chromosome ten) is a dual-specificity phosphatase that can act as an antagonist to the PI3 kinase/Akt pathway. ProNGF induces an increase in PTEN in BF neurons, even in the presence of BDNF, suggesting that proNGF might block survival signaling through PTEN. In the presence of BDNF, proNGF was unable to induce apoptosis when PTEN activity was inhibited both in vitro and in vivo. Also, the PTEN inhibitor blocked proNGF-induced inhibition of Akt phosphorylation by BDNF, suggesting that PTEN is a crucial factor mediating the balance between p75-induced apoptotic signaling and Trk-mediated survival signaling.
Taken together, the interaction of proneurotrophin-p75NTR and mature neurotrophin-Trk systems is partially determined by the balance of PTEN and Akt which eventually causes the cell to die or survive.
PhysicalDescription
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electronic resource
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x, 120 p. : ill.
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Note (type = degree)
Ph.D.
Note (type = bibliography)
Includes bibliographical references (p. 97-119)
Note (type = statement of responsibility)
by Wenyu Song
Name (ID = NAME-1); (type = personal)
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Song
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Wenyu
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1972
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author
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Wenyu Song
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Friedman
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Wilma
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chair
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Advisory Committee
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Wilma j Friedman
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Jonakait
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G
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internal member
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G Miller Jonakait
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Kim
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Haesun
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internal member
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Advisory Committee
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Haesun A Kim
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Dreyfus
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Cheryl
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outside member
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Advisory Committee
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Cheryl Dreyfus
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NamePart
Rutgers University
Role
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degree grantor
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Graduate School - Newark
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school
OriginInfo
DateCreated (point = ); (qualifier = exact)
2009
DateOther (qualifier = exact); (type = degree)
2009-05
Place
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xx
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TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
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ETD
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Title
Graduate School - Newark Electronic Theses and Dissertations
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rucore10002600001
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NjNbRU
Identifier (type = doi)
doi:10.7282/T3639PXS
Genre (authority = ExL-Esploro)
ETD doctoral
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RightsDeclaration (AUTHORITY = GS); (ID = rulibRdec0006)
The author owns the copyright to this work.
Copyright
Status
Copyright protected
Notice
Note
Availability
Status
Open
Reason
Permission or license
Note
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Name
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Song
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Wenyu
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Wenyu Song
Affiliation
Rutgers University. Graduate School - Newark
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Author Agreement License
Detail
I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
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application/pdf
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