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The inhibitor of DNA binding proteins in celluar proliferation and differentiation: regulation by the retinoic acid signaling pathway

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Title
The inhibitor of DNA binding proteins in celluar proliferation and differentiation: regulation by the retinoic acid signaling pathway
Name (ID = NAME001); (type = personal)
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Villano
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Caren M.
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Caren M. Villano
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Lori
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Advisory Committee
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Lori White
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chair
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Cooper
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Keith
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Advisory Committee
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Keith Cooper
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Richardson
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Jason
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Advisory Committee
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Jason Richardson
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Gordon
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Marion
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Advisory Committee
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Marion Gordon
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Quadro
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Loredana
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Advisory Committee
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Loredana Quadro
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Rutgers University
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degree grantor
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Graduate School - New Brunswick
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theses
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DateCreated (qualifier = exact)
2007
DateOther (qualifier = exact); (type = degree)
2007
Language
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English
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electronic
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x, 134 pages
Abstract
The Id (Inhibitor of differentiation or DNA binding) helix-loop-helix proteins mediate cellular differentiation and proliferation in a variety of cell types through regulation of gene expression. The goal of the experiments in this thesis is to determine the effect of the retinoic acid signaling pathway on Id expression using cell culture and whole animal models. Retinoids, vitamin A analogues, are powerful regulators of cell growth and differentiation and are widely used in the prevention and treatment of a variety of cancers in humans. We found that exposure of normal human keratinocytes to all-trans retinoic acid (RA) results in increased expression of Id1 and Id3, which is mediated by increased transcription involving cis- acting elements in the distal portion of the promoter. To examine the effect of the Id proteins in development, we used the zebrafish (Danio rerio) model. Morpholino knockdown of Id1 in the developing zebrafish embryo results in pericardial, yolk sac and/or brain edema, as well as an undulating notochord. Loss of Id1 in early zebrafish embryogenesis results in defects in larval development, such as decreased body size, lack of swim bladder inflation, and craniofacial defects. We conclude that Id1 is critical for early and late zebrafish development. Our findings also demonstrate that RA exposure decreases expression of Id1 specifically in the heart, and RA deficiency results in increased Id1 expression. Id1 knockdown results in increased expression of the cardiac-specific transcription factors gata5 and nkx2.5 which are also targets of the RA signaling pathway. To further examine the role of Id1 in differentiation and proliferation, we examined Id expression during caudal fin regeneration. Our data demonstrate that Id1 expression is induced in the blastema during caudal fin regeneration, and that exposure to RA during regeneration decreases Id1 expression. Taken together, the data presented in this thesis demonstrate that Id1 is a target for RA signaling in both human skin cells and in zebrafish. Further, these data suggest that Id1 may be an important intermediate in the RA signaling pathway, by altering expression of genes involved in proliferation and differentiation.
Note (type = degree)
Ph.D.
Note (type = bibliography)
Includes bibliographical references (p. 115-131).
Subject (ID = SUBJ1); (authority = RUETD)
Topic
Toxicology
Subject (ID = SUBJ2); (authority = ETD-LCSH)
Topic
DNA-binding proteins
Subject (ID = SUBJ3); (authority = ETD-LCSH)
Topic
DNA-protein interactions
Subject (ID = SUBJ4); (authority = ETD-LCSH)
Topic
Protein binding
Subject (ID = SUBJ5); (authority = ETD-LCSH)
Topic
Tretinoin
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Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier (type = local)
rucore19991600001
Identifier (type = hdl)
http://hdl.rutgers.edu/1782.2/rucore10001600001.ETD.16789
Identifier
ETD_552
Location
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NjNbRU
Identifier (type = doi)
doi:10.7282/T3G1617M
Genre (authority = ExL-Esploro)
ETD doctoral
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Name
Caren Villano
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Copyright holder
Affiliation
Rutgers University. Graduate School - New Brunswick
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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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