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Roles of SETD4 in radiation sensitivity and tumorigenesis

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TitleInfo
Title
Roles of SETD4 in radiation sensitivity and tumorigenesis
Name (type = personal)
NamePart (type = family)
FENG
NamePart (type = given)
XING
NamePart (type = date)
1987-
DisplayForm
XING FENG
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
Bunting
NamePart (type = given)
Samuel
DisplayForm
Samuel Bunting
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
chair
Name (type = personal)
NamePart (type = family)
Shen
NamePart (type = given)
Zhiyuan
DisplayForm
Zhiyuan Shen
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Denzin
NamePart (type = given)
Lisa
DisplayForm
Lisa Denzin
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Xie
NamePart (type = given)
Ping
DisplayForm
Ping Xie
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
outside member
Name (type = corporate)
NamePart
Rutgers University
Role
RoleTerm (authority = RULIB)
degree grantor
Name (type = corporate)
NamePart
School of Graduate Studies
Role
RoleTerm (authority = RULIB)
school
TypeOfResource
Text
Genre (authority = marcgt)
theses
OriginInfo
DateCreated (qualifier = exact)
2018
DateOther (qualifier = exact); (type = degree)
2018-10
CopyrightDate (encoding = w3cdtf)
2018
Place
PlaceTerm (type = code)
xx
Language
LanguageTerm (authority = ISO639-2b); (type = code)
eng
Abstract (type = abstract)
The SET domain protein methyltransferases play a critical role in histone modifications and global epigenetic regulations. Recent evidence suggests that some SET domain proteins may have the ability to modify non-histone proteins. The SET domain containing protein 4 (SETD4) was believed to be a non-histone methyltransferase, but no physiological substrate or biological functions of SETD4 has been identified. In this study, we constructed an inducible Setd4 knockout model and investigated the role of Setd4 in radiation sensitivity and tumorigenesis. We found that Setd4 deficient mice were significantly more resistant to radiation-induced hematopoietic syndrome than littermate wild type mice. Using several long-term bone marrow transplantation assays, we found that Setd4 deficient hematopoietic stem cells (HSCs) and progenitor cells (HPCs) have a slight in vivo growth advantage than the wild type cells, but are more sensitive to radiation. We also found that the Setd4 deficient recipient mice have an enhanced ability to engraft transplanted HSCs, suggesting an improved bone marrow niche for the Setd4 deficient animals. Using a radiation-induced thymic lymphoma model, we also found that Setd4 deletion delayed radiation-induced tumorigenesis. Collectively, our study suggests that Setd4 defect can enhance the recovery of radiation-induced bone marrow damage and suppress radiation-induced thymic lymphoma, and that Setd4 is a new gene involved in regulating bone marrow and hematopoietic functions in mice.
Subject (authority = RUETD)
Topic
Pharmacology, Cellular and Molecular
Subject (authority = ETD-LCSH)
Topic
Cancer--Gene therapy
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_9129
PhysicalDescription
Form (authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
1 online resource (137 pages) : illustrations
Note (type = degree)
Ph.D.
Note (type = bibliography)
Includes bibliographical references
Note (type = statement of responsibility)
by Xing Feng
RelatedItem (type = host)
TitleInfo
Title
School of Graduate Studies Electronic Theses and Dissertations
Identifier (type = local)
rucore10001600001
Location
PhysicalLocation (authority = marcorg); (displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier (type = doi)
doi:10.7282/t3-6h07-vn16
Genre (authority = ExL-Esploro)
ETD doctoral
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Rights

RightsDeclaration (ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
FENG
GivenName
XING
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2018-08-06 13:56:41
AssociatedEntity
Name
XING FENG
Role
Copyright holder
Affiliation
Rutgers University. School of Graduate Studies
AssociatedObject
Type
License
Name
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.
RightsEvent
Type
Embargo
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2018-10-31
DateTime (encoding = w3cdtf); (qualifier = exact); (point = end)
2020-10-30
Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after October 30th, 2020.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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Technical

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2018-09-18T18:22:34
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2018-09-18T18:22:34
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