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Role of Bcl-2 proteins in stress-induced apoptosis in a non-transformed mammary epithelial cell line
Descriptive
TitleInfo
Title
Role of Bcl-2 proteins in stress-induced apoptosis in a non-transformed mammary epithelial cell line
Name
(type = personal)
NamePart
(type = family)
Butler
NamePart
(type = given)
Kristie Lynn
NamePart
(type = date)
1989-
DisplayForm
Kristie Butler
Role
RoleTerm
(authority = RULIB)
author
Name
(type = personal)
NamePart
(type = family)
Cohick
NamePart
(type = given)
Wendie
DisplayForm
Wendie Cohick
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
chair
Name
(type = personal)
NamePart
(type = family)
Belden
NamePart
(type = given)
William
DisplayForm
William Belden
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Di
NamePart
(type = given)
Rong
DisplayForm
Rong Di
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = corporate)
NamePart
Rutgers University
Role
RoleTerm
(authority = RULIB)
degree grantor
Name
(type = corporate)
NamePart
Graduate School - New Brunswick
Role
RoleTerm
(authority = RULIB)
school
TypeOfResource
Text
Genre
(authority = marcgt)
theses
OriginInfo
DateCreated
(qualifier = exact)
2014
DateOther
(qualifier = exact);
(type = degree)
2014-05
Place
PlaceTerm
(type = code)
xx
Language
LanguageTerm
(authority = ISO639-2b);
(type = code)
eng
Abstract
(type = abstract)
Apoptosis is the process of programmed cell death characterized by morphological and physiological changes executed by cells in response to a stimulus. The apoptotic process contributes to the loss of milk secreting cells (i.e. mammary epithelial cells) that occurs in the bovine mammary gland once peak lactation has occurred. However, the specific mechanisms by which this occurs are unknown. The goal of this work was to examine the role of the Bcl-2 family of proteins in regulating apoptosis in the bovine mammary epithelial cell line, MAC-T. The Bcl-2 family is divided into three categories based on protein function and combinations of four Bcl-2 homology (BH) domains. Anti-apoptotic multidomain proteins, such as Bcl-2 and Mcl-1, prevent apoptosis by binding to pro-apoptotic members of the family. Pro-apoptotic multidomain proteins, such as Bax, help to regulate apoptosis at the mitochondrial outer membrane. Pro-apoptotic BH3-only proteins, such as Bad and Bim, act as messengers between the anti-apoptotic and pro-apoptotic proteins. To investigate the roles of Bcl-2 proteins in apoptosis, MAC-T cells were treated with anisomycin (ANS), an activator of the intrinsic apoptotic pathway. ANS had little effect on Bcl-2 or Bax mRNA levels while it induced a 40 to 60% decrease in levels of Bad mRNA. Protein expression of Bax did not change during apoptosis, while Bcl-2, Mcl-1, and Bad expression decreased to varying degrees. The greatest change in protein levels was observed for Mcl-1, whose expression was nearly non-detectable after 4 h of treatment with ANS. Bim was phosphorylated in response to ANS but this was not caused by JNK or p38 signaling. Knock-down of Bim using siRNA decreased the ability of ANS to induce apoptosis. Mcl-1 and Bim protein expression changed in a similar time frame, therefore, interactions between the two proteins were evaluated using co-immunoprecipitation experiments. Mcl-1 and Bim interacted both basally and after treatment with ANS. The significance of Bim phosphorylation, the kinase responsible for its phosphorylation, and the functional significance of the interaction between Bim and Mcl-1 in stress-induced apoptosis remain to be determined.
Subject
(authority = RUETD)
Topic
Microbiology and Molecular Genetics
RelatedItem
(type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier
(type = RULIB)
ETD
Identifier
ETD_5374
PhysicalDescription
Form
(authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
ix, 55 p. : ill.
Note
(type = degree)
M.S.
Note
(type = bibliography)
Includes bibliographical references
Note
(type = statement of responsibility)
by Kristie Lynn Butler
Subject
(authority = ETD-LCSH)
Topic
Apoptosis
Subject
(authority = ETD-LCSH)
Topic
Mammary glands--Secretions
Subject
(authority = ETD-LCSH)
Topic
Proteins--Affinity labeling
RelatedItem
(type = host)
TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier
(type = local)
rucore19991600001
Location
PhysicalLocation
(authority = marcorg);
(displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier
(type = doi)
doi:10.7282/T3KK993Q
Genre
(authority = ExL-Esploro)
ETD graduate
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Rights
RightsDeclaration
(ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder
(type = personal)
Name
FamilyName
Butler
GivenName
Kristie
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime
(encoding = w3cdtf);
(qualifier = exact);
(point = start)
2014-04-03 12:57:03
AssociatedEntity
Name
Kristie Butler
Role
Copyright holder
Affiliation
Rutgers University. Graduate School - New Brunswick
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.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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Technical
RULTechMD
(ID = TECHNICAL1)
ContentModel
ETD
OperatingSystem
(VERSION = 5.1)
windows xp
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