東華大學圖書館 |

Language: English

Help

回圖書館首頁

手機版館藏查詢

Back

Switch To: Labeled | MARC Mode | ISBD

Mechanisms of cell death regulation ...

Bailey, Jason P.

Linked to FindBook

Google Book

Amazon

博客來

Mechanisms of cell death regulation during mammary gland development and involution.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Mechanisms of cell death regulation during mammary gland development and involution./
Author:	Bailey, Jason P.
Description:	145 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1094.
Contained By:	Dissertation Abstracts International65-03B.
Subject:	Biology, Animal Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3127310
ISBN:	0496745743

Mechanisms of cell death regulation during mammary gland development and involution.
Bailey, Jason P.

Mechanisms of cell death regulation during mammary gland development and involution. - 145 p.

Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1094.

Thesis (Ph.D.)--University of Cincinnati, 2004.

Both prolactin (PRL) and transforming growth factor-beta (TGF-beta) regulate cell survival in mammary epithelial cells, but their mechanism(s) of interactions are not known. In primary mammary epithelial cells and the HC11 mouse mammary epithelial cell line, PRL prevented TGF-beta-induced apoptosis, as measured by terminal deoxynucleotidyltransferase dUTP nick-end labeling (TUNEL) staining and caspase-3 activation. Akt activity was inhibited by TGF-beta over a twenty to sixty minute time course. In TGF-beta treated cells, PRL disinhibited Akt in a PUK-dependent manner. Expression of dominant negative Akt (DN-Akt) blocked the protective effect of PRL in TGF-beta-induced apoptosis. Transgenic mice overexpressing a dominant-negative TGF-beta type II receptor (DNIIR) in the mammary epithelium undergo hyperplastic alveolar development, and this effect was PRL-dependent. Involution in response to teat-sealing was slowed by overexpression of DNIIR; furthermore, Akt and forkhead phosphorylation increased in the sealed mammary glands of DNIIR mice. Thus, Akt appears to be an essential component of the interaction between PRL and TGF-beta signaling in mammary epithelial cells both in vitro and in vivo.

ISBN: 0496745743Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Mechanisms of cell death regulation during mammary gland development and involution.
LDR:03347nmm 2200289 4500 001 1851272
005 20051216110241.5
008 130614s2004 eng d
020 $a 0496745743
035 $a (UnM)AAI3127310
035 $a AAI3127310
040 $a UnM $c UnM
100 1 $a Bailey, Jason P. $3 1939166
245 1 0 $a Mechanisms of cell death regulation during mammary gland development and involution.
300 $a 145 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1094.
500 $a Chair: Nelson D. Horseman.
502 $a Thesis (Ph.D.)--University of Cincinnati, 2004.
520 $a Both prolactin (PRL) and transforming growth factor-beta (TGF-beta) regulate cell survival in mammary epithelial cells, but their mechanism(s) of interactions are not known. In primary mammary epithelial cells and the HC11 mouse mammary epithelial cell line, PRL prevented TGF-beta-induced apoptosis, as measured by terminal deoxynucleotidyltransferase dUTP nick-end labeling (TUNEL) staining and caspase-3 activation. Akt activity was inhibited by TGF-beta over a twenty to sixty minute time course. In TGF-beta treated cells, PRL disinhibited Akt in a PUK-dependent manner. Expression of dominant negative Akt (DN-Akt) blocked the protective effect of PRL in TGF-beta-induced apoptosis. Transgenic mice overexpressing a dominant-negative TGF-beta type II receptor (DNIIR) in the mammary epithelium undergo hyperplastic alveolar development, and this effect was PRL-dependent. Involution in response to teat-sealing was slowed by overexpression of DNIIR; furthermore, Akt and forkhead phosphorylation increased in the sealed mammary glands of DNIIR mice. Thus, Akt appears to be an essential component of the interaction between PRL and TGF-beta signaling in mammary epithelial cells both in vitro and in vivo.
520 $a During involution substantial fragmentation of DNA can be readily detected; however, the role of endonucleases in mammary gland involution has not been investigated. Capase Activated DNase (CAD or DFF40) was reported to be essential for DNA fragmentation induced by several apoptotic stimuli. The dimer partner of DFF40, DFF45, has been knocked out. Analyses of the DFF45 mutant mouse mammary gland demonstrated that while pubertal mammary gland development was normal, involution was delayed. DFF45 mutant mice had delayed mammary gland involution and no DNA fragmentation as compared to wildtype controls. DFF45 was required for DNA fragmentation, and lack of this fragmentation prevented remodeling of the mammary gland; however, caspase-3 activation was unaffected. This is the first report of an endonuclease being involved in mammary gland involution. Virgin ductal outgrowth and terminal end bud apoptosis do not require the DFF40/DFF45 complex; however, this complex is indispensable for apoptosis during proper mammary gland involution to occur. Together these experiments provide a more complete and thorough understanding of the molecular mechanisms of apoptosis, which occurs during mammary gland involution.
590 $a School code: 0045.
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Biology, Cell. $3 1017686
690 $a 0433
690 $a 0379
710 2 0 $a University of Cincinnati. $3 960309
773 0 $t Dissertation Abstracts International $g 65-03B.
790 1 0 $a Horseman, Nelson D., $e advisor
790 $a 0045
791 $a Ph.D.
792 $a 2004
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3127310