語系:
繁體中文
English
說明(常見問題)
圖資館首頁
登入
回首頁
切換:
標籤
|
MARC模式
|
ISBD
ERBB4 regulated intramembrane proteo...
~
Rokicki, Jerzy Wayne.
ERBB4 regulated intramembrane proteolysis is stimulated by estradiol and the 4ICD product controls progesterone receptor expression.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
ERBB4 regulated intramembrane proteolysis is stimulated by estradiol and the 4ICD product controls progesterone receptor expression.
作者:
Rokicki, Jerzy Wayne.
面頁冊數:
124 p.
附註:
Source: Dissertation Abstracts International, Volume: 72-07, Section: B, page: .
附註:
Adviser: Frank Jones.
Contained By:
Dissertation Abstracts International72-07B.
標題:
Biology, Molecular.
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3454208
ISBN:
9781124630755
ERBB4 regulated intramembrane proteolysis is stimulated by estradiol and the 4ICD product controls progesterone receptor expression.
Rokicki, Jerzy Wayne.
ERBB4 regulated intramembrane proteolysis is stimulated by estradiol and the 4ICD product controls progesterone receptor expression.
- 124 p.
Source: Dissertation Abstracts International, Volume: 72-07, Section: B, page: .
Thesis (Ph.D.)--Tulane University, 2011.
ERBB4 is a unique member of the ERBB receptor tyrosine kinase family that can undergo regulated intramembrane proteolysis (RIP) to generate the 4ICD cytosolic fragment. ERBB4 RIP occurs upon the binding of cognate ligand. Increased levels of 4ICD have been observed after estrogen stimulation of breast cancer cells. Using cell culture, genetic, and pharmacological approaches we investigated if E2 treatment stimulates RIP. E2 stimulation lead to increased cytosolic levels of 4ICD after 60 minutes and was estrogen receptor alpha (ERalpha) dependent. Furthermore, RIP occurred thought the pathway identified for ligand induced RIP. Due to the short response time, it was hypothesized that membrane ERalpha was involved. However, it was demonstrated that non-membrane ERalpha mediates this activity.
ISBN: 9781124630755Subjects--Topical Terms:
226919
Biology, Molecular.
ERBB4 regulated intramembrane proteolysis is stimulated by estradiol and the 4ICD product controls progesterone receptor expression.
LDR
:03003nmm 2200337 4500
001
309723
005
20111105132456.5
008
111212s2011 ||||||||||||||||| ||eng d
020
$a
9781124630755
035
$a
(UMI)AAI3454208
035
$a
AAI3454208
040
$a
UMI
$c
UMI
100
1
$a
Rokicki, Jerzy Wayne.
$3
531065
245
1 0
$a
ERBB4 regulated intramembrane proteolysis is stimulated by estradiol and the 4ICD product controls progesterone receptor expression.
300
$a
124 p.
500
$a
Source: Dissertation Abstracts International, Volume: 72-07, Section: B, page: .
500
$a
Adviser: Frank Jones.
502
$a
Thesis (Ph.D.)--Tulane University, 2011.
520
$a
ERBB4 is a unique member of the ERBB receptor tyrosine kinase family that can undergo regulated intramembrane proteolysis (RIP) to generate the 4ICD cytosolic fragment. ERBB4 RIP occurs upon the binding of cognate ligand. Increased levels of 4ICD have been observed after estrogen stimulation of breast cancer cells. Using cell culture, genetic, and pharmacological approaches we investigated if E2 treatment stimulates RIP. E2 stimulation lead to increased cytosolic levels of 4ICD after 60 minutes and was estrogen receptor alpha (ERalpha) dependent. Furthermore, RIP occurred thought the pathway identified for ligand induced RIP. Due to the short response time, it was hypothesized that membrane ERalpha was involved. However, it was demonstrated that non-membrane ERalpha mediates this activity.
520
$a
The ERBB family members ERBB1 and ERBB2 are heavily involved in the pathogenesis of breast cancer, while the role of ERBB4 is less clear. Breast cancer is the most commonly diagnosed and second leading cause of cancer related death in North American. The clinical prognosis of breast cancer is based on the expression status of a number of molecular markers, the most widely used being estrogen receptor alpha (ERalpha), progesterone receptor (PR), and ERBB2. The central role of ERalpha in the pathogenesis of breast cancer is undisputed; however, the phenotypes of ERBB4 and PR knockout mouse models overlap. Here we investigated the possibility that ERBB4 regulates estrogen stimulated PR expression in the breast. Using genetic, cell culture, and mouse model approaches we were able to demonstrate that ERBB4 coactivates PR expression in models of breast cancer and in the developing mammary gland. Furthermore, in human pathological samples, nuclear localized ERBB4/4ICD was significantly associated with increased levels of PR expression in breast tumors.
590
$a
School code: 0235.
650
4
$a
Biology, Molecular.
$3
226919
650
4
$a
Biology, Cell.
$3
226967
690
$a
0307
690
$a
0379
710
2
$a
Tulane University.
$b
Biomedical Sciences.
$3
531064
773
0
$t
Dissertation Abstracts International
$g
72-07B.
790
1 0
$a
Jones, Frank,
$e
advisor
790
1 0
$a
Agrawal, Krishna
$e
committee member
790
1 0
$a
Deininger, Prescott
$e
committee member
790
1 0
$a
Hill, Steve
$e
committee member
790
1 0
$a
Rowan, Brian
$e
committee member
790
$a
0235
791
$a
Ph.D.
792
$a
2011
856
4 0
$u
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3454208
筆 0 讀者評論
全部
電子館藏
館藏
1 筆 • 頁數 1 •
1
條碼號
館藏地
館藏流通類別
資料類型
索書號
使用類型
借閱狀態
預約狀態
備註欄
附件
000000060135
電子館藏
1圖書
學位論文
TH 2011
一般使用(Normal)
在架
0
1 筆 • 頁數 1 •
1
多媒體
多媒體檔案
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3454208
評論
新增評論
分享你的心得
Export
取書館別
處理中
...
變更密碼
登入