東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

The role ofv-Abl tyrosine kinase in ...

Hinrichs-Sterling, Karen.

FindBook

Google Book

Amazon

博客來

The role ofv-Abl tyrosine kinase in transformation and apoptosis.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The role ofv-Abl tyrosine kinase in transformation and apoptosis./
作者:	Hinrichs-Sterling, Karen.
面頁冊數:	292 p.
附註:	Adviser: Kathryn Calame.
Contained By:	Dissertation Abstracts International63-10B.
標題:	Chemistry, Biochemistry. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3066852
ISBN:	0493862641

The role ofv-Abl tyrosine kinase in transformation and apoptosis.
Hinrichs-Sterling, Karen.

The role ofv-Abl tyrosine kinase in transformation and apoptosis. - 292 p.

Adviser: Kathryn Calame.

Thesis (Ph.D.)--Columbia University, 2002.

The v-Abl tyrosine kinase is a constitutively active form of the cellular kinase c-Abl. While causing pre-B cell lymphomas <italic>in vivo</italic>, v-Abl can transform pre-B cells, as well as some fibroblasts and myeloid cells <italic> in vitro</italic>. This thesis explores the initial response of primary cells to v-Abl expression and the circumstances under which primary cells undergo apoptosis, or become transformed, by v-Abl. v-Abl-dependent induction of <italic> p19arf</italic> transcription is presented as one mechanism by which v-Abl can cause apoptosis in fibroblasts. We identified an EN binding site as the v-Abl response element in the human <italic>p14ARF</italic> promoter, and an E2F as well as two overlapping Sp1 binding sites as v-Abl response elements in the murine <italic>p19arf</italic> promoter. In addition, we compared the extent of v-Abl-dependent apoptosis and transformation in primary mouse embryo fibroblasts (MEFs) and pre-B lymphocytes of wild type, p53<super>−/− </super>, and p73<super>−/−</super> genetic backgrounds and found that v-Abl-mediated apoptosis in pre-B cells, but not MEFs, is p53-independent. Finally, we identified <italic>c-myc</italic> gene amplification as an event that contributes to v-Abl-dependent transformation of p53<super>−/− </super> mouse embryo fibroblasts. Apoptosis versus transformation by other oncogenes, as well as potential determinants of the pre-B cell preference of v-Abl for transformation <italic>in vivo</italic> are discussed.

ISBN: 0493862641Subjects--Topical Terms:

1017722
Chemistry, Biochemistry.

The role ofv-Abl tyrosine kinase in transformation and apoptosis.
LDR:02408nam 2200277 a 45 001 927805
005 20110425
008 110425s2002 eng d
020 $a 0493862641
035 $a (UnM)AAI3066852
035 $a AAI3066852
040 $a UnM $c UnM
100 1 $a Hinrichs-Sterling, Karen. $3 1251368
245 1 0 $a The role ofv-Abl tyrosine kinase in transformation and apoptosis.
300 $a 292 p.
500 $a Adviser: Kathryn Calame.
500 $a Source: Dissertation Abstracts International, Volume: 63-10, Section: B, page: 4656.
502 $a Thesis (Ph.D.)--Columbia University, 2002.
520 $a The v-Abl tyrosine kinase is a constitutively active form of the cellular kinase c-Abl. While causing pre-B cell lymphomas <italic>in vivo</italic>, v-Abl can transform pre-B cells, as well as some fibroblasts and myeloid cells <italic> in vitro</italic>. This thesis explores the initial response of primary cells to v-Abl expression and the circumstances under which primary cells undergo apoptosis, or become transformed, by v-Abl. v-Abl-dependent induction of <italic> p19arf</italic> transcription is presented as one mechanism by which v-Abl can cause apoptosis in fibroblasts. We identified an EN binding site as the v-Abl response element in the human <italic>p14ARF</italic> promoter, and an E2F as well as two overlapping Sp1 binding sites as v-Abl response elements in the murine <italic>p19arf</italic> promoter. In addition, we compared the extent of v-Abl-dependent apoptosis and transformation in primary mouse embryo fibroblasts (MEFs) and pre-B lymphocytes of wild type, p53<super>−/− </super>, and p73<super>−/−</super> genetic backgrounds and found that v-Abl-mediated apoptosis in pre-B cells, but not MEFs, is p53-independent. Finally, we identified <italic>c-myc</italic> gene amplification as an event that contributes to v-Abl-dependent transformation of p53<super>−/− </super> mouse embryo fibroblasts. Apoptosis versus transformation by other oncogenes, as well as potential determinants of the pre-B cell preference of v-Abl for transformation <italic>in vivo</italic> are discussed.
590 $a School code: 0054.
650 4 $a Chemistry, Biochemistry. $3 1017722
650 4 $a Health Sciences, Immunology. $3 1017716
690 $a 0487
690 $a 0982
710 2 0 $a Columbia University. $3 571054
773 0 $t Dissertation Abstracts International $g 63-10B.
790 $a 0054
790 1 0 $a Calame, Kathryn, $e advisor
791 $a Ph.D.
792 $a 2002
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3066852