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

Endocytosis of DSL ligands and activ...

Wang, Weidong.

FindBook

Google Book

Amazon

博客來

Endocytosis of DSL ligands and activation of the Notch signaling pathway in Drosophila.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Endocytosis of DSL ligands and activation of the Notch signaling pathway in Drosophila./
作者:	Wang, Weidong.
面頁冊數:	216 p.
附註:	Source: Dissertation Abstracts International, Volume: 66-12, Section: B, page: 6403.
Contained By:	Dissertation Abstracts International66-12B.
標題:	Biology, Genetics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3199594
ISBN:	9780542463808

Endocytosis of DSL ligands and activation of the Notch signaling pathway in Drosophila.
Wang, Weidong.

Endocytosis of DSL ligands and activation of the Notch signaling pathway in Drosophila. - 216 p.

Source: Dissertation Abstracts International, Volume: 66-12, Section: B, page: 6403.

Thesis (Ph.D.)--Columbia University, 2006.

The DSL-Notch signaling pathway is a conserved signaling mechanism for cell-cell communication that dictates a wide range of developmental and physiological processes in organisms ranging from nematodes to humans. Delta/Serrate/Lag2 (DSL) ligands and their receptor, Notch, are single-pass transmembrane proteins. DSL ligands on the surface of signal-sending cells activate Notch on the surface of signal-receiving cells by triggering successive proteolytic cleavages of the receptor. Ligand-induced cleavage leads to the release and translocation of the Notch intracellular domain (NICD), a transcriptional activator, into nucleus, thereby transducing the signal. The mechanism by which DSL ligand binding activates Notch is not known.

ISBN: 9780542463808Subjects--Topical Terms:

1017730
Biology, Genetics.

Endocytosis of DSL ligands and activation of the Notch signaling pathway in Drosophila.
LDR:03280nmm 2200313 4500 001 1825437
005 20061211074630.5
008 130610s2006 eng d
020 $a 9780542463808
035 $a (UnM)AAI3199594
035 $a AAI3199594
040 $a UnM $c UnM
100 1 $a Wang, Weidong. $3 1250553
245 1 0 $a Endocytosis of DSL ligands and activation of the Notch signaling pathway in Drosophila.
300 $a 216 p.
500 $a Source: Dissertation Abstracts International, Volume: 66-12, Section: B, page: 6403.
500 $a Adviser: Gary Struhl.
502 $a Thesis (Ph.D.)--Columbia University, 2006.
520 $a The DSL-Notch signaling pathway is a conserved signaling mechanism for cell-cell communication that dictates a wide range of developmental and physiological processes in organisms ranging from nematodes to humans. Delta/Serrate/Lag2 (DSL) ligands and their receptor, Notch, are single-pass transmembrane proteins. DSL ligands on the surface of signal-sending cells activate Notch on the surface of signal-receiving cells by triggering successive proteolytic cleavages of the receptor. Ligand-induced cleavage leads to the release and translocation of the Notch intracellular domain (NICD), a transcriptional activator, into nucleus, thereby transducing the signal. The mechanism by which DSL ligand binding activates Notch is not known.
520 $a Herein, using transgenes that express altered forms of Delta (Dl), I demonstrate that signal-sending cells must endocytose DSL ligands in order to activate Notch in signal-receiving cells. I also show that mono-ubiquitination of DSL ligands is sufficient to target them for endocytosis, and is normally essential for their signaling activity.
520 $a To better understand the requirements for mono-ubiquitination and endocytosis in DSL signaling, I have defined the roles of two genes, liquid facets (lqf), and mind bomb (dmib) that encode, respectively, the conserved endocytic protein Epsin and a ubiquitin ligase; both of these genes are selectively required in signal-sending cells for activating Notch in signal-receiving cells. By using mutations and transgenes to manipulate the functions of Epsin, Dmib, and a functionally related ubiquitin ligase, Neuralized (Neur), I demonstrate that under normal conditions, (i) mono-ubiquitination of DSL ligands by either Dmib or Neur is required to target them for endocytosis by Epsin, and (ii) DSL ligands enter the cell by multiple endocytic pathways, but only those that are internalized via the action of Epsin activate Notch. These findings indicate that signaling activity does not depend on endocytosis of DSL ligands, per se, but rather on entry of the ligands into a select, Epsin-mediated endocytic pathway. I propose two general classes of models to explain the essential role of Epsin-mediated endocytosis in DSL-Notch signaling, involving the recruitment of DSL ligands to a special class of endocytic structures, or to a special recycling pathway.
590 $a School code: 0054.
650 4 $a Biology, Genetics. $3 1017730
650 4 $a Biology, Cell. $3 1017686
650 4 $a Biology, Molecular. $3 1017719
690 $a 0369
690 $a 0379
690 $a 0307
710 2 0 $a Columbia University. $3 571054
773 0 $t Dissertation Abstracts International $g 66-12B.
790 1 0 $a Struhl, Gary, $e advisor
790 $a 0054
791 $a Ph.D.
792 $a 2006
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3199594