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Identification of novel signaling co...

Xiao, Changchun.

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Identification of novel signaling components of the Toll/IL-1R pathway and their functions in innate immunity and development.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Identification of novel signaling components of the Toll/IL-1R pathway and their functions in innate immunity and development./
作者:	Xiao, Changchun.
面頁冊數:	147 p.
附註:	Director: Sankar Ghosh.
Contained By:	Dissertation Abstracts International63-03B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3046255
ISBN:	0493605002

Identification of novel signaling components of the Toll/IL-1R pathway and their functions in innate immunity and development.
Xiao, Changchun.

Identification of novel signaling components of the Toll/IL-1R pathway and their functions in innate immunity and development. - 147 p.

Director: Sankar Ghosh.

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

The Toll pathway determines dorsoventral axis of Drosophila embryos and is essential for the antifungal response of adult flies. The mammalian homologs of Toll, Toll-like receptors (TLRs), are required for host defense against microbial infections. The cytoplasmic domain of Interleukin-1 Receptor (IL-1R) shares high homology with those of TLRs. IL-1R regulates the inflammatory response, a part of mammalian host defense. TLR and IL-1R signal transduction pathways share common components. Both pathways activate NFκB and AP-1. This thesis describes the identification, characterization, and functional studies of two novel signaling components of the Toll/IL-1R pathway: X and ECSIT. Both components are highly conserved evolutionarily. They play different roles in the Toll/IL-1R signal transduction pathway: ECSIT is an obligatory component for signal relay, whereas X negatively regulates it. Moreover, ECSIT is specific for the Toll/IL-1R pathway, whereas X inhibits other signal transduction pathways too. Mouse gene targeting experiments show that both components are indispensable for early embryo development: ECSIT is crucial for anterior-posterior axis formation and X is required for proper formation and differentiation of mesoderm. Analysis of homozygous null <italic>Ecsit</italic> mutant embryos revealed a possible link between the Toll pathway and the TGFβ pathways and further studies are ongoing to test this hypothesis.

ISBN: 0493605002Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

Identification of novel signaling components of the Toll/IL-1R pathway and their functions in innate immunity and development.
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502 $a Thesis (Ph.D.)--Yale University, 2002.
520 $a The Toll pathway determines dorsoventral axis of Drosophila embryos and is essential for the antifungal response of adult flies. The mammalian homologs of Toll, Toll-like receptors (TLRs), are required for host defense against microbial infections. The cytoplasmic domain of Interleukin-1 Receptor (IL-1R) shares high homology with those of TLRs. IL-1R regulates the inflammatory response, a part of mammalian host defense. TLR and IL-1R signal transduction pathways share common components. Both pathways activate NFκB and AP-1. This thesis describes the identification, characterization, and functional studies of two novel signaling components of the Toll/IL-1R pathway: X and ECSIT. Both components are highly conserved evolutionarily. They play different roles in the Toll/IL-1R signal transduction pathway: ECSIT is an obligatory component for signal relay, whereas X negatively regulates it. Moreover, ECSIT is specific for the Toll/IL-1R pathway, whereas X inhibits other signal transduction pathways too. Mouse gene targeting experiments show that both components are indispensable for early embryo development: ECSIT is crucial for anterior-posterior axis formation and X is required for proper formation and differentiation of mesoderm. Analysis of homozygous null <italic>Ecsit</italic> mutant embryos revealed a possible link between the Toll pathway and the TGFβ pathways and further studies are ongoing to test this hypothesis.
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