EGF receptor pathway substrate No.8 藉由增加TLR4-MyD88交互作用而促進內毒素誘導巨噬細胞進行吞噬作用

陳彥任

doi:10.6844/NCKU.2012.00535

3.232.133.141，Hello！

Close
Search Quick Search Advanced Search Publication Search	Personal Service Member Login Searching History Use Bonus Card SYMSKAN
Browse Browse by University of Graduate Thesis Browse by Pinyin of Graduate Thesis Browse by Conference Proceedings Topic Browse by Conference Proceedings Publisher Browse by Pinyin of Conference Proceedings Browse by eBook Category Browse by eBook Topic Browse by eBook Publisher
Customer Services Authorize Airiti Recommend a Journal

Search Symbol (Half-width)	Description of Search Symbols
Space	"AND" indicates the intertwining of key terms used in a search
Double Quotation Marks ("") ( " " )	Double quotation marks indicate the beginning and end of a phrase, and the search will only include terms that appear in the same order of those within the quotations. Example: "image process" ： " image process "
?	Indicates a variable letter. Entering two ? will indicate two variable letters, and so on. Example: "Appl?", search results will yield apple, apply… e , appl y … ( (often used to English word searches) )
*	Indicates an unlimited number of variable letters to follow, from 1~n. Example: Enter "appl*", search results will yield apple, apples, apply, applied, application…(often used in English word searches) e , appl es , appl y , appl ied , appl ication … ( (often used to English word searches) )
AND、OR、NOT	Boolean logic combinations of key words is a skill used to expand or refine search parameters. (1) AND (1) AND: Refines search parameters (2) OR (2) OR: Expands search parameters (3) NOT: Excludes irrelevant parameters

DOI stands for Digital Object Identifier （ D igital O bject I dentifier ） ,
and is the unique identifier for objects on the internet. It can be used to create persistent link and to cite articles.

Using DOI as a persistent link

To create a persistent link, add「http://dx.doi.org/」「 http://dx.doi.org/ 」 before a DOI.
For instance, if the DOI of an article is 10.5297/ser.1201.002 , you can link persistently to the article by entering the following link in your browser: http://dx.doi.org/ 10.5297/ser.1201.002 。
The DOI link will always direct you to the most updated article page no matter how the publisher changes the document's position, avoiding errors when engaging in important research.

Cite a document with DOI

When citing references, you should also cite the DOI if the article has one. If your citation guideline does not include DOIs, you may cite the DOI link.

DOIs allow accurate citations, improve academic contents connections, and allow users to gain better experience across different platforms. Currently, there are more than 70 million DOIs registered for academic contents. If you want to understand more about DOI, please visit airiti DOI Registration （ doi.airiti.com ）。

Data Source

Health & Medical Care > Basic Medical Science
College of Medicine > Graduate Institute of Basic Medical Sciences

Bibliography Management Tool

Related Links

Report an Issue

Purchase Single Articles

Download PDF

EGF receptor pathway substrate No.8 藉由增加TLR4-MyD88交互作用而促進內毒素誘導巨噬細胞進行吞噬作用

EGF receptor pathway substrate No.8 facilitates phagocytosis by increasing TLR4-MyD88 interaction in LPS-stimulated macrophages

陳彥任 , Ph.D　　Advisor：呂增宏　　

英文 DOI： 10.6844/NCKU.2012.00535

Eps8 ； Src ； Toll-like receptor 4 ；巨噬細胞；吞噬作用；內毒素； Eps8 ； Src ； Toll-like receptor 4 ； macrophage ； phagocytosis ； Lipopolysaccharide

Abstract │ Reference (91) │ Altmetrics

Abstract 〈TOP〉

Parallel Abstract 〈TOP〉

Macrophage-mediated phagocytosis and subsequent degradation of pathogens by macrophages play a pivotal role in host innate immune responses to microbial infection. Recent studies have shown that Toll-like receptors (TLRs) play an important role in promoting the clearance of bacteria by up-regulating the phagocytic activity of macrophages under LPS stimulation. However, the underlying mechanism is not well defined. In the present study, we demonstrated the induction of Src in LPS-treated macrophages was TLR4- and MyD88-dependent and attenuation of Src by src-specific siRNA reduced LPS-promoted phagocytosis. And reintroduction of siRNA-resistant Src could restore the defect. Interestingly, we observed Eps8 was also up-regulated under LPS stimulation in a Src-dependent manner and Eps8 knockdown or overexpression of PH-truncated Eps8 (i.e. 261-p97Eps8) decreased LPS-mediated macrophage phagocytosis. In addition, confocal microscopy indicated Eps8 and TLR4 were colocolized in the cytosol and at the phagosome in RAW264.7 cells. Consistently, both Eps8 and TLR4 immunoprecipitated together from the lysates of RAW264.7 cells with or without LPS stimulation. This Eps8-TLR4 complex formation was required for LPS-induced TLR4-MyD88 interaction and the following activation of Src, FAK, and p38 MAPK. Importantly, Eps8 knockdown reduced bacterium killing ability of macrophages. Thus, Eps8 is a key protein regulating LPS-stimulated TLR4-MyD88 interaction and the following macrophage phagocytosis.

Reference ( 91 ) 〈TOP〉

Abou-Kheir, W., Isaac, B., Yamaguchi, H., and Cox, D. (2008). Membrane targeting of WAVE2 is not sufficient for WAVE2-dependent actin polymerization: a role for IRSp53 in mediating the interaction between Rac and WAVE2. J Cell Sci 121, 379-390.
連結：
Aderem, A., and Underhill, D.M. (1999). Mechanisms of phagocytosis in macrophages. Annu Rev Immunol 17, 593-623.
連結：
Akira, S., Uematsu, S., and Takeuchi, O. (2006). Pathogen recognition and innate immunity. Cell 124, 783-801.
連結：
Allen, L.H., and Aderem, A. (1995). A role for MARCKS, the alpha isozyme of protein kinase C and myosin I in zymosan phagocytosis by macrophages. J Exp Med 182, 829-840.
連結：
Anand, R.J., Kohler, J.W., Cavallo, J.A., Li, J., Dubowski, T., and Hackam, D.J. (2007). Toll-like receptor 4 plays a role in macrophage phagocytosis during peritoneal sepsis. J Pediatr Surg 42, 927-932; discussion 933.
連結：

Altmetrics

〈TOP〉

E-mail ：

When an article is available to download, a notice will be sent to your mailbox address.

E-mail ：