This old version of Proteopedia is provided for student assignments while the new version is undergoing repairs. Content and edits done in this old version of Proteopedia after March 1, 2026 will eventually be lost when it is retired in about June of 2026.

Apply for new accounts at the new Proteopedia. Your logins will work in both the old and new versions.


2icf

From Proteopedia

(Difference between revisions)
Jump to: navigation, search
Line 1: Line 1:
-
[[Image:2icf.gif|left|200px]]
+
{{Seed}}
 +
[[Image:2icf.png|left|200px]]
<!--
<!--
Line 9: Line 10:
{{STRUCTURE_2icf| PDB=2icf | SCENE= }}
{{STRUCTURE_2icf| PDB=2icf | SCENE= }}
-
'''CRIg bound to C3b'''
+
===CRIg bound to C3b===
-
==Overview==
+
<!--
-
The complement system is a key part of the innate immune system, and is required for clearance of pathogens from the bloodstream. After exposure to pathogens, the third component of the complement system, C3, is cleaved to C3b which, after recruitment of factor B, initiates formation of the alternative pathway convertases. CRIg, a complement receptor expressed on macrophages, binds to C3b and iC3b mediating phagocytosis of the particles, but it is unknown how CRIg selectively recognizes proteolytic C3-fragments and whether binding of CRIg to C3b inhibits convertase activation. Here we present the crystal structure of C3b in complex with CRIg and, using CRIg mutants, provide evidence that CRIg acts as an inhibitor of the alternative pathway of complement. The structure shows that activation of C3 induces major structural rearrangements, including a dramatic movement (&gt;80 A) of the thioester-bond-containing domain through which C3b attaches to pathogen surfaces. We show that CRIg is not only a phagocytic receptor, but also a potent inhibitor of the alternative pathway convertases. The structure provides insights into the complex macromolecular structural rearrangements that occur during complement activation and inhibition. Moreover, our structure-function studies relating the structural basis of complement activation and the means by which CRIg inhibits the convertases provide important clues to the development of therapeutics that target complement.
+
The line below this paragraph, {{ABSTRACT_PUBMED_17051150}}, adds the Publication Abstract to the page
 +
(as it appears on PubMed at http://www.pubmed.gov), where 17051150 is the PubMed ID number.
 +
-->
 +
{{ABSTRACT_PUBMED_17051150}}
==About this Structure==
==About this Structure==
Line 30: Line 34:
[[Category: Crig]]
[[Category: Crig]]
[[Category: Immune system]]
[[Category: Immune system]]
-
''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Sun May 4 07:19:47 2008''
+
 
 +
''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Mon Jul 28 21:31:27 2008''

Revision as of 18:31, 28 July 2008

Image:2icf.png

Template:STRUCTURE 2icf

CRIg bound to C3b

Template:ABSTRACT PUBMED 17051150

About this Structure

2ICF is a Protein complex structure of sequences from Homo sapiens. Full crystallographic information is available from OCA.

Reference

Structure of C3b in complex with CRIg gives insights into regulation of complement activation., Wiesmann C, Katschke KJ, Yin J, Helmy KY, Steffek M, Fairbrother WJ, McCallum SA, Embuscado L, DeForge L, Hass PE, van Lookeren Campagne M, Nature. 2006 Nov 9;444(7116):217-20. Epub 2006 Oct 15. PMID:17051150

Page seeded by OCA on Mon Jul 28 21:31:27 2008

Proteopedia Page Contributors and Editors (what is this?)

OCA

Retrieved from "http://52.214.119.220/wiki/index.php/2icf"
Personal tools