1ik0

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[[Image:1ik0.png|left|200px]]
 
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{{STRUCTURE_1ik0| PDB=1ik0 | SCENE= }}
{{STRUCTURE_1ik0| PDB=1ik0 | SCENE= }}
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===Solution Structure of Human IL-13===
===Solution Structure of Human IL-13===
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{{ABSTRACT_PUBMED_11419948}}
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{{ABSTRACT_PUBMED_11419948}}
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==Disease==
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[[http://www.uniprot.org/uniprot/IL13_HUMAN IL13_HUMAN]] Defects in IL13 may be a cause of susceptibility to allergic rhinitis (ALRH) [MIM:[http://omim.org/entry/607154 607154]]. Allergic rhinitis is a common disease of complex inheritance and is characterized by mucosal inflammation caused by allergen exposure.
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==Function==
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[[http://www.uniprot.org/uniprot/IL13_HUMAN IL13_HUMAN]] Cytokine. Inhibits inflammatory cytokine production. Synergizes with IL2 in regulating interferon-gamma synthesis. May be critical in regulating inflammatory and immune responses.
==About this Structure==
==About this Structure==
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==Reference==
==Reference==
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<ref group="xtra">PMID:011419948</ref><references group="xtra"/>
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<ref group="xtra">PMID:011419948</ref><references group="xtra"/><references/>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Diblasio, E.]]
[[Category: Diblasio, E.]]

Revision as of 23:41, 24 March 2013

Template:STRUCTURE 1ik0

Contents

Solution Structure of Human IL-13

Template:ABSTRACT PUBMED 11419948

Disease

[IL13_HUMAN] Defects in IL13 may be a cause of susceptibility to allergic rhinitis (ALRH) [MIM:607154]. Allergic rhinitis is a common disease of complex inheritance and is characterized by mucosal inflammation caused by allergen exposure.

Function

[IL13_HUMAN] Cytokine. Inhibits inflammatory cytokine production. Synergizes with IL2 in regulating interferon-gamma synthesis. May be critical in regulating inflammatory and immune responses.

About this Structure

1ik0 is a 1 chain structure with sequence from Homo sapiens. Full experimental information is available from OCA.

See Also

Reference

  • Moy FJ, Diblasio E, Wilhelm J, Powers R. Solution structure of human IL-13 and implication for receptor binding. J Mol Biol. 2001 Jun 29;310(1):219-30. PMID:11419948 doi:10.1006/jmbi.2001.4764

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OCA

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