Document Detail


Transcriptional control of genes for soluble complement cascade regulatory proteins.
MedLine Citation:
PMID:  20869772     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The complement cascade of the immune system is an important mediator of the inflammatory response to infection; however it is crucial that this pathway is tightly regulated to prevent uncontrolled activation, which can lead to damage to host tissues. The complement system has many regulators that control activation; both membrane-bound and soluble factors. This review will focus on what is currently known about the transcriptional regulation of the soluble complement regulatory genes C1-inhibitor, complement factor I, complement factor H and C4-binding protein. The absence or mutation of these regulators is all associated with specific disease, and yet their contribution to disease is often poorly understood. It is through full understanding of these genes that we can comprehend the diseases with which they are implicated, and thus prove why knowledge of the transcriptional regulation of these genes is valuable.
Authors:
Laura A Fraczek; Brian K Martin
Publication Detail:
Type:  Journal Article; Review     Date:  2010-09-25
Journal Detail:
Title:  Molecular immunology     Volume:  48     ISSN:  1872-9142     ISO Abbreviation:  Mol. Immunol.     Publication Date:    2010 Nov-Dec
Date Detail:
Created Date:  2010-11-29     Completed Date:  2011-01-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905289     Medline TA:  Mol Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  9-13     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Ltd. All rights reserved.
Affiliation:
The Iowa Cancer Research Foundation, Urbandale, IA 50322, USA. laura-fraczek@uiowa.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Complement System Proteins / genetics*
Gene Expression
Gene Expression Regulation*
Humans
Chemical
Reg. No./Substance:
9007-36-7/Complement System Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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