Skip Navigation


Journal of Heredity Advance Access first published online on June 15, 2007
This version published online on June 27, 2007
Journal of Heredity, doi:10.1093/jhered/esm025
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
98/5/485    most recent
esm025v3
esm025v2
esm025v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Soller, J. T.
Right arrow Articles by Nolte, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Soller, J. T.
Right arrow Articles by Nolte, I.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The American Genetic Association. 2007. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Comparison of the Human and Canine Cytokines IL-1({alpha}/ß) and TNF-{alpha} to Orthologous Other Mammalians

Jan T. Soller, Hugo Murua Escobar, Saskia Willenbrock, Miriam Janssen, Nina Eberle, Jörn Bullerdiek, and Ingo Nolte

From the Small Animal Clinic, University of Veterinary Medicine, Bischofsholer Damm 15, 30137 Hanover, Germany (Soller, Escobar, Willenbrock, Eberle, and Nolte); and the Centre for Human Genetics, University of Bremen, Leobener Strasse ZHG, 28359 Bremen, Germany (Soller, Escobar, Willenbrock, Janssen, and Bullerdiek)

Address correspondence to Dr. I. Nolte at the address above, or e-mail: inolte{at}klt.tiho-hannover.de.

The cytokines interleukin-1 (IL-1{alpha} and IL-1ß) and the tumor necrosis factor-{alpha} (TNF-{alpha}) both play a major role in the initiation and regulation of inflammation and immunity responses. Polymorphisms within the gene sequences of these cytokines IL-1 and TNF-{alpha} have been proposed to play an important role in the pathogenesis of certain diseases. Affecting nearly every organ, various diseases, including some cancers, are described to be associated with an increased level of IL-1 and TNF-{alpha} proteins, for example, solid tumors, hematologic malignancies, malignant histiocytosis, autoimmune disorders, Alzheimer's disease, Parkinson's disease, sepsis, and rheumatoid arthritis. Regarding genetic backgrounds and pathways, numerous canine diseases show close similarities to their human counterparts. As a genetic model, the dog could be used to unravel the genetic mechanisms, for example, in particular the predispositions, the development, and progression of cancer and metabolic diseases. The identity comparison of gene and protein sequences of different species could be used to elucidate the structure and function of the genes and proteins by identifying the evolutionary conserved regions and domains. Herein we analyzed in detail the mRNA and protein structures and identities of the present known mammalian (human, canine, murine, rat, ovine, equine, feline, porcine, and bovine) TNF-{alpha}, IL-1{alpha}, and IL-1ß mRNAs and proteins. Additionally, based on the canine genome sequence, we derived in silico the complete mRNA structures of the IL-1{alpha} and IL-1ß mRNAs.

Corresponding Editor: Steven Hannah

The symposium paragraph for this article has been inserted.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.