MCB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kile, B. T.
Right arrow Articles by Alexander, W. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kile, B. T.
Right arrow Articles by Alexander, W. S.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, September 2001, p. 6189-6197, Vol. 21, No. 18
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.18.6189-6197.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Functional Analysis of Asb-1 Using Genetic Modification in Mice

Benjamin T. Kile,* Donald Metcalf, Sandra Mifsud, Ladina DiRago, Nicos A. Nicola, Douglas J. Hilton, and Warren S. Alexander

The Walter and Eliza Hall Institute of Medical Research and The Cooperative Research Centre for Cellular Growth Factors, Royal Melbourne Hospital, Victoria 3050, Australia

Received 30 March 2001/Returned for modification 8 June 2001/Accepted 11 June 2001

The Asbs are a family of ankyrin repeat proteins that, along with four other protein families, contain a C-terminal SOCS box motif, which was first identified in the suppressor of cytokine signaling (SOCS) proteins. While it is clear that the SOCS proteins are involved in the negative regulation of cytokine signaling, the biological roles of the other SOCS box-containing families are unknown. We have investigated Asb-1 function by generating mice that lack this protein, as well as mice that overexpress full-length or truncated Asb-1 in a wide range of tissues. Although Asb-1 is expressed in multiple organs, including the hematopoietic compartment in wild-type mice, Asb-1-/- mice develop normally and exhibit no anomalies of mature blood cells or their progenitors. While most organs in these mice appear normal, the testes of Asb-1-/- mice display a diminution of spermatogenesis with less complete filling of seminiferous tubules. In contrast, the widespread overexpression of Asb-1 in the mouse has no apparent deleterious effects.


* Corresponding author. Mailing address: The Walter and Eliza Hall Institute for Medical Research, Post Office, Royal Melbourne Hospital, Victoria 3050, Australia. Phone: 61-3-9345-2653. Fax: 61-3-9345-2616. E-mail: kile{at}wehi.edu.au.


Molecular and Cellular Biology, September 2001, p. 6189-6197, Vol. 21, No. 18
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.18.6189-6197.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2001 by the American Society for Microbiology. All rights reserved.