Skip Navigation

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 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 arrow Request Permissions
Google Scholar
Right arrow Articles by Kikuchi-Yanoshita, R.
Right arrow Articles by Kudo, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kikuchi-Yanoshita, R.
Right arrow Articles by Kudo, I.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

J. Biochem, 2003, Vol. 134, No. 5 699-709
© 2003 Japanese Biochemical Society

BIOCHEMISTRY

Induction of PYPAF1 during In Vitro Maturation of Mouse Mast Cells

Rei Kikuchi-Yanoshita1, Yoshitaka Taketomi1, Kumiko Koga1, Toshihiko Sugiki1, Yohei Atsumi1, Takanori Saito1, Shin-ichi Ishii2, Masato Hisada2, Tamiko Suzuki-Nishimura2, Masaatsu K. Uchida2, Tae-Chul Moon3, Hyeun-Wook Chang3, Masatsugu Sawada4, Naoki Inagaki4, Hiroichi Nagai4, Makoto Murakami*,1 and Ichiro Kudo1

1 Department of Health Chemistry, School of Pharmaceutical Sciences, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555; 2 Department of Pharmacology, Meiji Pharmaceutical University, 2-522-1 Nishio, Kiyose, Tokyo 204-8588; 3 College of Pharmacy, Yeungnam University, Gyonsan, Korea; and 4 Pharmacological Department, Gifu College of Pharmacy, 5-6-1 Mitahora Higashi, Gifu 502-8585

Coculture of mouse bone marrow-derived immature mast cells (BMMC) with Swiss 3T3 fibroblasts in the presence of stem cell factor (SCF) promotes morphological and functional maturation toward a connective tissue mast cell (CTMC)–like phenotype, which is accompanied by increased expression of several unique genes. Here we report the molecular identification of one of them, mast cell maturation–associated inducible gene (MMIG)-1. The MMIG-1 cDNA encodes a 117-kDa cytosolic protein that comprises an N-terminal PYRIN domain, a central nucleotide-binding domain, and nine C-terminal leucine-rich repeats. MMIG-1 shows >85% sequence similarity to human cryopyrin/PYPAF1, a causal gene for familial cold urticaria and Muckle-Wells syndrome. MMIG-1 was distributed in the cytosol of CTMC-like differentiated BMMC. MMIG-1 underwent alternative splicing in the leucine-rich repeats and each variant was induced differently in BMMC during coculture. Moreover, its expression was increased in the ears of mice with experimental atopic dermatitis. Thus, MMIG-1, a likely mouse PYPAF1 ortholog, may play a role in mast cell–directed inflammatory diseases.

* To whom correspondence should be addressed. Tel: +81-3-3784-8196, Fax: +81-3-3784-8245, E-mail: mako{at}pharm.showa-u.ac.jp


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


This article has been cited by other articles:


Home page
 J. Immunol.Home page
Y. Taketomi, K. Sunaga, S. Tanaka, M. Nakamura, S. Arata, T. Okuda, T.-C. Moon, H.-W. Chang, Y. Sugimoto, K. Kokame, et al.
Impaired Mast Cell Maturation and Degranulation and Attenuated Allergic Responses in Ndrg1-Deficient Mice
J. Immunol., June 1, 2007; 178(11): 7042 - 7053.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
P. Rosenstiel, K. Huse, A. Till, J. Hampe, S. Hellmig, C. Sina, S. Billmann, O. von Kampen, G. H. Waetzig, M. Platzer, et al.
A short isoform of NOD2/CARD15, NOD2-S, is an endogenous inhibitor of NOD2/receptor-interacting protein kinase 2-induced signaling pathways
PNAS, February 28, 2006; 103(9): 3280 - 3285.
[Abstract] [Full Text] [PDF]


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.