| A bacterial effector targets Mad2L2, an APC inhibitor, to modulate host cell cycling. | |
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MedLine Citation:
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PMID: 17719540 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The gut epithelium self-renews every several days, providing an important innate defense system that limits bacterial colonization. Nevertheless, many bacterial pathogens, including Shigella, efficiently colonize the intestinal epithelium. Here, we show that the Shigella effector IpaB, when delivered into epithelial cells, causes cell-cycle arrest by targeting Mad2L2, an anaphase-promoting complex/cyclosome (APC) inhibitor. Cyclin B1 ubiquitination assays revealed that APC undergoes unscheduled activation due to IpaB interaction with the APC inhibitor Mad2L2. Synchronized HeLa cells infected with Shigella failed to accumulate Cyclin B1, Cdc20, and Plk1, causing cell-cycle arrest at the G2/M phase in an IpaB/Mad2L2-dependent manner. IpaB/Mad2L2-dependent cell-cycle arrest by Shigella infection was also demonstrated in rabbit intestinal crypt progenitors, and the IpaB-mediated arrest contributed to efficient colonization of the host cells. These results strongly indicate that Shigella employ special tactics to influence epithelial renewal in order to promote bacterial colonization of intestinal epithelium. |
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Authors:
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Hiroki Iwai; Minsoo Kim; Yuko Yoshikawa; Hiroshi Ashida; Michinaga Ogawa; Yukihiro Fujita; Daniel Muller; Teruo Kirikae; Peter K Jackson; Shuji Kotani; Chihiro Sasakawa |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Cell Volume: 130 ISSN: 0092-8674 ISO Abbreviation: Cell Publication Date: 2007 Aug |
Date Detail:
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Created Date: 2007-08-27 Completed Date: 2007-10-19 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0413066 Medline TA: Cell Country: United States |
Other Details:
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Languages: eng Pagination: 611-23 Citation Subset: IM |
Affiliation:
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Department of Microbiology and Immunology, International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, 4-6-1, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Bacterial Proteins / metabolism* Cell Cycle / physiology* Cell Cycle Proteins / physiology Cell Division Dysentery, Bacillary / pathology G2 Phase Glutathione Transferase / metabolism Green Fluorescent Proteins / metabolism Hela Cells Humans Ileum / microbiology Immunohistochemistry Intestinal Mucosa / microbiology Models, Biological Precipitin Tests Proliferating Cell Nuclear Antigen / metabolism Proteins / genetics, metabolism* RNA Interference Rabbits Recombinant Proteins / metabolism Shigella / metabolism*, pathogenicity Two-Hybrid System Techniques Ubiquitin-Protein Ligase Complexes / antagonists & inhibitors* Ubiquitins / analysis |
| Chemical | |
Reg. No./Substance:
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0/Bacterial Proteins; 0/Cell Cycle Proteins; 0/MAD2L2 protein, human; 0/Proliferating Cell Nuclear Antigen; 0/Proteins; 0/Recombinant Proteins; 0/Ubiquitins; 127384-62-7/ipaB protein, Shigella; 147336-22-9/Green Fluorescent Proteins; EC 2.5.1.18/Glutathione Transferase; EC 6.3.2.19/Ubiquitin-Protein Ligase Complexes; EC 6.3.2.19/anaphase-promoting complex |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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