amtB:Quickview: Difference between revisions
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!align=left {{table_heading_style}} | | !align=left {{table_heading_style}} |Standard Name | ||
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!align=left {{table_heading_style}} | | !align=left {{table_heading_style}} |Gene Synonym(s) | ||
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!align=left {{table_heading_style}} | | !align=left {{table_heading_style}} |Product Desc. | ||
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!align=left {{table_heading_style}} |Knock-Out Phenotype | !align=left {{table_heading_style}} |Knock-Out Phenotype | ||
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!align=left {{table_heading_style}} |Regulation/Expression | !align=left {{table_heading_style}} |Regulation/Expression | ||
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!align=left {{table_heading_style}} |Regulation/Activity | !align=left {{table_heading_style}} |Regulation/Activity | ||
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Revision as of 20:09, 4 March 2009
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| Quickview | Gene | Gene Product(s) | Expression | Evolution | On One Page |
| References | Suggestions |
See Help:Quickview for help with entering information in the Quickview table.
| Standard Name |
|---|
| Gene Synonym(s) |
| Product Desc. |
| Product Synonyms(s) |
| Knock-Out Phenotype |
| Regulation/Expression |
| Regulation/Activity |
| edit table |
See Help:Quickview for help with entering information in the Quickview table.
Notes
AmtB is a trimeric inner membrane protein. Each subunit has 11 TM helices; a predicted N-terminal 12th TM helix is actually a cleaved signal peptide. Ammonium is proposed to bind to the periplasmic face of AmtB and then to be deprotonated to ammonia for diffusion through the AmtB channel, then reprotonated by water to hydrate the ammonia gas to ammonium ion in the cytoplasm. AmtB enables growth on ammonium as sole nitrogen source at low ammonium ion concentrations (Soupene, 1998). The human Rh proteins are AmtB homologs and have been variously proposed to act as ammonia channels or as carbon dioxide gas channels.[1]
References