dctR: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}} |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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Revision as of 20:23, 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
DctR is in the EvgAS regulon. Mutation reverses succinate growth defect of an atp operon deletion, as does a DctA overproducer. Overproduced DctR blocks growth on succinate, presumably by repressing dctA. Overexpression of DctR causes filamentous biofilm formation. DctR is a member of the LuxR family of regulatory proteins and is homologous to the DctR response regulator of R. capsulatus. DctR is possibly involved in the regulation of type III secretion systems in enterohemorrhagic E. coli O157:H7.[1]
References