Immunoatation of Rv2711
From DrugPedia: A Wikipedia for Drug discovery
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LAERLLVDVIGLPWEEVHAEACRWEHVMSEDVERRLVKVLNNPTTSPFGNPIPGLVELGVGPEPGADDANLVRLTELPAG | LAERLLVDVIGLPWEEVHAEACRWEHVMSEDVERRLVKVLNNPTTSPFGNPIPGLVELGVGPEPGADDANLVRLTELPAG | ||
SPVAVVVRQLTEHVQGDIDLITRLKDAGVVPNARVTVETTPGGGVTIVIPGHENVTLPHEMAHAVKVEKV | SPVAVVVRQLTEHVQGDIDLITRLKDAGVVPNARVTVETTPGGGVTIVIPGHENVTLPHEMAHAVKVEKV | ||
| + | |||
| + | =Human Homologue Blast Result= | ||
| + | |||
| + | <table border='1'><tr> | ||
| + | |||
| + | <td>subject ids</td><td>% identity</td><td>% positives</td><td>alignment length</td><td> evalue</td></tr> | ||
| + | |||
| + | <tr><td>sp|P07358</td><td> 30</td><td> 53</td><td> 39</td><td> 0.87</td></tr> | ||
| + | |||
| + | <tr><td>sp|Q8TEQ8</td><td> 40</td><td> 54</td><td> 35</td><td> 2.4</td></tr> | ||
| + | |||
| + | <tr><td>sp|Q9P273</td><td> 32</td><td> 50</td><td> 46</td><td> 5.2</td></tr> | ||
| + | |||
| + | <tr><td>sp|Q9NZQ8</td><td> 33</td><td> 50</td><td> 54</td><td> 7.5</td></tr> | ||
| + | |||
| + | <tr><td>sp|P25092</td><td> 27</td><td> 46</td><td> 80</td><td> 9.2</td></tr></table> | ||
Revision as of 08:58, 26 January 2010
| Immunoatation of Rv2711
| |
| Name | |
| IRON-dependent repressor and activator IDER | |
| Identifiers | |
| Swiss Prot | |
| Genbank | |
| PDB | |
| Chemical data | |
| Formula | ? |
| Mol. wt. | 25232.7 |
| Pharmacokinetic data | |
| Bioavailability | ? |
| Solubility | ? |
| Isoelectric-Point | 5.05 |
General
The mycobacterial IdeR protein is a metal-dependent regulator of the DtxR (diphtheria toxin repressor) family. In the presence of iron, it binds to a specific DNA sequence in the promoter regions of the genes that it regulates, thus controlling their transcription.A study has provided the evidence of ideR as an essential gene in Mycobacterium tuberculosis. ideR cannot normally be disrupted in this mycobacterium in the absence of a second functional copy of the gene. However, a rare ideR mutant was obtained in which the lethal effects of ideR inactivation were alleviated by a second-site suppressor mutation and which exhibited restricted iron assimilation capacity. Studies of this strain and a derivative in which IdeR expression was restored allowed to identify phenotypic effects resulting from ideR inactivation. Using DNA microarrays, the iron-dependent transcriptional profiles of the wild-type, ideR mutant, and ideR-complemented mutant strains were analyzed, and the genes regulated by iron and IdeR were identified. These genes encode a variety of proteins, including putative transporters, proteins involved in siderophore synthesis and iron storage, members of the PE/PPE family, a membrane protein involved in virulence, transcriptional regulators, and enzymes involved in lipid metabolism.
Protein Sequence
>Rv2711, TB.seq 3023562:3024251 MW:25234 MNELVDTTEMYLRTIYDLEEEGVTPLRARIAERLDQSGPTVSQTVSRMERDGLLRVAGDRHLELTEKGRALAIAVMRKHR LAERLLVDVIGLPWEEVHAEACRWEHVMSEDVERRLVKVLNNPTTSPFGNPIPGLVELGVGPEPGADDANLVRLTELPAG SPVAVVVRQLTEHVQGDIDLITRLKDAGVVPNARVTVETTPGGGVTIVIPGHENVTLPHEMAHAVKVEKV
Human Homologue Blast Result
| subject ids | % identity | % positives | alignment length | evalue |
| sp|P07358 | 30 | 53 | 39 | 0.87 |
| sp|Q8TEQ8 | 40 | 54 | 35 | 2.4 |
| sp|Q9P273 | 32 | 50 | 46 | 5.2 |
| sp|Q9NZQ8 | 33 | 50 | 54 | 7.5 |
| sp|P25092 | 27 | 46 | 80 | 9.2 |
