Difference between revisions of "IseA"
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− | '''Additional publications:''' {{PubMed|23033921}} | + | '''Additional publications:''' {{PubMed|23091053,23033921}} |
− | <pubmed>17581128,18761694,17483219, 20059685,22383849 | + | <pubmed>17581128,18761694,17483219, 20059685,22383849 </pubmed> |
[[Category:Protein-coding genes]] | [[Category:Protein-coding genes]] |
Revision as of 08:03, 24 October 2012
- Description: inhibits in vitro activity of cell wall endopeptidases LytE and LytF, inhibits cell separation
Gene name | iseA |
Synonyms | yoeB |
Essential | no |
Product | inhibitor of autolysins |
Function | protection against cell envelope stress |
Gene expression levels in SubtiExpress: iseA | |
Interactions involving this protein in SubtInteract: IseA | |
MW, pI | 19 kDa, 10.176 |
Gene length, protein length | 543 bp, 181 aa |
Immediate neighbours | yoeA, trnSL-Arg1 |
Get the DNA and protein sequences (Barbe et al., 2009) | |
Genetic context This image was kindly provided by SubtiList
| |
Expression at a glance PubMed |
Contents
Categories containing this gene/protein
cell wall degradation/ turnover, membrane proteins
This gene is a member of the following regulons
The gene
Basic information
- Locus tag: BSU18380
Phenotypes of a mutant
Database entries
- DBTBS entry: no entry
- SubtiList entry: [1]
Additional information
The protein
Basic information/ Evolution
- Catalyzed reaction/ biological activity:
- Protein family:
- Paralogous protein(s):
Extended information on the protein
- Kinetic information:
- Domains:
- Modification:
- Cofactor(s):
- Effectors of protein activity:
- Localization: cell membrane (according to Swiss-Prot), localized to cell separation sites
Database entries
- Structure:
- UniProt: O34841
- KEGG entry: [2]
- E.C. number:
Additional information
Expression and regulation
- Operon: iseA PubMed
- Sigma factor:
- Regulation:
- Additional information:
Biological materials
- Mutant:
- Expression vector:
- lacZ fusion:
- GFP fusion:
- two-hybrid system:
- Antibody:
Labs working on this gene/protein
Your additional remarks
References
Additional publications: PubMed