Difference between revisions of "McsB"

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(References)
(Original Publications)
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{{PubMed|19609260}}
 
{{PubMed|19609260}}
 
==Original Publications==
 
==Original Publications==
<pubmed> 11179229,9987115,8793870,16163393,16497325,19226326,,9987115, ,11544224, 20852588 </pubmed>
+
<pubmed> 11179229,9987115, 8793870,16163393,16497325,19226326, 9987115, 11544224, 20852588</pubmed>
 
'''Additional publications:''' {{PubMed|17380125,16163393,19498169}}
 
'''Additional publications:''' {{PubMed|17380125,16163393,19498169}}
 
[[Category:Protein-coding genes]]
 
[[Category:Protein-coding genes]]

Revision as of 09:05, 26 October 2010

  • Description: protein arginine kinase, modulator of CtsR-dependent repression

Gene name mcsB
Synonyms yacI
Essential no
Product protein arginine kinase
Function control of CtsR activity
Metabolic function and regulation of this protein in SubtiPathways:
Stress
MW, pI 40 kDa, 5.068
Gene length, protein length 1089 bp, 363 aa
Immediate neighbours mcsA, clpC
Get the DNA and protein sequences
(Barbe et al., 2009)
Genetic context
McsB context.gif
This image was kindly provided by SubtiList







The gene

Basic information

  • Locus tag: BSU00850

Phenotypes of a mutant

Database entries

  • DBTBS entry: [1]
  • SubtiList entry: [2]

Additional information

The protein

Basic information/ Evolution

  • Catalyzed reaction/ biological activity: targets non-functional CtsR for degradation by ClpP/ClpC PubMed


  • Protein family: ATP:guanido phosphotransferase family (according to Swiss-Prot)
  • Paralogous protein(s):

Extended information on the protein

  • Kinetic information:
  • Domains:
  • Cofactor(s):
  • Effectors of protein activity:
  • Localization:

Database entries

  • Structure:
  • KEGG entry: [3]
  • E.C. number:

Additional information

Expression and regulation

  • Regulatory mechanism:
  • 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

Reviews

PubMed

Original Publications

Additional publications: PubMed