Difference between revisions of "BshA"
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+ | = [[Categories]] containing this gene/protein = | ||
+ | {{SubtiWiki category|[[miscellaneous metabolic pathways]]}}, | ||
+ | {{SubtiWiki category|[[resistance against oxidative and electrophile stress]]}} | ||
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+ | = This gene is a member of the following [[regulons]] = | ||
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=The gene= | =The gene= | ||
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=The protein= | =The protein= | ||
Revision as of 13:28, 9 December 2010
- Description: L-malic acid glycosyltransferase, involved in bacillithiol synthesis
Gene name | bshA |
Synonyms | jojH, ypjH |
Essential | no |
Product | L-malic acid glycosyltransferase |
Function | biosynthesis of bacillithiol |
MW, pI | 41 kDa, 6.149 |
Gene length, protein length | 1131 bp, 377 aa |
Immediate neighbours | cca, bshB1 |
Get the DNA and protein sequences (Barbe et al., 2009) | |
Genetic context This image was kindly provided by SubtiList
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Contents
Categories containing this gene/protein
miscellaneous metabolic pathways, resistance against oxidative and electrophile stress
This gene is a member of the following regulons
The gene
Basic information
- Locus tag: BSU22460
Phenotypes of a mutant
Database entries
- DBTBS entry: no entry
- SubtiList entry: [1]
Additional information
The protein
Basic information/ Evolution
- Catalyzed reaction/ biological activity: UDP-GlcNAc + L-malate = GlcNAc(α1→2)L-malate PubMed; also uses D-malate as a substrate, but with much lower affinity PubMed
- Protein family: NamA subfamily (according to Swiss-Prot)
- Paralogous protein(s):
Extended information on the protein
- Kinetic information:
- Domains:
- Modification:
- Cofactor(s):
- Effectors of protein activity:
- Interactions:
- Localization:
Database entries
- UniProt: P42982
- KEGG entry: [2]
- E.C. number:
Additional information
Expression and regulation
- Regulation:
- Regulatory mechanism:
- Additional information:
Biological materials
- Mutant: bshA::mls available in John_Helmann lab
- Expression vector:
- lacZ fusion:
- GFP fusion:
- two-hybrid system:
- Antibody:
Labs working on this gene/protein
Your additional remarks
References
Additional references: PubMed