Difference between revisions of "PgcA"
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[[Category:Protein-coding genes]] | [[Category:Protein-coding genes]] |
Revision as of 18:14, 14 March 2012
- Description: alpha-phosphoglucomutase, required for UDP-glucose synthesis, inhibits FtsZ ring assembly (indirect effect due to a defect in UDP-glucose synthesis)
Gene name | pgcA |
Synonyms | yhxB, gtaC, gtaE |
Essential | no |
Product | alpha-phosphoglucomutase |
Function | interconversion of glucose 6-phosphate and alpha-glucose 1-phosphate |
Metabolic function and regulation of this protein in SubtiPathways: Lipid synthesis | |
MW, pI | 62 kDa, 4.913 |
Gene length, protein length | 1695 bp, 565 aa |
Immediate neighbours | glpD, yhcY |
Get the DNA and protein sequences (Barbe et al., 2009) | |
Genetic context This image was kindly provided by SubtiList
|
Contents
Categories containing this gene/protein
cell wall synthesis, lipid metabolism/ other, phosphoproteins
This gene is a member of the following regulons
The gene
Basic information
- Locus tag: BSU09310
Phenotypes of a mutant
Database entries
- DBTBS entry: no entry
- SubtiList entry: [1]
Additional information
The protein
Basic information/ Evolution
- Catalyzed reaction/ biological activity: Alpha-D-glucose 1-phosphate = alpha-D-glucose 6-phosphate (according to Swiss-Prot)
- Protein family: phosphohexose mutase family (according to Swiss-Prot)
- Paralogous protein(s):
Extended information on the protein
- Kinetic information:
- Domains:
- Cofactor(s):
- Effectors of protein activity:
Database entries
- Structure:
- UniProt: P18159
- KEGG entry: [2]
- E.C. number: 5.4.2.2
Additional information
PgcA inhibits FtsZ ring assembly (indirect effect due to a defect in UDP-glucose synthesis)PubMed
Expression and regulation
- Operon:
- 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
Original publications
Additional publications: PubMed