3.4.21.88: Repressor LexA
This is an abbreviated version!
For detailed information about Repressor LexA, go to the full flat file.
Word Map on EC 3.4.21.88
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3.4.21.88
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reca
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lambda
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phage
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single-stranded
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regulon
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umud
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prophage
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mitomycin
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dna-damaging
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damage-inducible
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colicins
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sos-induced
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coprotease
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uv-irradiated
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nalidixic
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autodigestion
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self-cleavage
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sula
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lexa-binding
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reca430
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lysogens
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reca-dependent
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lexa-regulated
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reca-mediated
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lexadef
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promoter-operator
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drug development
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translesion
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antirepressors
- 3.4.21.88
- reca
- lambda
- phage
-
single-stranded
-
regulon
- umud
- prophage
- mitomycin
-
dna-damaging
-
damage-inducible
- colicins
-
sos-induced
-
coprotease
-
uv-irradiated
-
nalidixic
-
autodigestion
-
self-cleavage
- sula
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lexa-binding
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reca430
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lysogens
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reca-dependent
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lexa-regulated
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reca-mediated
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lexadef
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promoter-operator
- drug development
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translesion
-
antirepressors
Reaction
Hydrolysis of Ala84-/-Gly bond in repressor LexA =
Synonyms
Cg2114, LexA, LexA protein, LexA repressor, LexA transcriptional repressor, LexA1, lexA_1, MtLexA, SOS regulatory protein dinR
ECTree
3.4.21.88 Repressor LexAAdvanced search results
results (
results (Engineering
Engineering on EC 3.4.21.88 - Repressor LexA
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
G85D
L89P/Q92W/E152A/K156A
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designed to trap protein in conformation required for cleavage. Crystallization data of tryptic fragment containing amino acids 68202
S119A
additional information
G85D
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change in cleavage site, that blocks autocleavage but has normal active site, crystallization data
S119A
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change in the active site, but normal cleavage site. Crystallization data of full length protein and of tryptic fragment containing amino acids 68202
S119A
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one subunit is well-ordered throughout and in the non-cleavable state, whereas the second subunit, whilst disordered in the amino-terminal domain, adopts the cleavable state in the carboxy-terminal domain
additional information
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deletion of lexA gene of strain ATCC 13032 to create the mutant strain NJ2114, which has an elongated cell morphology and an increased doubling time. Comparison of SOS regulon, the transcriptomes of NJ2114, and a DNA-damage-induced wild-type strain with the wild-type control using DNA microarray hybridization, overview
additional information
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K156A, L89P, Q92W, E152A quadruple mutant, K156A, Q92W, E152A mutant variant -89, K156A, L89P, E152A mutant variant -92, K156A, L89P, Q92W mutant variant -152, K156A, Q92W mutant variant, Q92W S119A mutant variant, expression of truncated variants
additional information
construction of knockout mutant DELTAlexA mutant, the decrease in gene transfer frequency from the DELTAlexA mutant is associated with a decrease in transcription of the RcGTA structural gene cluster, the -galactosidase activities of WTand DELTAlexA mutant cells containing a plasmid with the RcGTA promoter fused to lacZ are compared. RcGTA recipient capability is decreased in the DELTAlexA mutant, phenotype, and morphology of DELTAlexA mutant cells, overview
additional information
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construction of knockout mutant DELTAlexA mutant, the decrease in gene transfer frequency from the DELTAlexA mutant is associated with a decrease in transcription of the RcGTA structural gene cluster, the -galactosidase activities of WTand DELTAlexA mutant cells containing a plasmid with the RcGTA promoter fused to lacZ are compared. RcGTA recipient capability is decreased in the DELTAlexA mutant, phenotype, and morphology of DELTAlexA mutant cells, overview
additional information
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construction of knockout mutant DELTAlexA mutant, the decrease in gene transfer frequency from the DELTAlexA mutant is associated with a decrease in transcription of the RcGTA structural gene cluster, the -galactosidase activities of WTand DELTAlexA mutant cells containing a plasmid with the RcGTA promoter fused to lacZ are compared. RcGTA recipient capability is decreased in the DELTAlexA mutant, phenotype, and morphology of DELTAlexA mutant cells, overview
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additional information
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construction of knockout mutant DELTAlexA mutant, the decrease in gene transfer frequency from the DELTAlexA mutant is associated with a decrease in transcription of the RcGTA structural gene cluster, the -galactosidase activities of WTand DELTAlexA mutant cells containing a plasmid with the RcGTA promoter fused to lacZ are compared. RcGTA recipient capability is decreased in the DELTAlexA mutant, phenotype, and morphology of DELTAlexA mutant cells, overview
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additional information
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construction of knockout mutant DELTAlexA mutant, the decrease in gene transfer frequency from the DELTAlexA mutant is associated with a decrease in transcription of the RcGTA structural gene cluster, the -galactosidase activities of WTand DELTAlexA mutant cells containing a plasmid with the RcGTA promoter fused to lacZ are compared. RcGTA recipient capability is decreased in the DELTAlexA mutant, phenotype, and morphology of DELTAlexA mutant cells, overview
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additional information
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introduction of a mutation recAo6869 in the LexA binding site, in the promoter region of the recA gene, leads to dramatically decreased fitness of orally but not intraperitoneally inoculated recAo6869 cells. However, the SOS response of this mutant is induced normally, and there is no increase in the sensitivity of the strain toward DNA-damaging agents, bile salts, or alterations in pH. Nevertheless, recAo6869 cells are unable to swarm and their capacity to cross the intestinal epithelium is significantly reduced, phenotype, detailed overview. The rate of RecA protein accumulation increases about 5fold in mitomycin C-treated wild-type cells, whereas no induction is observed in the lexA3(Ind) strain
additional information
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introduction of a mutation recAo6869 in the LexA binding site, in the promoter region of the recA gene, leads to dramatically decreased fitness of orally but not intraperitoneally inoculated recAo6869 cells. However, the SOS response of this mutant is induced normally, and there is no increase in the sensitivity of the strain toward DNA-damaging agents, bile salts, or alterations in pH. Nevertheless, recAo6869 cells are unable to swarm and their capacity to cross the intestinal epithelium is significantly reduced, phenotype, detailed overview. The rate of RecA protein accumulation increases about 5fold in mitomycin C-treated wild-type cells, whereas no induction is observed in the lexA3(Ind) strain
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additional information
construction of a lexA deletion strain WP3DELTAlexA, no growth defect is observed. 481 and 108 genes are differentially expressed at 20°C and 4°C, respectively, as demonstrated by comparative whole genome microarray analysis
additional information
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construction of a lexA deletion strain WP3DELTAlexA, no growth defect is observed. 481 and 108 genes are differentially expressed at 20°C and 4°C, respectively, as demonstrated by comparative whole genome microarray analysis
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additional information
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construction of a lexA deletion strain WP3DELTAlexA, no growth defect is observed. 481 and 108 genes are differentially expressed at 20°C and 4°C, respectively, as demonstrated by comparative whole genome microarray analysis
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additional information
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site-directed mutagenesis of the Verrucomicrobium spinosum recA promoter confirms that LexA binds a 14 bp palindromic motif with consensus sequence TGTTC-N4-GAACA
additional information
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construction of strain BW27784 sulA6209 lexA71, that lacks LexA activity
