STRINGSTRING
lexA lexA recA recA MDS_1639 MDS_1639 MDS_2172 MDS_2172 MDS_3931 MDS_3931 MDS_3541 MDS_3541 dinB dinB MDS_2522 MDS_2522 MDS_2521 MDS_2521 MDS_1641 MDS_1641 MDS_2523 MDS_2523
Nodes:
Network nodes represent proteins
splice isoforms or post-translational modifications are collapsed, i.e. each node represents all the proteins produced by a single, protein-coding gene locus.
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colored nodes:
query proteins and first shell of interactors
white nodes:
second shell of interactors
Node Content
empty nodes:
proteins of unknown 3D structure
filled nodes:
a 3D structure is known or predicted
Edges:
Edges represent protein-protein associations
associations are meant to be specific and meaningful, i.e. proteins jointly contribute to a shared function; this does not necessarily mean they are physically binding to each other.
Known Interactions
from curated databases
experimentally determined
Predicted Interactions
gene neighborhood
gene fusions
gene co-occurrence
Others
textmining
co-expression
protein homology
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Neighborhood
Gene Fusion
Cooccurrence
Coexpression
Experiments
Databases
Textmining
[Homology]
Score
lexALexA repressor; Represses a number of genes involved in the response to DNA damage (SOS response), including recA and lexA. In the presence of single-stranded DNA, RecA interacts with LexA causing an autocatalytic cleavage which disrupts the DNA-binding part of LexA, leading to derepression of the SOS regulon and eventually DNA repair. (204 aa)    
Predicted Functional Partners:
recA
Recombinase A; Can catalyze the hydrolysis of ATP in the presence of single- stranded DNA, the ATP-dependent uptake of single-stranded DNA by duplex DNA, and the ATP-dependent hybridization of homologous single-stranded DNAs. It interacts with LexA causing its activation and leading to its autocatalytic cleavage; Belongs to the RecA family.
  
 
 0.945
MDS_1639
SOS cell division inhibitor SulA; Component of the SOS system and an inhibitor of cell division. Accumulation of SulA causes rapid cessation of cell division and the appearance of long, non-septate filaments. In the presence of GTP, binds a polymerization-competent form of FtsZ in a 1:1 ratio, thus inhibiting FtsZ polymerization and therefore preventing it from participating in the assembly of the Z ring. This mechanism prevents the premature segregation of damaged DNA to daughter cells during cell division.
  
  
 0.913
MDS_2172
Ultraviolet light resistance protein B.
 
 
 0.781
MDS_3931
DNA repair protein RecN; May be involved in recombinational repair of damaged DNA.
   
  
 0.778
MDS_3541
YebG family protein.
   
  
 0.769
dinB
DNA polymerase IV; Poorly processive, error-prone DNA polymerase involved in untargeted mutagenesis. Copies undamaged DNA at stalled replication forks, which arise in vivo from mismatched or misaligned primer ends. These misaligned primers can be extended by PolIV. Exhibits no 3'-5' exonuclease (proofreading) activity. May be involved in translesional synthesis, in conjunction with the beta clamp from PolIII.
 
 
 0.768
MDS_2522
DNA repair nucleotidyltransferase/DNA polymerase-like protein.
 
 
 0.755
MDS_2521
Cell division inhibitor SulA, putative.
 
   
 0.604
MDS_1641
TetR family transcriptional regulator.
     
 0.587
MDS_2523
Error-prone DNA polymerase.
 
   
 0.520
Your Current Organism:
Pseudomonas mendocina NK01
NCBI taxonomy Id: 1001585
Other names: P. mendocina NK-01, Pseudomonas mendocina NK-01, Pseudomonas mendocina str. NK-01, Pseudomonas mendocina strain NK-01
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