STRINGSTRING
lexA lexA recA recA AEF22876.1 AEF22876.1 AEF23152.1 AEF23152.1 dinB dinB AEF23564.1 AEF23564.1 AEF21002.1 AEF21002.1 AEF21452.1 AEF21452.1 dnaE2 dnaE2 AEF23151.1 AEF23151.1 AEF22874.1 AEF22874.1
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
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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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[Homology]
Score
lexASOS-response transcriptional repressor, LexA; 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
Protein recA; 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.
  
 
 0.967
AEF22876.1
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.
  
  
 0.911
AEF23152.1
KEGG: pmy:Pmen_1935 DNA repair nucleotidyltransferase/DNA polymerase-like protein.
 
 
 0.842
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.
  
 
 0.834
AEF23564.1
DNA repair protein RecN; May be involved in recombinational repair of damaged DNA.
   
  
 0.814
AEF21002.1
PFAM: Uncharacterised protein family YebG; KEGG: pmy:Pmen_3241 YebG family protein.
   
  
 0.784
AEF21452.1
KEGG: ppf:Pput_5030 DNA-directed DNA polymerase; PFAM: DNA-repair protein, UmuC-like.
 
 
 0.692
dnaE2
Error-prone DNA polymerase; DNA polymerase involved in damage-induced mutagenesis and translesion synthesis (TLS). It is not the major replicative DNA polymerase.
 
   
 0.655
AEF23151.1
KEGG: psa:PST_2344 cell division inhibitor SulA, putative.
 
   
 0.598
AEF22874.1
Regulatory protein TetR; PFAM: Transcription regulator, TetR-like, DNA-binding, bacterial/archaeal; KEGG: pmy:Pmen_1588 TetR family transcriptional regulator.
     
 0.562
Your Current Organism:
Pseudomonas fulva
NCBI taxonomy Id: 743720
Other names: P. fulva 12-X, Pseudomonas fulva 12-X, Pseudomonas fulva str. 12-X, Pseudomonas fulva strain 12-X
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