ADP Ribosylation
ADP ribosylation leads to the addition of a single or multiple ribose sugars and adenine diphosphate. This is a post translational modification ( modification of an already synthesize protein). The bacteria releases an exotoxin to a particular receptor site in which a protein that is normally active is inactivated or reduces protein function/ receptor preference. Most ADP ribosylation done by bacteria are divided into 2 categories. Diphtheria/diphtheria like toxins and cholera/cholera like toxins. In order for ADP ribosylation they need NAD+ to use ADP ribose moiety done by ADP ribosyl transferase.
A. Diphtheria toxin ( High Yield)
Inactivate EF-II
1. diphtheria toxin ( C. diphtheriae)
2. exotoxin A ( P.aeruginosa)
3. cholix toxin ( V. cholera)
B.Cholera Toxin
Inactivate GS High Yield
Cholera Toxin ( V. cholera)
Heat Labile Enterotoxin ( ETEC)
Inactivate Gi (B.pertussis) High Yield
Inactivate G-actin
CD toxin ( C. difficile)
Iota toxin ( C. perfringens)
C2 toxin (C. botulinum)
VIP ( B. cereus)
SpvB ( Salmonella sp.)
Inactivate Rho or Rho like proteins
C3bot ( C. botulinum)
C3 stau I( S.aureus)
ExoS ( P.aeruginosa)
ExoT ( P. aeruginosa)
Spy A ( S. pyogenes)
C3cer ( B. cereus)
In somes questions I have encounter they test if you know toxins that have similar mechanism in inactivating same protein target ( Pseudomona, C. diphtheriae). if they belong to ADP ribosylation family regardless of target protein ( Bordetella and C. diphtheriae) and what protein do they inactivate (for example EF-II). Proteins that inactivate Rho like proteins or G-actin are very low yield.
The author of other post was right in including ETEC. You can find article in this link. What I don't agree is B. anthracis. It is said that lethal factor of B. anthracis toxin has a similar target to ADP ribosylation of B. cereus toxin but does so in a different way (metalloprotease mechanism).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5846498/
ADP ribosylation leads to the addition of a single or multiple ribose sugars and adenine diphosphate. This is a post translational modification ( modification of an already synthesize protein). The bacteria releases an exotoxin to a particular receptor site in which a protein that is normally active is inactivated or reduces protein function/ receptor preference. Most ADP ribosylation done by bacteria are divided into 2 categories. Diphtheria/diphtheria like toxins and cholera/cholera like toxins. In order for ADP ribosylation they need NAD+ to use ADP ribose moiety done by ADP ribosyl transferase.
A. Diphtheria toxin ( High Yield)
Inactivate EF-II
1. diphtheria toxin ( C. diphtheriae)
2. exotoxin A ( P.aeruginosa)
3. cholix toxin ( V. cholera)
B.Cholera Toxin
Inactivate GS High Yield
Cholera Toxin ( V. cholera)
Heat Labile Enterotoxin ( ETEC)
Inactivate Gi (B.pertussis) High Yield
Inactivate G-actin
CD toxin ( C. difficile)
Iota toxin ( C. perfringens)
C2 toxin (C. botulinum)
VIP ( B. cereus)
SpvB ( Salmonella sp.)
Inactivate Rho or Rho like proteins
C3bot ( C. botulinum)
C3 stau I( S.aureus)
ExoS ( P.aeruginosa)
ExoT ( P. aeruginosa)
Spy A ( S. pyogenes)
C3cer ( B. cereus)
In somes questions I have encounter they test if you know toxins that have similar mechanism in inactivating same protein target ( Pseudomona, C. diphtheriae). if they belong to ADP ribosylation family regardless of target protein ( Bordetella and C. diphtheriae) and what protein do they inactivate (for example EF-II). Proteins that inactivate Rho like proteins or G-actin are very low yield.
The author of other post was right in including ETEC. You can find article in this link. What I don't agree is B. anthracis. It is said that lethal factor of B. anthracis toxin has a similar target to ADP ribosylation of B. cereus toxin but does so in a different way (metalloprotease mechanism).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5846498/