EC Number   |
Substrates |
Organism |
Products |
Reversibility |
|---|
   2.4.1.B62 | more |
enzyme glucosylates and inactivates small GTPases of the Rho or Ras families, culminating in cytotoxicity |
Clostridioides difficile |
? |
- |
? |
| 2.4.1.B62 | more |
a circular electron transfer reaction is suggested tha does not directly involve any residues from the toxin. The transfer starts with the split of the glycosidic bond leading to the most stable transient state. The split increases the pK of the phosphoryl oxygen atom, facilitating deprotonation of the accepor, and provides space for the nucleophilic attack |
Clostridium novyi |
? |
- |
? |
| 2.4.1.B62 | more |
a circular electron transfer reaction is suggested tha does not directly involve any residues from the toxin. The transfer starts with the split of the glycosidic bond leading to the most stable transient state. The split increases the pK of the phosphoryl oxygen atom, facilitating deprotonation of the accepor, and provides space for the nucleophilic attack |
Paeniclostridium sordellii |
? |
- |
? |
| 2.4.1.B62 | more |
in the absence of target proteins toxin A acts as hydrolase cleaving UDP-D-glucose to UDP and D-glucose |
Clostridioides difficile |
? |
- |
? |
| 2.4.1.B62 | more |
lethal toxin from Clostridium sordellii is a glucosyltransferase, which uses UDP-glucose as cosubstrate to modify low molecular mass GTPases. Lethal toxin selectively modifies Rac and Ras. In Rac, acceptor amino acid is residue threonine 35. No substrates: Rho, Cdc42, Rab, Arf |
Paeniclostridium sordellii |
? |
- |
? |
| 2.4.1.B62 | more |
UDP-alpha-D-glucose selectively serves as cosubstrate for toxin A-catalyzed modification. The acceptor amino acid of glucosylation is Thr37. Mutation of Thr37 to Ala completely abolishes glucosylation. No substrates: H-Ras, Rab5, and Arf1 |
Clostridioides difficile |
? |
- |
? |
| 2.4.1.B62 | more |
full-length hemorrhagic toxin TcsH exclusively glucosylates Rho-GTPases. The recombinant transferase domain glucosylates preferably Rho-GTPases but also Ras-GTPases to some extent. Vero cells treated with full length TcsH also show glucosylation of Ras, albeit to a lower extent than of Rho-GTPases |
Paeniclostridium sordellii |
? |
- |
? |
| 2.4.1.B62 | more |
Clostridioides difficile toxin B is not active on human Ras-GTPase in human epithelial colorectal adenocarcinoma Caco-2 cells |
Clostridioides difficile |
? |
- |
- |
| 2.4.1.B62 | more |
lethal toxin from Clostridium sordellii is a glucosyltransferase, which uses UDP-glucose as cosubstrate to modify low molecular mass GTPases. Lethal toxin selectively modifies Rac and Ras. In Rac, acceptor amino acid is residue threonine 35. No substrates: Rho, Cdc42, Rab, Arf |
Paeniclostridium sordellii 6018 |
? |
- |
? |
| 2.4.1.B62 | more |
Clostridioides difficile toxin B is not active on human Ras-GTPase in human epithelial colorectal adenocarcinoma Caco-2 cells |
Clostridioides difficile 10463 |
? |
- |
- |
