Ribosylation

Hydantocidin. Hydantocidin (182), C2H2QN2O3, is elaborated by S. hygroscopicus (278). It is unique in that the anomeric carbon of the ribosyl moiety forms the spHo bond of hydantoin (279). The ribofuranose moiety which has been reported to be in a Q -endo conformation (279) has been synthesized (280,281). Hydantocidin is a herbicidal nucleoside with activity against monocotyledenous and dicotyledenous plants. 

Adenine, 9- -D-2-deoxyribofuranosyl-, 5, 536 Adenine, 8-(2-deoxy-/3-D-ribosyl)-synthesis, 5, 585 Adenine, 2,8-dialkyl-synthesis, 5, 569 Adenine, 2,8-dichloro-reactions... 

Distannacyclodecanes synthesis, 1, 606 Disulfide, benzylpurinyl ribosylation, S, 560 Disulfide, bis(l-alkenyl) rearrangement thiophenes from, 4, 871 Disulfide, bis(4-phenyl-3-butenyl) cyclization, 4, 867-868 Disulfide, dibenzothiazolyl as vulcanization accelerator, 1, 402 Disulfide, di(2,6-dimethoxypyrimidin-4-yl) oxidation, 3, 96 Disulfide, dipyrimidinyl synthesis, 3, 137 Disulfide, di(tetrazol-5-yl)... 

ADP-Ribosyl transferase (from human placenta) [9026-30-6]. Purified by making an affinity absorbent for ADP-ribosyltransferase by coupling 3-aminobenzamide to Sepharose 4B. [Burtscher et al. Anal Biochem 152 285 1986.]... 

The first chemical synthesis of these substances, using a procedure which yields 1-ribofuranosyl derivatives by pyrimidine bases, was described by Hall. By using the mercuric salt of 6-azathymine and tribenzoate of D-ribofuranosyl chloride, he obtained a mixture of two monoribosyl derivatives and a diribosyl derivative. He determined the structure of the 3-substituted derivative by the similarity of spectra and other properties to those of 3-methyl-6-razauracil. The structure of the 1-ribosyl derivative was then determined from the similarity of the spectra with 6-azathymine deoxyriboside obtained enzymatically. 

Small GTPases of the Rho family are ADP-ribosylated (e.g., at Asn4l of RhoA) and inactivated by C3-like toxins from Clostridium botulinum, Clostridium limosum, and Staphylococcus aureus. These proteins have a molecular mass of 23-30 kDa and consist only of the enzyme domain. Specific inhibition of Rho functions (Rho but not Rac or Cdc42 are targets) is the reason why C3 is widely used as a pharmacological tool [2]. 

Diphtheria toxin, Pseudomonas exotoxin A Elongation factor 2 ADP-ribosylation Inhibition of protein synthesis (diphtheria, Pseudomonas infection)... 

Cholera toxin, heat labile coli toxins Gs proteins ADP-ribosylation Activation of adenylate cyclase (cholera, traveler -d iarrhea)... 

Pertussis toxin Gj,0 proteins ADP-ribosylation Inhibition ofG protein signaling (whooping cough)... 

C. botulinum C2-toxin and related toxins Actin ADP-ribosylation Inhibition of actin polymerization... 

C. botulinum C3-toxin and related toxins Rho proteins ADP-ribosylation Inhibition of RhoA, B,C Destruction of the cytoskeleton... 

Cholera toxin is a protein toxin of Vibrio choleme. Toxin ADP-ribosylates the a-subunit of the Gs heterotrimeric... 

GTP-binding protein at an arginine residue which is involved in GTP hydrolysis. ADP-ribosylation thus leads to constitutive activation of Gs. 

Nucleotidylation - the addition of adenylate-residues by Lnu enzymes - can also be the cause of resistance to lincosamide antibiotics in staphylococci and enterococci. A plasmid encoded ADP-ribosylating transferase (Arr-2) that leads to rifampicin resistance has been detected in various Enterobacteriaceae as well as in Pseudomonas aeruginosa. 

Researchers found that NAD serves as a substrate in poly(ADP-ribose) synthesis, a reaction important for DNA repair processes. In addition, it takes part in mono (ADP-ribosyl)ation reactions that are involved in endogenous regulation of many aspects of signal transduction and membrane trafficking in eukaryotic cells. 

Pertussis toxin is produced by the bacterium Bordetella pertussis. It covalently modifies G-proteins of the G/Go family (transfer of a ADP-ribose moiety of NAD onto G-protein a-subunits). ADP-ribosylated G-proteins are arrested in their inactive state and, as a consequence, functionally uncoupled from their respective effectors. Examples for pertussis toxin-sensitive cellular responses include the hormonal inhibition of adenylyl cyclases, stimulation ofK+ channels, inhibition of Ca2+ channels and stimulation ofthe cGMP-phosphodiesterase in retinal rods. 

Secondly, treatment of neutrophils with pertussis toxin, which ADP-ribosylates a neutrophil G protein and causes a loss of cell responsiveness via receptor-mediated pathways (40,41), has minimal effect on the response to HCH (Figure 11, lower panel). Thus it can be concluded that HCH activation of neutrophils is independent of receptor-mediated activation of G proteins. 

Free R has a low affinity. Processes which uncouple R from G, either guanine nucleotide binding to G or ribosylation of R, also give R a low affinity. 

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