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Literature summary for 2.7.8.29 extracted from

  • Kuge, O.; Saito, K.; Nishijima, M.
    Control of phosphatidylserine synthase II activity in Chinese hamster ovary cells (1999), J. Biol. Chem., 274, 23844-23849.
    View publication on PubMed

Protein Variants

Protein Variants Comment Organism
R97K in contrast to the PSS II wild-type transformant, the R97K transformant exhibits 4fold higher phosphatidylserine biosynthetic activity than that in CHO-K1 cells. The phosphatidylserine biosynthesis in the R97K transformant is not inhibited at all but elevated by the addition of phosphatidylserine Cricetulus griseus

Inhibitors

Inhibitors Comment Organism Structure
phosphatidylserine The phosphatidylserine synthesis in a CHO cell mutant which lacks PSS I, EC 2.7.8.8, but has normal PSS II activity, is almost completely inhibited by the addition of phosphatidylserine to the culture medium, like that in the wild-type CHO-K1 cells. The phosphatidylserine synthesis in a PSS II-overproducing stable transformant is reduced by 35% upon addition of phosphatidylserine. Residue Arg-97 is critical for the exogenous phosphatidylserine-mediated inhibition Cricetulus griseus

Organism

Organism UniProt Comment Textmining
Cricetulus griseus O08888
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Source Tissue

Source Tissue Comment Organism Textmining
CHO cell
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Cricetulus griseus
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General Information

General Information Comment Organism
physiological function PSS II activity is inhibited by exogenous phosphatidylserine and overproduction of PSS II leads to the loss of normal control of PSS II activity by exogenous phosphatidylserine. PSS II-overproducing cells cultivated without exogenous phosphatidylserine exhibit a normal phosphatidylserine biosynthetic rate similar to that in CHO-K1 cells. Stable transformation of R97K mutant PSS II, leads to a 4fold higher phosphatidylserine biosynthetic rate Cricetulus griseus