Abstract:
:Low plasma homoarginine has emerged as a risk marker for cardiovascular disease. We exploited cells of a patient with a rare inborn error of metabolism to explore potential pathways of homoarginine synthesis, using stable isotopes and mass spectrometry. Control lymphoblasts, as opposed to lymphoblasts from an arginine:glycine amidinotransferase (AGAT)-deficient patient, were able to synthesize homoarginine from arginine and lysine. In contrast, in a patient with a deficiency of the urea cycle enzyme argininosuccinate synthase, plasma homoarginine was not decreased. We conclude that promiscuous activity of AGAT, a key enzyme in creatine synthesis, plays a pivotal role in homoarginine synthesis.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Davids M,Ndika JD,Salomons GS,Blom HJ,Teerlink Tdoi
10.1016/j.febslet.2012.08.020subject
Has Abstractpub_date
2012-10-19 00:00:00pages
3653-7issue
20eissn
0014-5793issn
1873-3468pii
S0014-5793(12)00677-1journal_volume
586pub_type
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