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Novak et al., 1996

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In the case of At GSTF12, biochemical function can be linked to the observed phenotype of the knock-out, as inferred through metabolic profiling of the flavonoids present in the respective transparent testa 19 (TT19) mutants (Kitamura et al., 2004

We then summarize the evidence linking copper dyshomeostasis to atherosclerosis and elucidate the potential mechanisms underlying atherosclerosis development in terms of both copper excess and copper deficiency

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