Abstract
A new study shows that defects in SECIS-binding protein 2 (SBP2), a factor required for incorporation of selenium into proteins, produce alterations in thyroid hormone metabolism in humans but none of the other effects attributed to selenium deficiency or loss of selenoproteins. This finding suggests that SBP2 has a role in distinguishing between selenoproteins whose functions are essential and those with supporting roles in life and health.
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