Article ID Journal Published Year Pages File Type
8476317 Molecular and Cellular Endocrinology 2018 59 Pages PDF
Abstract
In conclusion, our results confirm the genetic heterogeneity of TG defects and the pathophysiological importance of the predicted TG misfolding and therefore thyroid hormone formation as a consequence of truncated TG proteins and/or missense mutations located within its ACHE-like domain.
Related Topics
Life Sciences Biochemistry, Genetics and Molecular Biology Cell Biology
Authors
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