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      Pre-Translational and Post-Translational Regulation of TSH Synthesis in Normal and Neoplastic Thyrotrophs

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          We are interested in the mechanisms by which endocrine and developmental factors regulate TSH synthesis at both pre-translational and post-translational levels. Thyroid hormone profoundly decreases transcription of the TSH-β gene, while TRH and agents modifying cyclic AMP increase transcription. To elucidate the molecular mechanisms underlying these effects, human embryonal kidney cells were transfected with constructs of the human TSH-β gene fused to the chloramphenicol acetyltransferase gene. The first exon of human TSH-β, contains an element that increases basal expression and mediates T<sub>3</sub>-induced gene repression, probably through a direct interaction with c-erbAβ. This transcriptional repression by T<sub>3</sub> appears aberrant in thyrotropic tumors. In contrast, TRH and agents modifying cyclic AMP mediate increased transcription of TSH-β through interacting with upstream regulatory elements. Thyroid hormone, TRH and developmental factors also regulate the branching pattern and relative sialylation of TSH carbohydrate chains, which may affect TSH action in vitro and in vivo. Certain thyrotropic tumors produce TSH with more complex carbohydrate branching patterns, which may increase its biologic activity.

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          Author and article information

          Horm Res Paediatr
          Hormone Research in Paediatrics
          S. Karger AG
          02 December 2008
          : 32
          : 1-3
          : 22-24
          MCNEB, NIDDK, National Institutes of Health, Bethesda, Md., USA
          181235 Horm Res 1989;32:22–24
          © 1989 S. Karger AG, Basel

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          Page count
          Pages: 3
          Peptide Hormone Secreting Tumors


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