The Claim
In the TαT1.1 pituitary thyrotroph cell line, depletion of thyroid hormone receptor beta (THRB) abolishes triiodothyronine (T3)-mediated down-regulation of Tshb mRNA at 10 nM T3, whereas depletion of thyroid hormone receptor alpha (THRA) has no effect, demonstrating that THRB is necessary for the negative feedback regulation of Tshb by physiological concentrations of T3.
What the research says
Not yet evaluated
We are still looking at what the research says.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
In a laboratory cell line derived from pituitary tissue, removing the thyroid hormone receptor beta prevents T3 from suppressing the production of Tshb mRNA, while removing receptor alpha does not, indicating that receptor beta is required for T3 to reduce Tshb mRNA levels under physiological conditions.
See the scientific wording
In a pituitary thyrotroph cell line (TαT1.1), thyroid hormone receptor beta (THRB) binds to the Tshb promoter, and its depletion abolishes triiodothyronine (T3)-mediated down-regulation of Tshb mRNA at 10 nM T3, while receptor alpha (THRA) depletion alone has no effect, indicating THRB is necessary for negative feedback regulation of Tshb at physiological T3 concentrations.
What the research says
1 studyIn simple terms, the study found that a specific protein called THRB is the key that turns off the Tshb gene when thyroid hormone levels are high — and removing it stops this shutdown. The other protein, THRA, doesn’t play a role in this process at normal hormone levels.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
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