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.

In a laboratory cell line derived from pituitary tissue, removing both versions of the thyroid hormone receptor prevents the hormone T3 from suppressing the production of Tshb mRNA, even when T3 is present at very high levels.

When the THRB protein is removed from a specific type of pituitary cell in the lab, more THRA protein binds to the DNA region that controls the Tshb gene.

In tumors that produce excess TSH hormone, the proteins that respond to thyroid hormones are not detectable, even though the genetic instructions to make them are present. This suggests a problem in converting those instructions into functional proteins, which could disrupt the body's normal control of TSH levels.

In certain pituitary tumors that overproduce TSH, the genetic instructions for thyroid hormone receptors are present and readable, but the receptors themselves are not made, suggesting a problem occurs after the genetic code is copied but before the protein is assembled.

In certain benign tumors of the pituitary gland that overproduce TSH, the lack of thyroid hormone receptors prevents thyroid hormone from signaling the tumor to stop releasing TSH, leading to elevated thyroid hormone levels alongside abnormally high TSH.