TSH

The TSHR, long known to signal via cAMP, can induce both the phospholipase C (PLC) and the protein kinase A signal transduction systems. Intracellular Ca2+ and PLC regulate iodide efflux, H2O2 production, and thyroglobulin iodination, while adenylate cyclase and cAMP regulate iodide uptake and transcription of thyroglobulin (Tg), thyroid peroxidase (TPO), and the sodium-iodide symporter.

Presumably by protein disulfide isomerase leading to release of the α subunit from the membrane-bound receptor.

High-normal TSH-values are associated with an adverse lipid profile, high blood pressure, high body mass index (BMI), metabolic syndrome and fatal coronary heart disease.

It is known that the majority of the metabolically active T3 in the brain is not derived from the circulation, but produced locally by the effect of D2 on T4. Locally produced T3 largely acts on the hypothalamus and pituitary glands to control TSH levels.

Thyroid stimulating hormone receptors have been identified in mammalian heart, bone, kidneys, brain, skin, adipose, hair follicles, thymus, lymphocytes, astrocyte cultures and in fish testes.

Levothyroxine is recommended for long-term TSH suppression.

Including thyroid,lymphocytes, the pituitary, thymus, testes, kidney, brain, adipose tissue, and fibroblasts.

The only established biologic function of thyroid stimulating hormone (TSH) is to regulate the synthesis and secretion of thyroid hormone from thyroid follicular cells.

In response to low circulating thyroid hormone levels, the basal medial hypothalamus releases thyrotropin-releasing hormone (TRH) which then stimulates production of thyroid-stimulating hormone (TSH) from the thyrotropes of the anterior pituitary gland.

Other substances like serotonin, gonadotropin-releasing hormone, and estrogen can also stimulate prolactin release.

In thyroid cancer, the TSH protein may have a role in promoting the proliferation and growth of cancer cells. Therefore, for some high-risk groups, such as patients with postoperative thyroidectomy, inhibition of TSH protein production and activity can reduce the risk of cancer recurrence.

The secretion of TSH protein is regulated by a variety of factors, including negative feedback regulation of the hypothalamic-pituitary-thyroid axis, thyroxine levels, and the regulatory mechanism of anterior pituitary cells.

The polymorphisms of the TSH protein are partly related to the genetic variation of individuals. TSH proteins of different genotypes may affect an individual's sensitivity to TSH and regulation of thyroid function.

TSH protein activates intracellular signaling pathways by binding to TSH receptors on the surface of thyroid cells, promoting thyroxine synthesis and secretion. It enhances the production of thyroxine by positively regulating iodine uptake, thyroglobulin synthesis, and thyroid peroxidase activity.

The TSH protein plays a key role in clinical diagnosis. By measuring serum TSH levels, it is possible to assess whether the thyroid gland is functioning normally for diagnosis and follow-up of thyroid-related diseases.

Yes, the TSH protein can interact with TSH receptors on the surface of thyroid cells, triggering a series of signaling. In addition, TSH protein interacts with other cytokines and regulators to regulate thyroid function.