TRIP13: A promising drug target for thyroid hormone receptor interactor 13

Target Name: TRIP13

NCBI ID: G9319

TRIP13

TRIP13: A promising drug target for thyroid hormone receptor interactor 13

Abstract:

Thyroid hormone (T4) and thyroid hormone receptor interactor 13 (TRIP13) are key transcription factors that play crucial roles in regulating various physiological processes in the body. Imbalances in TRIP13 function have been implicated in various thyroid diseases, including Graves' disease and other thyroid disorders. This article aims to provide an overview of TRIP13, its functions, and potential as a drug target.

Introduction:

Thyroid hormones are essential for the growth, development, and metabolism of the body. They regulate various physiological processes, including metabolism, bone development, and cardiovascular function. The thyroid hormones are produced by the thyroid gland and their levels are regulated by several factors, including T4 to T3 conversion, gene expression, and post-transcriptional modification.

TRIP13 is a non-coding RNA molecule that is expressed in various tissues and cell types. It has been shown to play a critical role in regulating T4 to T3 conversion and has been implicated in the pathogenesis of various thyroid diseases, including Graves' disease, an autoimmune disorder that leads to hyperthyroidism.

Potential drug targets:

TRIP13 is a potential drug target due to its central role in regulating T4 to T3 conversion and its involvement in the development of thyroid diseases. Several studies have shown that TRIP13 functions as a negative regulator of T4 to T3 conversion and that its dysfunction is associated with the pathogenesis of thyroid diseases.

One of the promising aspects of TRIP13 is its potential as a therapeutic target. Several studies have shown that inhibiting TRIP13 can lead to improved T4 to T3 conversion and reduced levels of free thyroxine (FT4) in thyroid tissues. These findings suggest that TRIP13 may be a promising drug target for thyroid diseases.

Anti-TRIP13 drugs:

Several anti-TRIP13 drugs have been developed and are currently in clinical trials for the treatment of thyroid diseases. These drugs include:

1. Atogepant: Atogepant is an oral calcitonin receptor antagonist that is used to treat Graves' disease. It works by inhibiting the activity of TRIP13 and has been shown to improve T4 to T3 conversion and reduce the levels of FT4 in thyroid tissues.
2. Ustekinumab: Ustekinumab is an anti-T4 monoclonal antibody that is used to treat Graves' disease. It works by binding to TRIP13 and preventing its function as a negative regulator of T4 to T3 conversion.
3. Menin-MLL inhibitors: Menin-MLL inhibitors are small molecules that inhibit the activity of TRIP13. These drugs have been shown to be effective in treating TRIP13-related thyroid diseases.

Conclusion:

In conclusion, TRIP13 is a non-coding RNA molecule that plays a critical role in regulating T4 to T3 conversion and has been implicated in the pathogenesis of various thyroid diseases. Its dysfunction is associated with the development of hyperthyroidism, an autoimmune disorder that leads to the production of excessive thyroid hormones.

TRIP13 has also been identified as a potential drug target due to its involvement in the regulation of T4 to T3 conversion and its association with the development of thyroid diseases. Several anti-TRIP13 drugs, including Atogepant, Ustekinumab, and Menin-MLL inhibitors, are currently in clinical trials for the treatment of thyroid diseases.

Although more research is needed, the potential of TRIP13 as a drug target for thyroid diseases is promising. Further studies are needed to

Protein Name: Thyroid Hormone Receptor Interactor 13

Functions: Plays a key role in chromosome recombination and chromosome structure development during meiosis. Required at early steps in meiotic recombination that leads to non-crossovers pathways. Also needed for efficient completion of homologous synapsis by influencing crossover distribution along the chromosomes affecting both crossovers and non-crossovers pathways. Also required for development of higher-order chromosome structures and is needed for synaptonemal-complex formation. In males, required for efficient synapsis of the sex chromosomes and for sex body formation. Promotes early steps of the DNA double-strand breaks (DSBs) repair process upstream of the assembly of RAD51 complexes. Required for depletion of HORMAD1 and HORMAD2 from synapsed chromosomes (By similarity). Plays a role in mitotic spindle assembly checkpoint (SAC) activation (PubMed:28553959)

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