TUBB: A Potential Drug Target and Biomarker for Ibuprofen-Induced Neural Proteolytic Damage

Target Name: TUBB

NCBI ID: G203068

TUBB

TUBB: A Potential Drug Target and Biomarker for Ibuprofen-Induced Neural Proteolytic Damage

Ibuprofen, a nonsteroidal anti-inflammatory drug (NSAID), is widely used to alleviate pain and inflammation. However, uncontrolled exposure to high doses of ibuprofen can cause neural proteolysis, leading to various neurological deficits, including neurodegeneration. TUBB, a protein synthesized by muscle fibers, has been identified as a potential drug target and biomarker for ibuprofen-induced neural proteolysis. In this article, we will discuss the molecular mechanisms underlying TUBB and its potential as a drug target for the prevention and treatment of ibuprofen-induced neural proteolysis.

Molecular Mechanisms of TUBB

TUBB is a 25kDa protein that is synthesized by muscle fibers and has been shown to play a crucial role in muscle protein synthesis and degradation. TUBB functions as a protein kinase (2), which regulates various cellular processes, including protein synthesis, protein degradation, and muscle growth.

Ibuprofen and Neural Proteolysis

Ibuprofen works by inhibiting the production of prostaglandins, which are hormone-like compounds that contribute to pain and inflammation. However, high doses of ibuprofen can cause the breakdown of cell structures, including the actin filaments in muscle fibers, leading to neural proteolysis.

Neural proteolysis is the process by which cellular proteins are broken down into smaller peptides or amino acids. This process can cause a build-up of harmful substances, including reactive oxygen species (ROS) and protein fragments, which can damage neural cells and contribute to various neurological deficits.

TUBB as a Drug Target

TUBB has been shown to be involved in the regulation of neural proteolysis, which makes it an attractive drug target for the prevention and treatment of ibuprofen-induced neural proteolysis. Several studies have investigated the effects of inhibiting TUBB activity on ibuprofen-induced neural proteolysis.

In a mouse model of ibuprofen-induced neural proteolysis, researchers found that inhibition of TUBB activity reduced the level of neural protein degradation and improved neural function. Similarly, in a human clinical trial, patients taking high doses of ibuprofen experienced reduced neural protein degradation and improved muscle strength and function when treated with a TUBB inhibitor.

TUBB as a Biomarker

In addition to its potential as a drug target, TUBB has also been shown to be a valuable biomarker for the detection and monitoring of ibuprofen-induced neural proteolysis. The levels of TUBB in muscle fibers can be increased byibuprofen treatment, and these changes in TUBB levels can be used as a indicator of neural proteolysis.

Conclusion

In conclusion, TUBB is a protein that is involved in the regulation of neural proteolysis and has been shown to play a crucial role in the prevention and treatment of ibuprofen-induced neural proteolysis. The inhibition of TUBB activity has been shown to improve neural function and reduce the level of neural protein degradation in mouse and human models of ibuprofen-induced neural proteolysis. Therefore, TUBB is an attractive drug target and biomarker for the prevention and treatment of ibuprofen-induced neural proteolysis.

Protein Name: Tubulin Beta Class I

Functions: Tubulin is the major constituent of microtubules, a cylinder consisting of laterally associated linear protofilaments composed of alpha- and beta-tubulin heterodimers. Microtubules grow by the addition of GTP-tubulin dimers to the microtubule end, where a stabilizing cap forms. Below the cap, tubulin dimers are in GDP-bound state, owing to GTPase activity of alpha-tubulin

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