Unlocking the Potential of TUBA3C as a Drug Target and Biomarker

Target Name: TUBA3C

NCBI ID: G7278

TUBA3C

Unlocking the Potential of TUBA3C as a Drug Target and Biomarker

Tubulin, alpha 2 (TUBA2) is a protein that plays a critical role in the structure and function of microtubules, which are essential components of the cytoskeleton in eukaryotic cells. The misfolding of tubulin伪2 has been implicated in various neurological and psychiatric disorders, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. As a result, targeting tubulin伪2 has become an attractive research focus in the pharmaceutical industry, with a goal of developing new treatments for various neurological disorders.

TUBA3C, a specific tubulin伪2 isoform, has been identified as a potential drug target and biomarker. In this article, we will explore the biology of TUBA3C, its dysfunction in various neurological disorders, and the potential for it as a drug target.

biology and functions of TUBA3C

Tubulin伪2, also known as TUBA2, is a transmembrane protein that plays a central role in the cytoskeleton structure and function. It consists of four distinct isoforms,伪2, 尾, 纬, and 未, each with distinct functions in microtubule dynamics and stability.伪2 is the most abundant isoform and is responsible for the formation and stability of microtubules.

TUBA3C, the most abundant of the 伪2 isoforms, is a 14-kDa protein that is involved in the formation and stability of microtubules. It has been shown to play a critical role in the regulation of microtubule dynamics and stability, and is often targeted by drugs that aim to modulate microtubule function.

disorders associated with TUBA2 dysfunction

TUBA2 dysfunction has been implicated in various neurological disorders, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. These disorders are characterized by the misfolding and aggregation of TUBA2, leading to the formation of insoluble aggregates that cause structural and functional changes in the brain.

Alzheimer's disease is a neurodegenerative disorder that is characterized by the accumulation of insoluble aggregates of TUBA2 in the brain. The accumulation of TUBA2 in the brain is thought to contribute to the neurofibrillary tangles and neurogenic infarctions that are observed in Alzheimer's disease.

Parkinson's disease is a neurodegenerative disorder that is characterized by the symptoms of tremor, rigidity, and bradykinesia. The misfolding and aggregation of TUBA2 have been implicated in the development and progression of Parkinson's disease.

Huntington's disease is a genetic disorder that is characterized by the accumulation of insoluble aggregates of TUBA2 in the brain. The accumulation of TUBA2 in the brain is thought to contribute to the neurofibrillary tangles and neurogenic infarctions that are observed in Huntington's disease.

potential of TUBA3C as a drug target

The misfolding and aggregation of TUBA2 have led to the formation of insoluble aggregates that are thought to contribute to the development and progression of various neurological disorders. Targeting TUBA2 with small molecules or antibodies has the potential to treat these disorders.

One approach to targeting TUBA2 is through the use of small molecules that can inhibit the formation of insoluble aggregates. One such compound, known as TUBA3C inhibitor, has been shown to inhibit the formation of insoluble aggregates of TUBA2 in a cell culture model

Protein Name: Tubulin Alpha 3c

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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The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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