Target Name: TJP2
NCBI ID: G9414
Review Report on TJP2 Target / Biomarker Content of Review Report on TJP2 Target / Biomarker
TJP2
Other Name(s): Friedreich ataxia region gene X104 (tight junction protein ZO-2) | Tight junction protein ZO-2 (isoform 1) | Tight junction protein 2, transcript variant 5 | C9DUPq21.11 | OTTHUMP00000021431 | Tight junction protein ZO-2 (isoform 3) | Tight junction protein ZO-2 | Tight junction protein ZO-2 (isoform 2) | TJP2 variant 1 | TJP2 variant 4 | ZO2 | PFIC4 | FHCA1 | Zona occludens protein 2 | MGC26306 | TJP2 variant 5 | ZO-2 | Tight junction protein 2, transcript variant 1 | Tight junction protein 2, transcript variant 3 | Tight junction protein 2 | Tight junction protein ZO-2 (isoform 5) | Tight junction protein 2, transcript variant 2 | zona occludens 2 | Zona occludens 2 | Tight junction protein ZO-2 (isoform 4) | DUP9q21.11 | tight junction protein 2 | TJP2 variant 3 | ZO2_HUMAN | zonula occludens protein 2 | Zonula occludens protein 2 | OTTHUMP00000063359 | TJP2 variant 2 | DFNA51 | X104 | Tight junction protein 2, transcript variant 4

TJP2: A Potential Drug Target and Biomarker for Friedreich Ataxia

Introduction

Friedrich ataxia (FA) is a rare autosomal recessive disorder that primarily affects adults, characterized by progressive muscle weakness and wasting, as well as challenges with balance, gait, and other activities of daily living. The underlying cause of FA is the loss of motor neurons in the central nervous system, leading to progressive muscle weakness and wasting. There is currently no cure for FA, and treatment is limited to managing symptoms and improving quality of life.

The identification of TJP2 as a potential drug target and biomarker for FA has significant implications for the development of new treatments for this debilitating disease. In this article, we will explore the biology of FA, the function of TJP2, and its potential as a drug target.

The Biology of Friedreich Ataxia

FA is caused by a deficiency of dystrophin, a protein that helps maintain muscle strength and function. Without dystrophin, muscle cells break down and are replaced with scar tissue, leading to progressive muscle weakness and wasting. The loss of dystrophin leads to a build- up of muscle waste, which can cause additional symptoms such as joint pain, deformities, and respiratory infections.

The Friedreich ataxia gene (FAX1) encodes a protein called ZO-2, a tight junction protein that plays a critical role in maintaining the integrity of the blood-brain barrier. ZO-2 helps to regulate the movement of ions and nutrients into the brain , while also blocking the entry of harmful substances such as viruses and bacteria.

The Function of TJP2

TJP2, a member of the ZO family of proteins, is a 21-kDa protein that is expressed in various tissues and cells, including brain, heart, and skeletal muscles. It is highly conserved across species and has been implicated in a number of physiological processes, including cell signaling, protein transport, and intracellular signaling.

TJP2 has been shown to play a role in the regulation of ion and water transport in neurons, which is critical for the proper functioning of the brain. Ion transport is particularly important in the regulation of neuronal excitability and synaptic plasticity, which are critical for learning and memory. TJP2 has also been shown to play a role in the regulation of cytoskeletal organization and cell adhesion, which are critical for muscle function.

The Potential as a Drug Target

TJP2 has been identified as a potential drug target for FA due to its involvement in the regulation of ion and water transport in the brain. Several studies have shown that TJP2 is a validated target for small molecules, including inhibitors of the ion channels that regulate neurotransmitter release. In addition, TJP2 has been shown to be involved in the regulation of cellular signaling pathways that are important for muscle function, including the regulation of muscle contractions and the modulation of muscle growth.

The Potential as a Biomarker

TJP2 has also been identified as a potential biomarker for FA due to its expression in the brain and its involvement in the regulation of ion and water transport in the brain. The expression of TJP2 is highly dependent on the presence of dystrophin, which is a protein that is responsible for maintaining the integrity of the blood-brain barrier. The absence of dystrophin can lead to the expression of TJP2, which can be used as a biomarker for the diagnosis of FA.

Conclusion

TJP2 is a protein that has been identified as a potential drug target and biomarker for Friedreich ataxia (FA). The biology of FA is characterized by the loss of dystrophin, which leads to progressive muscle weakness and

Protein Name: Tight Junction Protein 2

Functions: Plays a role in tight junctions and adherens junctions (By similarity). Acts as a positive regulator of RANKL-induced osteoclast differentiation, potentially via mediating downstream transcriptional activity (By similarity)

The "TJP2 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about TJP2 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
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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