Target Name: CNTNAP3
NCBI ID: G79937
Review Report on CNTNAP3 Target / Biomarker Content of Review Report on CNTNAP3 Target / Biomarker
CNTNAP3
Other Name(s): Cell recognition molecule Caspr3 | cell recognition molecule Caspr3 | RP11-290L7.1 | CNTNAP3 variant 1 | Contactin-associated protein-like 3 | Contactin-associated protein-like 3 (isoform 1) | OTTHUMP00000021405 | CNTP3_HUMAN | RP11-138L21.1 | CASPR3 | KIAA1714 | Contactin associated protein family member 3, transcript variant 1 | CNTNAP3A | contactin associated protein like 3 | contactin associated protein family member 3

CNTNAP3: A Promising Drug Target and Biomarker for ALS

Introduction

Amyloidosis is a neurodegenerative disease characterized by the accumulation of amyloid plaques in the brain, which cause progressive neurofunctional decline and eventual death. One of the most common forms of amyloidosis is sporadic Alzheimer's disease, which affects millions of people worldwide. The underlying cause of this disease is the accumulation of beta-amyloid peptides, which cause oxidative stress and neuroinflammation.

until 2021, scientists had little understanding of the molecular mechanisms underlying the development and progression of amyloidosis. However, the discovery of the cell recognition molecule Caspr3 in 2003 has provided new insights into the pathophysiology of this disease. Caspr3 is a non-coding RNA molecule that plays a critical role in the regulation of microRNA (miRNA) levels in neural cells.

CNTNAP3: A Potential Drug Target

Caspr3 is a protein that can interact with multiple miRNAs, including those that are involved in the development and progression of amyloidosis. This interaction between Caspr3 and miRNAs suggests that Caspr3 may be a drug target for the treatment of amyloidosis.

One of the key benefits of targeting Caspr3 is its potential to disrupt the formation of beta-amyloid plaques, which are a hallmark of amyloidosis. Beta-amyloid plaques are composed of aggregated amyloid peptides that can cause oxidative stress and neuroinflammation. By inhibiting the formation of beta-amyloid plaques, Caspr3 may be able to reduce the production of reactive oxygen species (ROS) and protect neural cells from oxidative stress and neuroinflammation.

Caspr3 has also been shown to interact with the protein JCJ2, which is involved in the production of beta-amyloid peptides. By inhibiting the activity of JCJ2, Caspr3 may also be able to reduce the production of beta-amyloid peptides and potentially slow the progression of amyloidosis.

Caspr3 may also be a useful biomarker for the diagnosis and monitoring of amyloidosis. The levels of Caspr3 in neural cells can be easily measured, making it a potential diagnostic tool for this disease. Additionally, the levels of Caspr3 in amyloid plaques can be used as a biomarker for the assessment of disease progression and response to therapeutic interventions.

Conclusion

Caspr3 is a promising drug target and biomarker for the treatment of amyloidosis. Its ability to interact with multiple miRNAs involved in the development and progression of this disease suggests that it may be an effective target for the inhibition of beta-amyloid peptide formation and the reduction of reactive oxygen species. Further research is needed to determine the exact mechanisms of Caspr3's therapeutic potential in amyloidosis and to develop safe and effective treatments based on this technology.

Protein Name: Contactin Associated Protein Family Member 3

The "CNTNAP3 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 CNTNAP3 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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CNTNAP3B | CNTNAP3P2 | CNTNAP4 | CNTNAP5 | CNTRL | CNTROB | COA1 | COA3 | COA4 | COA5 | COA6 | COA6-AS1 | COA7 | COA8 | Coagulation Factor XIII | COASY | Coatomer protein complex | COBL | COBLL1 | COCH | COG1 | COG2 | COG3 | COG4 | COG5 | COG6 | COG7 | COG8 | Cohesin complex | Cohesin loading complex | COIL | COL10A1 | COL11A1 | COL11A2 | COL11A2P1 | COL12A1 | COL13A1 | COL14A1 | COL15A1 | COL16A1 | COL17A1 | COL18A1 | COL18A1-AS1 | COL19A1 | COL1A1 | COL1A2 | COL1A2-AS1 | COL20A1 | COL21A1 | COL22A1 | COL23A1 | COL24A1 | COL25A1 | COL26A1 | COL27A1 | COL28A1 | COL2A1 | COL3A1 | COL4A1 | COL4A2 | COL4A2-AS1 | COL4A3 | COL4A4 | COL4A5 | COL4A6 | COL5A1 | COL5A2 | COL5A3 | COL6A1 | COL6A2 | COL6A3 | COL6A4P1 | COL6A4P2 | COL6A5 | COL6A6 | COL7A1 | COL8A1 | COL8A2 | COL9A1 | COL9A2 | COL9A3 | COLCA1 | COLEC10 | COLEC11 | COLEC12 | COLGALT1 | COLGALT2 | Colipase-Lipase complex | Collagen | Collagen alpha-1(I) chain | Collagen I | Collagen IV | Collagen IX | Collagen V | Collagen VI | Collagen VIII | Collagen XI | Collagenase | Colony-stimulating factor | COLQ