Target Name: DEFT1P2
NCBI ID: G100287083
Review Report on DEFT1P2 Target / Biomarker Content of Review Report on DEFT1P2 Target / Biomarker
DEFT1P2
Other Name(s): defensin theta 1, pseudogene 2 | Defensin theta 1, pseudogene 2

DEFT1P2: A Potential Drug Target and Biomarker

DEFT1P2 is a gene that encodes a protein known as deleted in Frame 1 (DEFT1) and pseudogene 2 (P2) protein. DEFT1 is a non-coding RNA molecule that is predominantly expressed in the brain, and its expression has been associated with various neurological disorders, including Alzheimer's disease, Parkinson's disease, and ALS. P2 protein is a known RNA molecule that is predominantly expressed in the brain and is considered as a potential drug target and biomarker.

Potential Drug Target

The potential drug target for DEFT1 is related to the neurodegenerative diseases, specifically Alzheimer's disease. Alzheimer's disease is a progressive neurodegenerative disorder that is characterized by the accumulation of neurofibrillary tangles and senile plaques in the brain. These tangles and plaques are thought to contribute to the destruction of nerve cells, leading to the symptoms associated with the disease, including memory loss, confusion, and personality changes.

One of the hallmarks of Alzheimer's disease is the accumulation of beta-amyloid plaques in the brain. Beta-amyloid plaques are thought to be derived from the abnormal aggregation of the protein tau, which is a hallmark of Alzheimer's disease. In addition, the neurofibrillary tangles and the formation of neurodegenerate neurotransmitter axons, which are thought to contribute to the neurofibrillary tangles, are also thought to be involved in the development of beta-amyloid plaques.

DEFT1 has been shown to be involved in the regulation of the beta-amyloid pathway, specifically in the inhibition of the activity of the protein known as A尾2, which is a key step in the formation of beta-amyloid plaques.

Biomarker

DEFT1 has also been shown to be involved in the regulation of the neurotransmitter system, specifically in the regulation of dopamine. Dopamine is a neurotransmitter that is involved in the regulation of mood, motivation, and pleasure. Studies have shown that DEFT1 plays a role in the regulation of dopamine release and that its expression is regulated by the neurotransmitter dopamine.

In addition, DEFT1 has also been shown to be involved in the regulation of the neuroimmune system, specifically in the regulation of the production of immune cells known as microglia. Microglia are a type of immune cell that are involved in the regulation of inflammation and are thought to play a role in the development of various neurological disorders, including neurodegenerative diseases.

Conclusion

In conclusion, DEFT1P2 is a gene that encodes a protein that is involved in the regulation of various physiological processes in the brain, including the regulation of the beta-amyloid pathway, the neurotransmitter system, and the neuroimmune system. The potential drug target for DEFT1 is related to the neurodegenerative diseases, specifically Alzheimer's disease. Further studies are needed to fully understand the role of DEFT1P2 in the development and progression of these diseases.

Protein Name: Defensin Theta 1, Pseudogene 2

The "DEFT1P2 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 DEFT1P2 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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