LINC01565: A Potential Drug Target for Neurodegenerative Diseases

Target Name: LINC01565

NCBI ID: G23434

LINC01565

LINC01565: A Potential Drug Target for Neurodegenerative Diseases

LINC01565 is a protein located on chromosome 3 open reading frame 27 (ORF27) that has been identified as a potential drug target in the field of neurodegenerative diseases. ORF27 is a gene that is often lost or deleted in individuals with neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases. The loss of ORF27 has been linked to the development of these debilitating conditions, and therefore, targeting this gene has the potential to provide new treatments for these diseases.

LINC01565 is a transmembrane protein that is expressed in a variety of tissues, including brain, spleen, and peripheral tissues. It is characterized by a unique structure that includes a N-terminal cytoplasmic domain, a transmembrane region, and a C-terminal T- cell receptor alpha chain domain. The T-cell receptor alpha chain domain is a protein that is involved in cell signaling and is a potential drug target in its own right.

One of the key features of LINC01565 is its ability to interact with the protein PDGF-R2. PDGF-R2 is a potent growth factor that is involved in the development and maintenance of tissues, including brain. LINC01565 has been shown to interact with PDGF- R2 and can regulate its activity. This interaction between LINC01565 and PDGF-R2 has implications for the development of neurodegenerative diseases, as the loss of ORF27 has been linked to the decreased production of PDGF-R2 in these conditions.

Another potential mechanism by which LINC01565 may contribute to the development of neurodegenerative diseases is its role in the regulation of cellular stress responses. Stress can have a negative impact on the structure and function of cellular components, including proteins like LINC01565. Studies have shown that LINC01565 is involved in the regulation of cellular stress responses and that its loss can lead to increased cellular stress. This increased stress can contribute to the development of neurodegenerative diseases, as it can lead to the loss of cellular components and the development of damage to tissues.

In addition to its potential role in the regulation of cellular stress responses, LINC01565 is also involved in the development and maintenance of tissues. Studies have shown that LINC01565 is involved in the development of the blood-brain barrier and that its loss can lead to the leakage of toxic substances into the brain. This increased toxicity can have a negative impact on the structure and function of the brain and contribute to the development of neurodegenerative diseases.

Finally, LINC01565 is also involved in the regulation of cellular signaling pathways. Studies have shown that LINC01565 is involved in the regulation of several signaling pathways, including the TGF-beta pathway and the Wnt signaling pathway. These signaling pathways are involved in the development and maintenance of tissues and are potential targets for new drugs. The loss of LINC01565 has been linked to the decreased production of several signaling molecules, including TGF-beta and Wnt, which can contribute to the development of neurodegenerative diseases.

In conclusion, LINC01565 is a protein that is involved in several important cellular processes that are involved in the development and maintenance of tissues. Its loss has been linked to the development of neurodegenerative diseases, and its potential as a drug target makes it an attractive target for researchers to investigate. Further studies are needed to fully understand the role of LINC01565 in the development and progression of neurodegenerative diseases.

Protein Name: Long Intergenic Non-protein Coding RNA 1565

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•   general information;
•   protein structure and compound binding;
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•   the target screening and validation;
•   expression level;
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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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