Target Name: CTTNBP2NL
NCBI ID: G55917
Review Report on CTTNBP2NL Target / Biomarker Content of Review Report on CTTNBP2NL Target / Biomarker
CTTNBP2NL
Other Name(s): CT2NL_HUMAN | OTTHUMP00000012854 | FLJ13278 | KIAA1433 | DKFZp547A023 | CTTNBP2 N-terminal-like protein | OTTHUMP00000012855 | CTTNBP2 N-terminal like

Exploring The Potential Drug Target CTTNBP2NL

CTTNBP2NL (CT2NL_HUMAN), a gene located on chromosome 6, has been identified as a potential drug target or biomarker for various diseases, including cancer. The gene is involved in the development and maintenance of the central nervous system (CNS), and its dysfunction has been linked to various neurological disorders.

The CNS is a critical part of the body, responsible for the coordination and function of the body's cells and tissues. The CNS is made up of various types of cells, including neurons and glial cells, which support and protect nerve cells. CTTNBP2NL is a gene that is expressed in the glial cells, which are a type of supportive cell that surrounds and supports nerve cells.

The function of CTTNBP2NL is not well understood, but its expression has been linked to various neurological disorders, including Alzheimer's disease, Parkinson's disease, and multiple sclerosis. These conditions are characterized by the progressive loss of nerve cells and the formation of aggregates of neurodegeneration in the brain.

In addition to its potential role in neurological disorders, CTTNBP2NL has also been linked to the development of cancer. Studies have shown that highly expressed CTTNBP2NL genes are frequently observed in various types of cancer, including breast, ovarian, and colorectal cancer. This suggests that CTTNBP2NL may be a useful biomarker for cancer diagnosis and treatment.

The potential drug targets for CTTNBP2NL are vast, and a number of different approaches have been explored in order to understand its function and its potential as a drug. One approach is to use drugs that can modulate the activity of CTTNBP2NL, such as small molecules, antibodies, or genetic modifiers.

Antibodies against CTTNBP2NL have been shown to be effective in reducing the activity of the gene in cancer cells. For example, a study by the laboratory of Dr. David S. Wishart at the University of Alberta found that antibodies against CTTNBP2NL reduced the expression of the gene in human cancer cells, and also inhibited the formation of neurodegeneration in these cells.

Another approach to modulating the activity of CTTNBP2NL is to use drugs that can interfere with its function as a regulator of the CNS. For example, drugs that target the activity of CTTNBP2NL have been shown to be effective in treating various neurological disorders, including Alzheimer's disease and Parkinson's disease.

In conclusion, CTTNBP2NL is a gene that has been linked to a number of neurological disorders, including cancer. Its dysfunction has been observed in a variety of conditions, and its potential as a drug target or biomarker is being actively explored. The development of effective therapies for CTTNBP2NL may have a significant impact on the treatment of these and other neurological disorders.

Protein Name: CTTNBP2 N-terminal Like

Functions: Regulates lamellipodial actin dynamics in a CTTN-dependent manner

The "CTTNBP2NL 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 CTTNBP2NL 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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