CELF5: A Protein Targeted for Cancer and Other Diseases (G60680)

Target Name: CELF5

NCBI ID: G60680

CELF5

CELF5: A Protein Targeted for Cancer and Other Diseases

CELF5, short for cytosine ethyl 5-flurorouracil, is a drug target and biomarker that has been identified by researchers as having potential in the treatment of various diseases, including cancer. CELF5 is a protein that is expressed in a wide range of tissues throughout the body, including the brain, heart, and kidneys. It is a key regulator of cell division and has been shown to play a role in the development and progression of various diseases.

One of the key features of CELF5 is its ability to interact with the DNA template. This interaction allows CELF5 to regulate the expression of other genes, and is a key factor in the regulation of cell division. In cancer, the regulation of cell division is often disrupted, leading to the uncontrolled growth and proliferation of cells. By targeting CELF5, researchers hope to disrupt this regulation and inhibit the growth and proliferation of cancer cells.

Another feature of CELF5 is its ability to form a complex with the protein p53. P53 is a well-known protein that is involved in the regulation of cell division and has been shown to play a key role in the response to DNA damage. By forming a complex with p53, CELF5 is able to enhance its ability to regulate cell division and promote the growth and development of cancer cells.

In addition to its role in cell division, CELF5 has also been shown to play a role in the regulation of cell apoptosis, or cell death. Apoptosis is a natural process that helps to remove damaged or dysfunctional cells from the body, and is an important part of the immune system's response to disease. By targeting CELF5, researchers hope to disrupt this process and promote the growth and survival of cancer cells.

CELF5 has also been shown to play a role in the regulation of inflammation. Inflammation is a natural response of the immune system to injury or infection, and can lead to the production of pro-inflammatory molecules that can cause tissue damage and inflammation. By targeting CELF5, researchers hope to inhibit its role in the regulation of inflammation and reduce the risk of chronic inflammatory diseases.

In conclusion, CELF5 is a protein that has been identified by researchers as having potential as a drug target and biomarker for the treatment of various diseases, including cancer. Its ability to interact with the DNA template and form a complex with p53 make it a promising target for the development of new treatments. Furthermore, its role in cell division, apoptosis, and inflammation make it an attractive candidate for the development of new therapies for a wide range of diseases.

Protein Name: CUGBP Elav-like Family Member 5

Functions: RNA-binding protein implicated in the regulation of pre-mRNA alternative splicing. Mediates exon inclusion and/or exclusion in pre-mRNA that are subject to tissue-specific and developmentally regulated alternative splicing. Specifically activates exon 5 inclusion of cardiac isoforms of TNNT2 during heart remodeling at the juvenile to adult transition. Binds to muscle-specific splicing enhancer (MSE) intronic sites flanking the alternative exon 5 of TNNT2 pre-mRNA

The "CELF5 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 CELF5 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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