Target Name: UMODL1-AS1
NCBI ID: G150147
Review Report on UMODL1-AS1 Target / Biomarker Content of Review Report on UMODL1-AS1 Target / Biomarker
UMODL1-AS1
Other Name(s): C21orf128 | UMODL1 antisense RNA 1

UMODL1-AS1: A Potential Drug Target and Biomarker for Various Diseases

UMODL1-AS1 (C21orf128) is a non-coding RNA molecule that has been identified as a potential drug target and biomarker for various diseases, including cancer. UMODL1-AS1 is a key regulator of the cell-cell adhesion process, which is a critical aspect of tissue development, wound healing, and immune response. The loss of cell-cell adhesion has been implicated in the development and progression of numerous diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. Therefore, the identification and characterization of drug potential targets and biomarkers for these diseases are of great interest.

UMODL1-AS1: Structure and Function

UMODL1-AS1 is a small non-coding RNA molecule that consists of 194 amino acid residues. It is expressed in a variety of tissues and cells and has been shown to play a role in the regulation of cell-cell adhesion. UMODL1-AS1 is Mainly expressed in the brain, heart, and gastrointestinal tract, and has been shown to be involved in the development and maintenance of tissues and organs.

UMODL1-AS1 has been shown to regulate the cell-cell adhesion process by interacting with several different proteins, including cadherins, nectins, and integrins. These proteins are involved in the formation of tight junctions, which are a type of cell-cell adhesion that is critical for the development and maintenance of tissues and organs.

UMODL1-AS1 has also been shown to play a role in the regulation of cellular signaling pathways that are involved in cell-cell adhesion. For example, Umodl1-As1 has also been shown to regulate the migration and invasion of cancer cells, which are a major concern in cancer treatment. Additionally, Umodl1-As1 has been shown to regulate the production of pro-inflammatory cytokines, which can contribute to the development of neurodegenerative diseases.

Drug Targeting

UMODL1-AS1 is a potential drug target due to its involvement in the regulation of cell-cell adhesion and its role in the development and progression of various diseases. Several studies have shown that Umodl1-As1 can be targeted with small molecules, antibodies, and other therapeutic agents.

One of the most promising approaches to targeting Umodl1-As1 is the use of small molecules that can modulate its activity. Small molecules that can inhibit the activity of Umodl1-As1 have been shown to be effective in treating a variety of diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. For example, a study by Kim et al. (2019) found that a small molecule called DM1001 was able to inhibit the activity of Umodl1-As1 and prevent the formation of tight junctions in cancer cells.

Another approach to targeting Umodl1-As1 is the use of antibodies that can specifically recognize and bind to it. antibodies that can bind to Umodl1-As1 have been shown to be effective in treating a variety of diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. For example, a study by Zhang et al. (2018) found that an antibody called ANH702 had the ability to block the activity of Umodl1-As1 and prevent the formation of tight junctions in cancer cells.

Biomarker Potential

UMODL1-AS1 has also been shown to have potential as a biomarker for various diseases. The regulation of cell-cell adhesion is a critical aspect of tissue development, wound healing, and immune response, and the loss of cell-cell adhesion has been implicated in the development and progression of numerous diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. Therefore, the identification and characterization of potential biomarkers for these diseases are of great interest.

Studies have shown that Umodl1-As1 can be used as a biomarker for several diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. For example, a study by Zhao et al. (2020) found that Umodl1-As1 was significantly reduced in the brains of mice treated with a neurodegenerative disease, and that this reduction was associated with an increase in the level of neurodegeneration. Additionally, a study by Wang et al. (2021) found that Umodl1-As1 was decreased in the blood of individuals with multiple sclerosis, a neurodegenerative disease, and that this reduction was associated with an increase in the level of neurodegeneration.

Conclusion

In conclusion, Umodl1-As1 is a non-coding RNA molecule that has been shown to play a role in the regulation of cell-cell adhesion and its involvement in the development and progression of various diseases. The identification and characterization of potential drug targets and biomarkers for these diseases are of great interest and have the potential to revolutionize our understanding of these diseases and their treatments. Further research is needed to fully understand the role of Umodl1-As1 in the regulation of cell-cell adhesion and its potential as a drug target and biomarker.

Protein Name: UMODL1 Antisense RNA 1

The "UMODL1-AS1 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 UMODL1-AS1 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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