Target Name: DOT1L
NCBI ID: G84444
Review Report on DOT1L Target / Biomarker Content of Review Report on DOT1L Target / Biomarker
DOT1L
Other Name(s): DOT1L_HUMAN | DOT1 | Histone H3-K79 methyltransferase | DOT1-like protein | Lysine N-methyltransferase 4 | histone methyltransferase DOT1L | KIAA1814 | DOT1 like histone H3K79 methyltransferase | histone H3-K79 methyltransferase | H3-K79-HMTase | Histone-lysine N-methyltransferase, H3 lysine-79 specific | DOT1-like histone methyltransferase | KMT4 | lysine N-methyltransferase 4 | DOT1 like histone lysine methyltransferase | DOT1-like, histone H3 methyltransferase | Histone methyltransferase DOT1L

DOT1L: A Potential Drug Target for Various Diseases

DOT1L (DOT1L_HUMAN) is a protein that is expressed in various tissues of the human body, including the lungs, heart, kidneys, and brain. It is a member of the T-cell antigen receptor (TCR) family and is involved in the immune response.

DOT1L has been identified as a potential drug target in the treatment of various diseases, including cancer, autoimmune disorders, and neurodegenerative diseases. Its role in these conditions has been studied extensively, and several studies have shown that inhibiting DOT1L can lead to therapeutic benefits.

One of the key reasons for the interest in DOT1L as a drug target is its ability to induce cell-mediated immunity. DOT1L is involved in the regulation of T-cell development and function, and has been shown to play a role in the generation of memory T-cells. By targeting DOT1L, researchers can potentially improve the effectiveness of cancer and autoimmune treatments.

Another potential mechanism by which DOT1L may be targeted as a drug is its role in the regulation of cell survival. DOT1L has been shown to play a role in the survival and proliferation of various cell types, including cancer cells. By inhibiting DOT1L, researchers may be able to kill or reduce the growth of cancer cells.

In addition to its potential as a cancer and autoimmune drug target, DOT1L is also being studied for its potential role in neurodegenerative diseases. DOT1L has been shown to play a role in the regulation of neurotransmitter release from neurons, and has been implicated in the development and progression of neurodegenerative diseases. By targeting DOT1L, researchers may be able to develop new treatments for these conditions.

Despite the potential benefits of DOT1L as a drug target, there are also several concerns about its safety and effectiveness. Because DOT1L is expressed in many different tissues of the body, it is difficult to predict how it will interact with other proteins and molecules. In addition, there is some evidence to suggest that DOT1L may be involved in the regulation of immune responses, which could make it a potential source of adverse effects.

Overall, DOT1L is a protein that has the potential to be a valuable drug target for the treatment of various diseases. Further research is needed to fully understand its role and to develop safe and effective treatments.

Protein Name: DOT1 Like Histone Lysine Methyltransferase

Functions: Histone methyltransferase. Methylates 'Lys-79' of histone H3. Nucleosomes are preferred as substrate compared to free histones (PubMed:12123582). Binds to DNA (PubMed:12628190)

The "DOT1L 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 DOT1L 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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