DNMT3A: A Drug Target and Biomarker for the Treatment of Genetic Disorders

Target Name: DNMT3A

NCBI ID: G1788

DNMT3A

DNMT3A: A Drug Target and Biomarker for the Treatment of Genetic Disorders

DNA damage Response (DDR) is a cellular stress response mechanism that protects the genome from damage caused by various agents, including environmental stressors and genetic mutations. DNA damage can result in the development of genetic disorders, such as cancer, neurodegenerative diseases, and systemic illnesses. The DNA damage response is a critical pathway that regulates cell growth and division, and it is closely monitored by various proteins and enzymes.

DNMT3A, which stands for DNA damage-inducible NNAT3-ASF4, is a non-coding RNA molecule that plays a critical role in the DNA damage response. It is a key regulator of the DDR, and it is involved in the repair of DNA damage caused by various stressors, including double-strand breaks, single-strand breaks, and insertions/deletions (indels).

DNMT3A is a drug target and a biomarker for the treatment of genetic disorders. Its role in the DDR and its potential as a drug target make it an attractive target for researchers to investigate and develop new treatments for genetic disorders.

The Importance of the DNA Damage Response

The DNA damage response is a critical pathway that regulates the integrity and function of the genome. It is a complex process that involves the interaction of various proteins and enzymes, including DNA damage repair proteins, DNA polymerases, and transcription factors. The DNA damage response is essential for the regulation of cell growth, apoptosis, and senescence, and it is involved in the development and progression of numerous genetic disorders.

DNMT3A is a key regulator of the DNA damage response. It is a DNA damage-inducible gene that is expressed in response to DNA damage, such as double-strand breaks, single-strand breaks, or insertions/deletions. DNMT3A plays a critical role in the repair of DNA damage by promoting the formation of a double-strand break repair complex and facilitating the recruitment of repair enzymes to the site of damage.

DNMT3A is also involved in the regulation of DNA replication, transcription, and apoptosis. It is a critical regulator of DNA polymerase, which is responsible for the replication of the genome during S-phase. DNMT3A promotes the growth of the replication complex and ensures the accuracy of DNA replication by preventing the formation of incorrect base pairs during the replication process.

In addition to its role in the DNA damage response, DNMT3A is also a biomarker for the treatment of genetic disorders. Its expression is often reduced in genetic disorders, such as cancer, neurodegenerative diseases, and systemic illnesses, and its levels are often elevated in individuals with these disorders. Therefore, DNMT3A is an attractive biomarker for the diagnosis and monitoring of genetic disorders.

DNMT3A as a Drug Target

DNMT3A is a drug target for the treatment of genetic disorders because its regulation of the DNA damage response is disrupted in these disorders. The disruption of the DNA damage response can lead to the development of genetic mutations, which can then lead to the development of genetic disorders.

DNMT3A has been shown to be involved in the development of various genetic disorders, including cancer, neurodegenerative diseases, and systemic illnesses. For example, studies have shown that DNMT3A is involved in the development of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, by promoting the formation of DNA damage-inducible cell stress pathways.

In addition to its role in the development of genetic disorders, DNMT3A is also a potential therapeutic target for the treatment of these disorders. Studies have shown that inhibiting DNMT3A can lead to the rescue of neural cells from the effects of neurotoxins, indicating that DNMT3A may have potential as a neuroprotectant.

DNMT3A has also been shown to be involved in the regulation of cancer cell growth and division. For example, studies have shown that DNMT3A is involved in the regulation of the growth and survival of cancer cells, and that its inhibition can lead to the growth inhibition of these cells. Therefore, DNMT3A may have potential as a therapeutic target for cancer.

Conclusion

DNMT3A is a non-coding RNA molecule that plays a critical role in the DNA damage response. Its regulation of the DNA damage response is disrupted in various genetic disorders, and its levels are often elevated in individuals with these disorders. Therefore, DNMT3A is an attractive drug target and biomarker for the treatment of genetic disorders.

The DNA damage response is a critical pathway that regulates the integrity and function of the genome, and its regulation by DNMT3A is involved in the development and progression of numerous genetic disorders. The potential of DNMT3A as a drug target and biomarker makes it an attractive target for researchers to investigate and develop new treatments for genetic disorders.

Protein Name: DNA Methyltransferase 3 Alpha

Functions: Required for genome-wide de novo methylation and is essential for the establishment of DNA methylation patterns during development (PubMed:12138111, PubMed:16357870, PubMed:30478443). DNA methylation is coordinated with methylation of histones (PubMed:12138111, PubMed:16357870, PubMed:30478443). It modifies DNA in a non-processive manner and also methylates non-CpG sites (PubMed:12138111, PubMed:16357870, PubMed:30478443). May preferentially methylate DNA linker between 2 nucleosomal cores and is inhibited by histone H1 (By similarity). Plays a role in paternal and maternal imprinting (By similarity). Required for methylation of most imprinted loci in germ cells (By similarity). Acts as a transcriptional corepressor for ZBTB18 (By similarity). Recruited to trimethylated 'Lys-36' of histone H3 (H3K36me3) sites (By similarity). Can actively repress transcription through the recruitment of HDAC activity (By similarity). Also has weak auto-methylation activity on Cys-710 in absence of DNA (By similarity)

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•   general information;
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•   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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