METTL3: A Key Enzyme in DNA Methylation and MicroRNA Regulation

Target Name: METTL3

NCBI ID: G56339

METTL3

Other Name(s): Methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit | methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit | Spo8 | adoMet-binding subunit of the hum

METTL3: A Key Enzyme in DNA Methylation and MicroRNA Regulation

METTL3, or Methyltransferase 3, N6-Adenosine-Methyltransferase Complex Catalytic Subunit, is a protein that plays a crucial role in the regulation of DNA methylation. METTL3 is a member of the N6-Adenosine-Methyltransferase Complex (NMT), which is a complex of DNA methyltransferase and an enzyme that removes methyl groups from DNA. METTL3 is responsible for catalyzing the conversion of N6-adenosine to N6-methyl-dCMP, which is then converted to N6-adducts. METTL3 is a key enzyme in the removal of methyl groups, which is critical for the regulation of gene expression and DNA methylation.

METTL3 is a 23-kDa protein that is expressed in a variety of tissues, including muscle, heart, liver, and brain. It is highly conserved, with a calculated pI of 10.03 and a predicted localization in the cytoplasm. METTL3 is a non-essential protein, which means that it is not essential for life, but it is required for the proper functioning of many cellular processes.

METTL3 is involved in the regulation of DNA methylation by removing methyl groups from the promoter region of a gene. Methylation of the promoter region is a common technique used to repress gene expression, and it is critical for the regulation of stem cell and cancer growth. METTL3 is responsible for the removal of the methyl groups that are present in the promoter region of a gene, allowing for the activation of gene expression.

In addition to its role in DNA methylation, METTL3 is also involved in the regulation of microRNA (miRNA) levels. miRNA is a small non-coding RNA molecule that plays a critical role in post-transcriptional gene regulation. METTL3 is involved in the regulation of miRNA levels by removing the methyl groups that are present in the miRNA precursors. This allows for the activation and translation of miRNA into the cytoplasm.

METTL3 is a protein that is being targeted as a potential drug target for a variety of diseases. One of the main targets of METTL3 is cancer. METTL3 has been shown to be involved in the regulation of cancer cell growth and progression. In addition, METTL3 has also been shown to be involved in the regulation of cell cycle progression, which is critical for the development and progression of cancer.

Another potential target of METTL3 is neurodegenerative diseases. METTL3 is involved in the regulation of the translation of miRNA into the cytoplasm, which is important for the regulation of miRNA levels. METTL3 has been shown to be involved in the regulation of the translation of miRNA into the cytoplasm in neurodegenerative diseases, which may be caused by the translation of miRNA into the cytoplasm and the regulation of cellular processes.

In conclusion, METTL3 is a protein that plays a crucial role in the regulation of DNA methylation and the translation of miRNA into the cytoplasm. METTL3 is a key enzyme in the N6-Adenosine-Methyltransferase Complex and is involved in the regulation of gene expression and cellular processes. METTL3 is a potential drug target for a variety of diseases, including cancer and neurodegenerative diseases. Further research is needed to fully understand the role of METTL3 in these processes and to develop effective treatments.

Protein Name: Methyltransferase 3, N6-adenosine-methyltransferase Complex Catalytic Subunit

Functions: The METTL3-METTL14 heterodimer forms a N6-methyltransferase complex that methylates adenosine residues at the N(6) position of some RNAs and regulates various processes such as the circadian clock, differentiation of embryonic and hematopoietic stem cells, cortical neurogenesis, response to DNA damage, differentiation of T-cells and primary miRNA processing (PubMed:22575960, PubMed:24284625, PubMed:25719671, PubMed:25799998, PubMed:26321680, PubMed:26593424, PubMed:27627798, PubMed:27373337, PubMed:27281194, PubMed:28297716, PubMed:30428350, PubMed:29506078, PubMed:29348140, PubMed:9409616). In the heterodimer formed with METTL14, METTL3 constitutes the catalytic core (PubMed:27627798, PubMed:27373337, PubMed:27281194). N6-methyladenosine (m6A), which takes place at the 5'-[AG]GAC-3' consensus sites of some mRNAs, plays a role in mRNA stability, processing, translation efficiency and editing (PubMed:22575960, PubMed:24284625, PubMed:25719671, PubMed:25799998, PubMed:26321680, PubMed:26593424, PubMed:28297716, PubMed:9409616). M6A acts as a key regulator of mRNA stability: methylation is completed upon the release of mRNA into the nucleoplasm and promotes mRNA destabilization and degradation (PubMed:28637692). In embryonic stem cells (ESCs), m6A methylation of mRNAs encoding key naive pluripotency-promoting transcripts results in transcript destabilization, promoting differentiation of ESCs (By similarity). M6A regulates the length of the circadian clock: acts as an early pace-setter in the circadian loop by putting mRNA production on a fast-track for facilitating nuclear processing, thereby providing an early point of control in setting the dynamics of the feedback loop (By similarity). M6A also regulates circadian regulation of hepatic lipid metabolism (PubMed:30428350). M6A regulates spermatogonial differentiation and meiosis and is essential for male fertility and spermatogenesis (By similarity). Also required for oogenesis (By similarity). Involved in the response to DNA damage: in response to ultraviolet irradiation, METTL3 rapidly catalyzes the formation of m6A on poly(A) transcripts at DNA damage sites, leading to the recruitment of POLK to DNA damage sites (PubMed:28297716). M6A is also required for T-cell homeostasis and differentiation: m6A methylation of transcripts of SOCS family members (SOCS1, SOCS3 and CISH) in naive T-cells promotes mRNA destabilization and degradation, promoting T-cell differentiation (By similarity). Inhibits the type I interferon response by mediating m6A methylation of IFNB (PubMed:30559377). M6A also takes place in other RNA molecules, such as primary miRNA (pri-miRNAs) (PubMed:25799998). Mediates m6A methylation of Xist RNA, thereby participating in random X inactivation: m6A methylation of Xist leads to target YTHDC1 reader on Xist and promote transcription repression activity of Xist (PubMed:27602518). M6A also regulates cortical neurogenesis: m6A methylation of transcripts related to transcription factors, neural stem cells, the cell cycle and neuronal differentiation during brain development promotes their destabilization and decay, promoting differentiation of radial glial cells (By similarity). METTL3 mediates methylation of pri-miRNAs, marking them for recognition and processing by DGCR8 (PubMed:25799998). Acts as a positive regulator of mRNA translation independently of the methyltransferase activity: promotes translation by interacting with the translation initiation machinery in the cytoplasm (PubMed:27117702). Its overexpression in a number of cancer cells suggests that it may participate in cancer cell proliferation by promoting mRNA translation (PubMed:27117702). During human coronorivus SARS-CoV-2 infection, adds m6A modifications in SARS-CoV-2 RNA leading to decreased RIGI binding and subsequently dampening the sensing and activation of innate immune responses (PubMed:33961823)

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•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
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•   the target screening and validation;
•   expression level;
•   disease relevance;
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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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