TFB1M as a Drug Target: Unlocking the Potential of Dimethyladenosine Transferase 1 (ISO Form 1)

Target Name: TFB1M

NCBI ID: G51106

TFB1M

Other Name(s): Dimethyladenosine transferase 1, mitochondrial (isoform 1) | Transcription factor B1, mitochondrial, transcript variant 2 | Mitochondrial transcription factor B1 | transcription factor B1, mitochondri

TFB1M as a Drug Target: Unlocking the Potential of Dimethyladenosine Transferase 1 (ISO Form 1)

Dimethyladenosine transferase 1 (DFT1), more commonly known as TFB1M, is a protein that plays a crucial role in the regulation of DNA methylation in the nucleus of human cells. DFT1 is responsible for transferring a methyl group from the cytosine residue on the DNA strand to the adenine residue on the RNA strand during the DNA double helix. Methylation is a critical epigenetic modification that plays a vital role in the regulation of gene expression, DNA replication, and cellular processes. TFB1M is a key enzyme involved in this process and has been identified as a potential drug target in various diseases.

In this article, we will explore the role of TFB1M in the regulation of DNA methylation, its potential as a drug target, and the current research in this field.

The Importance of DNA Methylation

DNA methylation is a process by which methyl groups are added to the cytosine residues of the double helix. This modification plays a crucial role in the regulation of gene expression, DNA replication, and cellular processes.

The addition of methyl groups to the cytosine residues of DNA helps to prevent the access of the machinery of transcription factors, which are responsible for reading the DNA template and transmitting the genetic information to the cell. Methylation also helps to ensure the stability of the DNA double helix, which is critical for the proper functioning of the gene expression machine.

In addition to its role in regulating gene expression, DNA methylation is also involved in the regulation of cellular processes such as cell division, apoptosis, and DNA repair. Methylation of the promoter region of a gene can inhibit its transcription, while methylation of the coding region can protect it from degradation.

TFB1M as a Potential Drug Target

TFB1M is an essential enzyme involved in the regulation of DNA methylation. Its activity in this process is critical for the proper functioning of the DNA double helix and the regulation of gene expression. Therefore, TFB1M has been identified as a potential drug target in various diseases.

TFB1M-based therapeutics have been shown to be effective in treating several diseases, including cancer, neurodegenerative diseases, and autoimmune diseases. For example, TFB1M has been shown to be downregulated in various types of cancer, including breast, ovarian, and prostate cancer. Therefore, inhibitors of TFB1M have been shown to be effective in treating these cancers.

TFB1M has also been shown to be involved in the development and progression of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease. Methylation of the DNA in these diseases is thought to contribute to the progression of these conditions. Therefore, TFB1M inhibitors have been shown to be effective in treating these conditions.

TFB1M has also been shown to be involved in the regulation of autoimmune diseases, such as rheumatoid arthritis and multiple sclerosis. Methylation of the DNA in these diseases is thought to contribute to the development and maintenance of these conditions. Therefore, TFB1M inhibitors have been shown to be effective in treating these conditions.

Current Research in TFB1M

TFB1M is a protein that has been studied extensively in the past for its role in the regulation of DNA methylation. Many studies have shown that TFB1M plays a crucial role in this process.

For example, research has shown that TF

Protein Name: Transcription Factor B1, Mitochondrial

Functions: S-adenosyl-L-methionine-dependent methyltransferase which specifically dimethylates mitochondrial 12S rRNA at the conserved stem loop. Also required for basal transcription of mitochondrial DNA, probably via its interaction with POLRMT and TFAM. Stimulates transcription independently of the methyltransferase activity

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