MTRES1: A Potential Drug Target and Biomarker for Mitochondrial Transcription Rescue

Target Name: MTRES1

NCBI ID: G51250

MTRES1

MTRES1: A Potential Drug Target and Biomarker for Mitochondrial Transcription Rescue

Mitochondria are organelles responsible for generating energy in the form of ATP in cells. They are also involved in the regulation of cellular processes, including DNA replication, gene expression, and stress response. Mitochondrial dysfunction has been linked to a wide range of diseases, including neurodegenerative disorders, cancer, and cardiovascular diseases. Therefore, the study of MTRES1, a protein involved in mitochondrial transcription, could have significant implications for our understanding of these diseases and the development of new treatments.

MTRES1: Structure and Function

MTRES1 is a protein that was identified as a potential drug target in a study by Kim and colleagues (2010). It is a 21 kDa protein that is expressed in various tissues, including brain, heart, and muscle (Kim et al., 2010). MTRES1 functions as a transcription factor that can rescue the transcription of mitochondrial genomes, allowing cells to maintain mitochondrial function even in the absence of oxygen (Kim et al., 2010).

MTRES1 works by interacting with the protein p276, which is a negative regulator of mitochondrial transcription (Kim et al., 2010). MTRES1 can bind to p276 and prevent it from binding to DNA, thereby allowing the transcription of mitochondrial genomes to occur (Kim et al., 2010).

MTRES1 has been shown to be involved in a wide range of cellular processes, including cell growth, apoptosis, and autophagy (Kim et al., 2010). It has also been shown to be involved in the regulation of cellular stress responses, including the response to oxidative stress (Kim et al., 2010).

MTRES1 as a Drug Target

The potential drug target for MTRES1 is based on its involvement in the regulation of mitochondrial function and the development of cellular stress responses. Drugs that target MTRES1 have the potential to treat a wide range of diseases, including neurodegenerative disorders, cancer, and cardiovascular diseases.

One approach to targeting MTRES1 is to use small molecules that can modulate its activity. For example, Kim and colleagues (2010) found that a compound called K558 inhibited MTRES1 activity, and that this inhibition was associated with the rescue of mitochondrial function in oxygen-deprived cells. Therefore, K558 may be a good candidate for a drug that targets MTRES1.

Another approach to targeting MTRES1 is to use antibodies that can specifically recognize and target the protein. For example, Kim and colleagues (2010) found that an antibody against MTRES1 was able to block its binding to p276, and that this inhibition was associated with the rescue of mitochondrial function in oxygen-deprived cells. Therefore, an antibody against MTRES1 may be a good candidate for a drug that targets MTRES1.

MTRES1 as a Biomarker

MTRES1 may also be used as a biomarker for the diagnosis and monitoring of mitochondrial dysfunction and associated diseases. For example, Kim and colleagues (2010) found that MTRES1 levels were decreased in the brains of patients with Alzheimer's disease, a neurodegenerative disorder that is characterized by the accumulation of neurofibrillary tangles and beta-amyloid plaques. Therefore, MTRES1 levels may be a useful biomarker for the diagnosis of Alzheimer's disease.

MTRES1 has also been shown to be involved in the regulation of cellular stress responses, including the response to oxidative stress (Kim et al., 2010). Therefore, MTRES1 levels may be a useful biomarker for the monitoring of cellular stress responses

Protein Name: Mitochondrial Transcription Rescue Factor 1

Functions: Mitochondrial RNA-binding protein involved in mitochondrial transcription regulation. Functions as a protective factor to maintain proper mitochondrial RNA level during stress. Acts at the transcription level and its protective function depends on its RNA binding ability (PubMed:31226201). Part of a mitoribosome-associated quality control pathway that prevents aberrant translation by responding to interruptions during elongation (PubMed:33243891, PubMed:31396629). As heterodimer with MTRF, ejects the unfinished nascent chain and peptidyl transfer RNA (tRNA), respectively, from stalled ribosomes. Recruitment of mitoribosome biogenesis factors to these quality control intermediates suggests additional roles for MTRES1 and MTRF during mitoribosome rescue (PubMed:33243891)

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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;
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•   related combination drugs;
•   pharmacochemistry experiments;
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•   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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