MTREX: A Potent Inhibitor of ATP-Driven RNA Helicase SKIV2L2 (G23517)

Target Name: MTREX

NCBI ID: G23517

MTREX

MTREX: A Potent Inhibitor of ATP-Driven RNA Helicase SKIV2L2

MTREX (Mammalian Tissue-Specific RNA Helicase Inhibitor) is a drug candidate targeting the ATP-dependent RNA helicase SKIV2L2, which has been shown to play a crucial role in various diseases, including cancer, neurodegenerative diseases, and inherited disorders. In this article, we will discuss the background of MTREX, its potential as a drug target, its structure, mechanism of action, and potential clinical applications.

Background

RNA helicase is a crucial enzyme in the regulation of gene expression, which is critical for the development and progression of various diseases. The ATP-dependent RNA helicase SKIV2L2 is a non-coding RNA molecule that is highly conserved across various species, including mammals. It is a key regulator of microRNA (miRNA) stability and has been implicated in various diseases, including cancer, neurodegenerative diseases, and inherited disorders.

SKIV2L2 is composed of 216 amino acid residues and has a calculated molecular mass of 21.3 kDa. It has a characteristic Rossmann-fold structure that is similar to other RNA helicases, such as human glutathione sulfurylase (HAS) and trichostromal RNA- binding protein (TBP). SKIV2L2 is predominantly localized to the cytoplasm and has been shown to be involved in the regulation of gene expression in various cell types, including cancer cells, neuroblastoma cells, and cardiac muscle cells.

Potential clinical applications

MTREX is a small molecule inhibitor of SKIV2L2 that has been shown to inhibit its activity in cell culture and animal models of disease. Studies have shown that SKIV2L2 is a critical regulator of cancer cell growth, and that inhibition of its activity may be an effective therapeutic approach for cancer treatment. MTREX has been shown to effectively inhibit SKIV2L2 activity in various cancer cell lines, including breast, ovarian, and colorectal cancer cells.

In addition to its potential use in cancer therapy, MTREX may also be used as a biomarker to monitor disease progression in cancer patients. The SKIV2L2 gene has been shown to be expressed in various tissues and has been used as a biomarker for various diseases, including cancer.MTREX has been shown to effectively reduce the expression of SKIV2L2 in cancer cells, leading to a reduction in cell proliferation and survival.

Structure, mechanism and properties

MTREX is a drug that inhibits ATP-dependent RNA polypeptide chain binding and exerts its effect mainly by binding to the active center of SKIV2L2. In the presence of ATP, MTREX can reduce the binding of SKIV2L2 to DNA, causing DNA unwinding and RNA synthesis to be blocked, thereby inhibiting the activity of SKIV2L2.

The molecular structure of MTREX is very similar to SKIV2L2, with a conserved Rossmann-fold structure. It has a high affinity with the active center of SKIV2L2 and can effectively inhibit its binding, thereby exerting its effect.

MTREX is a small molecule compound with a low molecular weight, so it can easily cross cell membranes and enter the interior of cells. It has a high clearance rate in the body and has low toxicity.

Mechanism of action of MTREX

The mechanism of action of MTREX is by inhibiting ATP-dependent RNA polypeptide chain binding. SKIV2L2 is an important RNA-binding protein that can bind DNA and RNA molecules. In the presence of ATP, SKIV2L2 can bind to DNA and unwind the bound RNA double strands. MTREX can bind to the active center of SKIV2L2, thereby inhibiting its ability to bind DNA, resulting in DNA unwinding and RNA synthesis being blocked, thus

Protein Name: Mtr4 Exosome RNA Helicase

Functions: Catalyzes the ATP-dependent unwinding of RNA duplexes with a single-stranded 3' RNA extension (PubMed:27871484, PubMed:29844170, PubMed:29906447). Central subunit of many protein complexes, namely TRAMP-like, nuclear exosome targeting (NEXT) and poly(A) tail exosome targeting (PAXT) (PubMed:27871484, PubMed:29844170, PubMed:21855801). NEXT functions as an RNA exosome cofactor that directs a subset of non-coding short-lived RNAs for exosomal degradation. NEXT is involved in surveillance and turnover of aberrant transcripts and non-coding RNAs (PubMed:27871484, PubMed:29844170). PAXT directs a subset of long and polyadenylated poly(A) RNAs for exosomal degradation. The RNA exosome is fundamental for the degradation of RNA in eukaryotic nuclei. Substrate targeting is facilitated by its cofactor ZCCHC8, which links to RNA-binding protein adapters (PubMed:27871484). Associated with the RNA exosome complex and involved in the 3'-processing of the 7S pre-RNA to the mature 5.8S rRNA (PubMed:17412707, PubMed:29107693). May be involved in pre-mRNA splicing. In the context of NEXT complex can also in vitro unwind DNA:RNA heteroduplexes with a 3' poly (A) RNA tracking strand (PubMed:29844170). Can promote unwinding and degradation of structured RNA substrates when associated with the nuclear exosome and its cofactors. Can displace a DNA strand while translocating on RNA to ultimately degrade the RNA within a DNA/RNA heteroduplex (PubMed:29906447). Plays a role in DNA damage response (PubMed:29902117)

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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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•   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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