CHTOP: A Potential Drug Target and Biomarker for PRMT1-Induced Genomic Rewiring

Target Name: CHTOP

NCBI ID: G26097

CHTOP

CHTOP: A Potential Drug Target and Biomarker for PRMT1-Induced Genomic Rewiring

Introduction

PRMT1 (PR elongating histone 1) is a key regulator of DNA double-strand break repair, which is crucial for maintaining the integrity of genomic DNA.DNA double-strand breaks are often caused by mutations, such as those caused by ionizing radiation or other forms of stress. Damage to the DNA double-stranded structure can lead to the development of various diseases, including cancer.

PRMT1 plays a vital role in repairing these breaks. When a double-strand break occurs, PRMT1 recruits a complex of proteins to the site of the break. These proteins work together to repair the damage to the DNA double-strand.

One of the proteins that PRMT1 recruits to the site of a double-strand break is CHTOP (Chromatin-remodeling protein TAMP), a protein that is highly conserved across various species. CHTOP is essential for the proper functioning of PRMT1, as it helps to physically alter the chromatin structure at the site of the double-strand break.

In this article, we will discuss the potential implications of CHTOP as a drug target and biomarker for PRMT1-induced genomic rewiring.

Potential Drug Target

The study of CHTOP and its function in PRMT1-induced genomic rewiring suggests that it may be a valuable drug target for the treatment of various diseases. For example, CHTOP has been shown to promote the formation of distinct chromatin domains at the site of a double -strand break, which can potentially lead to the development of Chromosomal Defects (CDs) and other forms of cancer.

In addition, the alteration of chromatin structure at the site of a double-strand break by CHTOP has been linked to the development of various diseases, including cancer. For instance, studies have shown that the alteration in chromatin structure at the site of a double -strand break by CHTOP is a key predictor of the development of certain types of cancer.

Potential Biomarkers

CHTOP has also been shown to serve as a potential biomarker for PRMT1-induced genomic rewiring. The alteration in chromatin structure at the site of a double-strand break by CHTOP can be detected using various techniques, including qRT-PCR, RNA-seq, andChIP-seq. These techniques allow researchers to quantify the levels of different genes in the cell and to identify changes in gene expression that occur at the site of a double-strand break.

One of the potential benefits of CHTOP as a biomarker is its ability to be used to diagnose diseases that are caused by changes in the DNA double-strand structure. For example, the development of cancer is often associated with the alteration of chromatin structure at the site of a double-strand break. By detecting changes in chromatin structure at this site, researchers can identify individuals at risk for the development of cancer and monitor the effectiveness of various treatments.

Conclusion

In conclusion, CHTOP is a protein that plays a crucial role in the regulation of PRMT1-induced genomic rewiring. Its ability to physically alter the chromatin structure at the site of a double-strand break makes it a potential drug target and biomarker for various diseases . Further research is needed to fully understand the role of CHTOP in the development and progression of various diseases.

Protein Name: Chromatin Target Of PRMT1

Functions: Plays an important role in the ligand-dependent activation of estrogen receptor target genes (PubMed:19858291). May play a role in the silencing of fetal globin genes (PubMed:20688955). Recruits the 5FMC complex to ZNF148, leading to desumoylation of ZNF148 and subsequent transactivation of ZNF148 target genes (By similarity). Plays an important role in the tumorigenicity of glioblastoma cells. Binds to 5-hydroxymethylcytosine (5hmC) and associates with the methylosome complex containing PRMT1, PRMT5, MEP50 and ERH. The CHTOP-methylosome complex associated with 5hmC is recruited to selective sites on the chromosome, where it methylates H4R3 and activates the transcription of genes involved in glioblastomagenesis (PubMed:25284789)

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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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