RAD51B: A Non-Coding RNA Molecule as A Potential Drug Target for Cancer

Target Name: RAD51B

NCBI ID: G5890

RAD51B: A Non-Coding RNA Molecule as A Potential Drug Target for Cancer

RAD51B is a non-coding RNA molecule that is found in various tissues of the body. It is a part of the hREC2 gene family, which is responsible for encoding histone modifications on the DNA of chromosome 9. RAD51B has been shown to play a crucial role in the regulation of gene expression and has been linked to various diseases, including cancer. In this article, we will discuss the research on RAD51B as a drug target and its potential applications in cancer treatment.

The hREC2 gene family

The hREC2 gene family is a cluster of non-coding RNAs that are characterized by the presence of a specific intron in their primary transcript. The hREC2 cluster includes several non-coding RNAs, including RAD51B, RAD51C, and RAD51D. These RNAs are involved in the regulation of gene expression and have been shown to play a role in various cellular processes, including DNA replication, transcription, and post-transcriptional modification.

RAD51B function

RAD51B is a non-coding RNA molecule that is found in various tissues of the body. It is a part of the hREC2 gene family and has been shown to play a crucial role in the regulation of gene expression. RAD51B is made up of 1,188 base pairs of RNA and has a molecular weight of 29 kDa. It is expressed in various tissues of the body, including the brain, heart, and testes.

RAD51B has been shown to play a role in the regulation of gene expression by binding to specific DNA sequences. It has been shown to interact with the protein SIRT1, which is a NAD+-dependent antioxidant that has been shown to play a role in various cellular processes, including DNA repair and stress response.

In addition to its role in gene expression, RAD51B has also been shown to play a role in the regulation of DNA replication. It has been shown to interact with the protein DnaC, which is involved in the regulation of DNA replication.

Potential drug targets

RAD51B has been shown to play a crucial role in the regulation of gene expression and has been linked to various diseases, including cancer. As a result, RAD51B has emerged as a potential drug target for cancer treatment.

One of the main advantages of RAD51B as a drug target is its ability to interact with multiple proteins, including SIRT1 and DNAC. This makes it a more versatile drug target than many other RNA molecules. Additionally, RAD51B is expressed in various tissues of the body, which makes it a more accessible drug target than some other RNA molecules.

Another advantage of RAD51B as a drug target is its role in the regulation of DNA replication. This makes it a potential drug target for cancer cells that are dependent on DNA replication for their growth and survival.

In addition to its potential as a drug target, RAD51B has also been shown to be a useful biomarker for the diagnosis and prognosis of various diseases, including cancer. Its expression has been shown to be associated with the development and progression of various diseases, including cancer.

Conclusion

In conclusion, RAD51B is a non-coding RNA molecule that is expressed in various tissues of the body and has been shown to play a crucial role in the regulation of gene expression and the regulation of DNA replication. Its potential as a drug target for cancer treatment is due to its ability to interact with multiple proteins and its role in the regulation of DNA replication. Further research is needed to fully understand the potential applications of RAD51B as a drug target for cancer treatment.

Protein Name: RAD51 Paralog B

Functions: Involved in the homologous recombination repair (HRR) pathway of double-stranded DNA breaks arising during DNA replication or induced by DNA-damaging agents. May promote the assembly of presynaptic RAD51 nucleoprotein filaments. Binds single-stranded DNA and double-stranded DNA and has DNA-dependent ATPase activity. Part of the RAD51 paralog protein complex BCDX2 which acts in the BRCA1-BRCA2-dependent HR pathway. Upon DNA damage, BCDX2 acts downstream of BRCA2 recruitment and upstream of RAD51 recruitment. BCDX2 binds predominantly to the intersection of the four duplex arms of the Holliday junction and to junction of replication forks. The BCDX2 complex was originally reported to bind single-stranded DNA, single-stranded gaps in duplex DNA and specifically to nicks in duplex DNA. The BCDX2 subcomplex RAD51B:RAD51C exhibits single-stranded DNA-dependent ATPase activity suggesting an involvement in early stages of the HR pathway

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