Helicase B: A Protein Involved in DNA Replication and Repair (G92797)

Target Name: HELB

NCBI ID: G92797

HELB

Helicase B: A Protein Involved in DNA Replication and Repair

Helicase (DNA) B, also known as HELB, is a protein that plays a crucial role in the regulation of DNA replication and repair in various organisms, including humans. It is a key component of the complex machinery that ensures the faithful transmission of genetic information from one generation to the next.

HELB is a 26-kDa protein that consists of a catalytic domain and a transmembrane region. The catalytic domain, which is the part of the protein that interacts with DNA, consists of a single domain that contains a single active site. This domain is responsible for the protein's catalytic activity, which is essential for its function in DNA replication and repair.

One of the unique features of HELB is its ability to interact with DNA in a specific way. It can form a stable complex with the double-stranded DNA, allowing it to exert a persistent influence on the replication process. This interaction between HELB and DNA is critical for ensuring that the DNA is replicated correctly and that any errors in replication are corrected.

In addition to its role in DNA replication, HELB is also involved in the regulation of DNA repair. When DNA replication fails or is damaged, HELB helps to ensure that the necessary repairs are made to maintain the integrity of the genetic material. This is done through the formation of a complex between HELB and the DNA damage repair system.

HELB is a protein that is expressed in most organisms, including humans. It is found in a variety of tissues and cells, including the cytoplasm, the nucleus, and the mitochondria. It is also expressed in various signaling pathways, including the cell cycle and the DNA replication/repair pathways.

Due to its involvement in so many cellular processes, HELB is a potential drug target. Studies have shown that HELB is a good candidate for inhibition, either alone or in combination with other drugs, in a variety of diseases, including cancer, neurodegenerative diseases, and autoimmune disorders.

In cancer, HELB has been shown to be involved in the regulation of DNA replication and repair, which makes it a potentially attractive target for cancer treatment. For example, studies have shown that inhibiting HELB can lead to a reduction in the growth of cancer cells. This is because HELB is involved in the formation of the double-stranded DNA structure that is necessary for cell growth, and inhibiting its activity can disrupt this structure.

In neurodegenerative diseases, HELB has been shown to be involved in the regulation of protein synthesis and may play a role in the development of these diseases. For example, studies have shown that HELB is involved in the regulation of the production of the protein involved in neurotransmitter synthesis, which is important for the function of many neurons.

In autoimmune disorders, HELB has been shown to be involved in the regulation of immune cell function and may play a role in the development of these disorders. For example, studies have shown that HELB is involved in the regulation of the production of antibodies, which are important for the immune response.

Overall, HELB is a protein that plays a crucial role in the regulation of DNA replication and repair in various organisms. Its ability to interact with DNA in a specific way makes it a potential drug target in a variety of diseases. Further research is needed to fully understand the role of HELB in cellular processes and to develop effective treatments for diseases in which it is involved.

Protein Name: DNA Helicase B

Functions: 5'-3' DNA helicase involved in DNA damage response by acting as an inhibitor of DNA end resection (PubMed:25617833, PubMed:26774285). Recruitment to single-stranded DNA (ssDNA) following DNA damage leads to inhibit the nucleases catalyzing resection, such as EXO1, BLM and DNA2, possibly via the 5'-3' ssDNA translocase activity of HELB (PubMed:26774285). As cells approach S phase, DNA end resection is promoted by the nuclear export of HELB following phosphorylation (PubMed:26774285). Acts independently of TP53BP1 (PubMed:26774285). Unwinds duplex DNA with 5'-3' polarity. Has single-strand DNA-dependent ATPase and DNA helicase activities. Prefers ATP and dATP as substrates (PubMed:12181327). During S phase, may facilitate cellular recovery from replication stress (PubMed:22194613)

The "HELB Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about HELB comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   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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