APOBEC-3D: A Potential Drug Target and Biomarker for DNA Damage Response

Target Name: APOBEC3D

NCBI ID: G140564

APOBEC3D

APOBEC-3D: A Potential Drug Target and Biomarker for DNA Damage Response

Several diseases are caused by DNA damage, which can lead to various health issues, including cancer. DNA damage can occur due to various factors, such as exposure to radiation, infection, or genetic mutations. The damage to DNA can result in the development of cancer, which is a leading cause of death worldwide.

DNA repair mechanisms are essential for maintaining the integrity of DNA and preventing the development of cancer. The DNA damage response is a series of cellular pathways that occur when DNA is damaged or repaired. One of the critical pathways in the DNA damage response is the apoptosis pathway, which is a self-destruction mechanism that helps remove damaged DNA from the cell.

Probable DNA damage response enzyme APOBEC-3D

APOBEC-3D is a DNA repair enzyme that is involved in the apoptosis pathway. It is a protein that is present in the cytoplasm of various cell types and is responsible for editing the DNA in the double helix.

APOBEC-3D functions as an enzyme that can remove damaged DNA from the double helix. It does this by using a specific set of nucleotides, which are called APOBEC-3D-targeting lesions. These lesions cause a double-strand break in the DNA, which can result in the formation of an abnormally stable DNA molecule.

APOBEC-3D-targeting lesions are specific to the APOBEC-3D enzyme and can cause double-strand breaks in specific regions of the DNA. These lesions can occur due to various factors, such as exposure to radiation, UV radiation, or chemical mutagens.

APOBEC-3D-editing activity

APOBEC-3D is also involved in editing the DNA in the double helix. It uses a specific set of nucleotides called APOBEC-3D-editing lesions to remove damaged DNA and create a more stable double-strand break.

APOBEC-3D-editing lesions can cause changes in the nucleotide base, such as a substitution or deletion. These changes can result in the formation of a more stable double-strand break than the original double-strand break. This increase in stability can result in the formation of a more stable and repairable DNA molecule.

APOBEC-3D in cancer

The APOBEC-3D enzyme is involved in the DNA damage response and has been implicated in the development and progression of several types of cancer.

Studies have shown that APOBEC-3D is involved in the development of cancer by promoting the double-strand break repair system. By removing damaged DNA from the double-strand break, APOBEC-3D can prevent the formation of more stable and repairable DNA molecules, which can lead to the formation of cancer cells.

In addition to its role in cancer development, APOBEC-3D has also been shown to contribute to the maintenance of cancer stem cells. Cancer stem cells are a subset of cancer cells that have the ability to self-replify and promote the growth and progression of cancer.

APOBEC-3D as a drug target

The APOBEC-3D enzyme is a potential drug target for cancer treatment. By inhibiting the activity of APOBEC-3D, cancer cells can be damaged and repaired more efficiently, leading to the formation of more stable and repairable DNA molecules.

In addition to its role in cancer development, APOBEC-3D has also been shown to be a potential biomarker for cancer. The level of APOBEC-3D in cancer cells can be used as a measure of the severity of DNA damage and the effectiveness of cancer treatments.

Conclusion

In conclusion, APOBEC-3D is a probable DNA damage response enzyme that can contribute to the development and progression of cancer. It is involved in editing the DNA in the double

Protein Name: Apolipoprotein B MRNA Editing Enzyme Catalytic Subunit 3D

Functions: DNA deaminase (cytidine deaminase) which acts as an inhibitor of retrovirus replication and retrotransposon mobility via deaminase-dependent and -independent mechanisms (PubMed:16920826, PubMed:20062055, PubMed:21835787). Exhibits antiviral activity against HIV-1. After the penetration of retroviral nucleocapsids into target cells of infection and the initiation of reverse transcription, it can induce the conversion of cytosine to uracil in the minus-sense single-strand viral DNA, leading to G-to-A hypermutations in the subsequent plus-strand viral DNA (PubMed:16920826). The resultant detrimental levels of mutations in the proviral genome, along with a deamination-independent mechanism that works prior to the proviral integration, together exert efficient antiretroviral effects in infected target cells. Selectively targets single-stranded DNA and does not deaminate double-stranded DNA or single- or double-stranded RNA. Inhibits also the mobility of LTR and non-LTR retrotransposons (PubMed:27428332)

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