DCLRE1A

Official Full Name

DNA cross-link repair 1A

Organism

Homo sapiens

GeneID

9937

Background

This gene encodes a conserved protein that is involved in the repair of DNA interstrand cross-links. DNA cross-links suppress transcription, replication, and DNA segregation. The encoded protein is a regulator of the mitotic cell cycle checkpoint. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Nov 2012]

Synonyms

PSO2; SNM1; SNM1A;

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Detailed Information

DNA cross-link repair 1A (DCLRE1A) gene is an essential player in the maintenance of genome stability. DCLRE1A belongs to the family of DNA repair genes that are responsible for repairing DNA damage, which can lead to mutations and potentially cause cancer.

Function And Mechanism of DCLRE1A

The DCLRE1A gene encodes a protein that is involved in the repair of DNA cross-links. DNA cross-links are chemical bonds that form between DNA strands, causing structural and functional abnormalities. These cross-links can result from various environmental and endogenous factors, such as UV radiation, chemotherapy drugs, and reactive oxygen species. The formation of cross-links can lead to DNA damage, which if not repaired, can result in mutations, cell death, or cancer.

The exact mechanism of how DCLRE1A repairs DNA cross-links is still being unraveled. However, it is known that DCLRE1A interacts with other DNA repair proteins and forms a complex that targets the damaged DNA. This complex then processes the cross-linked DNA, enabling the repair of the damage.

DCLRE1A in Disease

Mutations in the DCLRE1A gene have been associated with various diseases, including cancer, developmental disorders, and neurodegenerative diseases. In cancer, defects in DNA repair mechanisms can lead to unrepaired DNA damage, enabling the accumulation of mutations and promoting tumorigenesis. Impairment of DCLRE1A function has been implicated in the development of various types of cancer, including breast, colon, and prostate cancer.

In addition to cancer, defects in DCLRE1A have been linked to developmental disorders such as cataracts, microcephaly, and growth retardation. Furthermore, DCLRE1A has been implicated in neurodegenerative diseases such as Alzheimer's disease and Huntington's disease. The exact role of DCLRE1A in these diseases is not fully understood, but it is believed that defects in DNA repair can contribute to the accumulation of toxic proteins and mutations, leading to cellular dysfunction and ultimately disease progression.

Recent Advances And Therapeutic Implications

The study of DCLRE1A has gained significant attention in recent years, leading to the identification of new therapeutic targets and approaches for the treatment of various diseases. For example, researchers have discovered that DCLRE1A is a target for certain chemotherapeutic agents, which can lead to the inhibition of DNA repair and sensitize cancer cells to treatment. Researchers have been exploring the use of small molecules that modulate DCLRE1A activity for the treatment of various diseases. For instance, the development of small molecules that enhance DCLRE1A activity has shown potential in the treatment of cancer and neurodegenerative diseases. On the other hand, inhibitors of DCLRE1A have also been developed and shown to be effective in preclinical models of cancer and other diseases.

Reference:

Kellum, Andrew H Jr et al. "Structure of a Stable Interstrand DNA Cross-Link Involving a β-N-Glycosyl Linkage Between an N6-dA Amino Group and an Abasic Site." Biochemistry vol. 60,1 (2021): 41-52. doi:10.1021/acs.biochem.0c00596

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