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RAD51 recombinase

The RAD51 gene provides instructions for making a protein that is essential for repairing damaged DNA. Exposure to radiation, ultraviolet light, or certain chemicals can cause breaks in DNA. Breaks also occur when chromosomes exchange genetic material in preparation for cell division. The RAD51 protein attaches (binds) to the DNA at the site of a break and encases it in a protein sheath, which is an essential step in the repair process.

Normal function

The RAD51 gene provides instructions for making a protein that is essential for repairing damaged DNA. Exposure to radiation, ultraviolet light, or certain chemicals can cause breaks in DNA. Breaks also occur when chromosomes exchange genetic material in preparation for cell division. The RAD51 protein attaches (binds) to the DNA at the site of a break and encases it in a protein sheath, which is an essential step in the repair process.

In the nucleus of many cells, the RAD51 protein interacts with many other proteins, including other RAD51 proteins, BRCA1, and BRCA2. The RAD51 protein needs to bind to other RAD51 proteins to function effectively. The BRCA2 protein regulates the activity of the RAD51 protein by transporting it to sites of DNA damage in the nucleus. The interaction between the BRCA1 protein and the RAD51 protein is less clear, although research suggests that BRCA1 may also activate RAD51 in response to DNA damage. By helping repair DNA, these three proteins play a role in maintaining the stability of a cell's genetic information.

The RAD51 protein is also thought to play a role in the developing nervous system, specifically in the development of nerve cells (neurons) that extend down the spinal cord (corticospinal tracts). These neurons send electrical signals that lead to voluntary muscle movement.

Conditions referring to this gene or chromosome

Other names

HRAD51

HsRAD51

RAD51_HUMAN

RAD51A

RECA

Leitura adicional e referências

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As informações nesta página são escritas e revisadas por clínicos qualificados.
  • 19 May 2025 | Última versão
  • 1 May 2025 | Publicado originalmente

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