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WRN gene
Reviewed by Medicinsk Expert•Last updated: 2026-10-22•Gene

WRN gene

The WRN gene provides instructions for producing the Werner protein, which is essential for maintaining the structure and integrity of DNA.

Normal Function

The WRN gene provides instructions for producing the Werner protein, which plays a critical role in repairing damaged DNA. The Werner protein functions as a type of enzyme called a helicase. Helicase enzymes generally unwind and separate double-stranded DNA. The Werner protein also functions as an enzyme called an exonuclease. Exonucleases trim the broken ends of damaged DNA by removing DNA building blocks (nucleotides). Research suggests that the Werner protein first unwinds the DNA and then removes abnormal DNA structures that have been accidentally generated.

Overall, the Werner protein helps maintain the structure and integrity of a person's DNA. This protein plays an important role in copying (replicating) DNA before cell division and transferring the information in genes to the cell machinery that makes proteins (transcription). Additionally, recent studies suggest that the Werner protein may be particularly important for maintaining DNA at the ends of chromosomes (telomeres).

Health Conditions Related to Genetic Changes

Werner syndrome

More than 60 mutations in the WRN gene are known to cause Werner syndrome. Most of these mutations result in an abnormally short, nonfunctional Werner protein. Research suggests that this shortened protein is not transported into the cell's nucleus, where it normally interacts with DNA. Furthermore, the shortened protein is broken down more quickly than the normal Werner protein, reducing the amount of this protein in the cell. Without normal Werner protein in the nucleus, DNA replication, repair, and transcription are disrupted.

Prostate cancer

MedlinePlus Genetics provides information about Prostate cancer.

Cancers

Some changes to a person's genes are acquired during that person's lifetime and are present only in certain cells. These differences, called somatic changes, are not inherited. Somatic changes in the WRN gene are found in nonhereditary tumors and involve a process called methylation. Methylation is a chemical modification that attaches small molecules called methyl groups to certain segments of DNA. When too many methyl groups are attached to the WRN gene (hypermethylation), the gene is turned off and the Werner protein is not produced. Without this protein, cells do not respond normally to DNA damage, allowing mutations to accumulate and potentially leading to cancerous tumors. Hypermethylation of the WRN gene has been found in many different types of tumors, including colon, rectal, lung, stomach, prostate, breast, and thyroid tumors.

Other Names for This Gene

  • RECQ3
  • RECQL2
  • RECQL3
  • Werner syndrome
  • Werner Syndrome helicase
  • Werner syndrome protein
  • Werner syndrome, RecQ helicase-like
  • WRN_HUMAN

Frequently Asked Questions

The loss of WRN helicase activity impairs DNA repair, leading to genomic instability. Consequently, individuals with Werner syndrome have a markedly higher risk of cancers such as osteosarcoma, colorectal cancer, and breast cancer, often developing at a younger age than the general population. Regular cancer screening (e.g., colonoscopy, mammography, and imaging for bone lesions) is advised starting in the third decade.
While no cure exists, maintaining a heart‑healthy lifestyle—low sodium, regular exercise, and smoking cessation—can reduce cardiovascular complications. Antioxidant‑rich diets, routine skin care, and early treatment of infections may also help. Some clinicians trial low‑dose statins or metformin to address metabolic disturbances, but evidence is limited; decisions should be individualized.
Because WRN mutations are autosomal recessive, carrier testing for relatives is recommended. Prenatal testing or preimplantation genetic diagnosis can be offered to couples who wish to avoid affected offspring. A genetic counselor can explain recurrence risks, testing procedures, and support resources.
Typical early indicators include premature graying or hair loss before age 30, skin changes such as atrophic or scleroderma‑like lesions, and the onset of cataracts or atherosclerotic cardiovascular disease in the 30s or 40s. If these features appear together, a genetic test for WRN mutations should be considered.
Source: MedlinePlus, National Library of Medicine

MedlinePlus brings together authoritative health information from the National Library of Medicine (NLM), the National Institutes of Health (NIH), and other government agencies and health-related organizations.

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