Target intelligence / Profile preview

Double-strand break repair protein MRE11 (MRE11)

Target
MRE11
Molecular classification
Enzyme (nuclease), DNA repair protein
01

Overview

Double-strand break repair protein MRE11 is a highly conserved nuclear enzyme with both exonuclease and endonuclease activity, encoded by the MRE11A gene in humans. It functions primarily in the detection and repair of DNA double-strand breaks, crucial for maintaining genomic stability. MRE11 forms the MRN complex with Rad50 and NBS1, facilitating both homologous recombination and nonhomologous DNA end joining, and has important roles in telomere maintenance. Deficiency or mutation of MRE11 impairs DNA repair, leading to increased susceptibility to cancer and genomic disorders.

Other names
Meiotic recombination 11 homologMRE11 meiotic recombination 11 homolog A (in humans)MRE11A (gene symbol for human protein)
02

Mechanism of action

If targeted, drugs would likely inhibit its nuclease activity, impairing the repair of DNA double-strand breaks and sensitizing cells to DNA-damaging agents (e.g., radiotherapy, chemotherapy)

03

Biological functions

Homologous recombinationDNA double-strand break repairTelomere length maintenanceNonhomologous DNA end joining
04

Disease associations

Cancer (mutations can contribute to genome instability and cancer predisposition)Other (rare genetic disorders involving DNA repair deficiency)
05

Safety considerations

Potential concern is genomic instability resulting from loss of MRE11 function, leading to increased cancer risk or progression, bone marrow failure, and developmental disorders
06

Interacting drugs

Currently, no approved drugs directly target MRE11; however, inhibitors of the MRE11-RAD50-NBS1 (MRN) complex are in preclinical development. MRE11 activity contributes to resistance or sensitivity to chemotherapeutics that induce DNA damage (e.g., PARP inhibitors in cancer therapy)
07

Biomarkers

MRE11 expression and mutation status are being researched as biomarkers for predicting response to DNA-damaging therapies (e.g., PARP inhibitors) in cancers

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