MRE11 homolog, double strand break repair nuclease
DNA double-strand break repair protein Mre11
Calcineurin-like phosphoesterase domain, ApaH type
Mre11, DNA-binding domain, protein family
single-stranded DNA endodeoxyribonuclease activity
mitotic intra-S DNA damage checkpoint signaling
ATM activation by DNA double-strand breaks through the Mre11-Rad50-Nbs1 complex
Nuclease Activities in a Complex of Human Recombination and DNA Repair Factors Rad50, Mre11, and p95
The hMre11/hRad50 Protein Complex and Nijmegen Breakage Syndrome: Linkage of Double-Strand Break Repair to the Cellular DNA Damage Response
MRNIP/C5orf45 Interacts with the MRN Complex and Contributes to the DNA Damage Response
SAMHD1 acts at stalled replication forks to prevent interferon induction
ATRX dysfunction induces replication defects in primary mouse cells
SAMHD1 Promotes DNA End Resection to Facilitate DNA Repair by Homologous Recombination.
ATM-dependent phosphorylation of ATF2 is required for the DNA damage response
CDK targets Sae2 to control DNA-end resection and homologous recombination
EXD2 promotes homologous recombination by facilitating DNA end resection
UBQLN4 Represses Homologous Recombination and Is Overexpressed in Aggressive Tumors
Tyrosine dephosphorylation of H2AX modulates apoptosis and survival decisions
MDC1 directly binds phosphorylated histone H2AX to regulate cellular responses to DNA double-strand breaks
MRE11-RAD50-NBS1 is a critical regulator of FANCD2 stability and function during DNA double-strand break repair
DNA end resection by CtIP and exonuclease 1 prevents genomic instability
Huntingtin interacting proteins are genetic modifiers of neurodegeneration
SIRT1 regulates the function of the Nijmegen breakage syndrome protein
Intranuclear targeting and nuclear export of the adenovirus E1B-55K protein are regulated by SUMO1 conjugation
NBS1 localizes to gamma-H2AX foci through interaction with the FHA/BRCT domain
CtIP tetramer assembly is required for DNA-end resection and repair
Crystal Structure of Human Mre11: Understanding Tumorigenic Mutations
PTIP associates with MLL3- and MLL4-containing histone H3 lysine 4 methyltransferase complex
Five dysfunctional telomeres predict onset of senescence in human cells
Rad17 recruits the MRE11-RAD50-NBS1 complex to regulate the cellular response to DNA double-strand breaks
Phospho-dependent interactions between NBS1 and MDC1 mediate chromatin retention of the MRN complex at sites of DNA damage
PML isoforms IV and V contribute to adenovirus-mediated oncogenic transformation by functionally inhibiting the tumor-suppressor p53.
TERRA-reinforced association of LSD1 with MRE11 promotes processing of uncapped telomeres
The 3′ to 5′ Exonuclease Activity of Mre11 Facilitates Repair of DNA Double-Strand Breaks