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Minichromosome maintenance 9 homologous recombination repair factor (MCM9)

Target
MCM9
Molecular classification
Enzyme (helicase), DNA repair protein
01

Overview

Minichromosome maintenance 9 homologous recombination repair factor (MCM9) is a member of the mini-chromosome maintenance (MCM) protein family that acts as an ATP-dependent helicase involved in DNA mismatch repair and homologous recombination repair[2][3]. MCM9 forms a complex with MCM8 (the MCM8-MCM9 complex) that is essential for the repair of double-stranded DNA breaks and interstrand crosslinks via homologous recombination mechanisms; it helps recruit and promote the activity of the MRN (MRE11-RAD50-NBN) complex and RAD51 to sites of DNA damage, and also recruits MLH1 for mismatch repair[2]. Unlike the essential replicative helicase MCM2-7, MCM9 is dispensable for DNA replication under normal conditions in mammals, but it is important for genome integrity under replication stress, maintenance of germ-line stem cells, and tumor suppression[3][1]. Genetic loss of MCM9 leads to increased genomic instability, defective cell cycle reentry after replication stress, germ-cell depletion, and higher susceptibility to specific cancers[3]. MCM9 has roles in chromatin licensing and interacts positively with CDT1, a DNA replication licensing factor[2]. Disease associations include primary ovarian insufficiency, ovarian dysgenesis, and cancer predisposition. Currently, no drugs directly target MCM9, nor are mechanisms of drug action or clinical biomarkers established specifically for this molecule[2][3][1].

Other names
DNA helicase MCM9C6orf61MCMDC1hMCM9MGC35304dJ329L24.1dJ329L24.3FLJ20170Mini-chromosome maintenance deficient domain-containing protein 1ODG4DNA replication licensing factor MCM9minichromosome maintenance complex component 9
02

Biological functions

Homologous recombination repair (HR)DNA mismatch repair (MMR)Genome stability maintenanceReplication fork progression and protectionChromatin licensing and DNA replication origin licensingCell cycle regulation
03

Disease associations

Cancer (tumor suppression)Primary ovarian insufficiencyOvarian dysgenesis
04

Safety considerations

Genetic deficiency or loss-of-function leads to increased genomic instability, elevated cancer risk, and reproductive system dysfunction (e.g., germ-cell depletion, premature ovarian failure)[2][3]
05

Biomarkers

Genomic instability markersDisease association: Ovarian dysgenesis, premature ovarian failure

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