Fanconi anemia group M protein

Definition:

DNA-dependent ATPase component of the Fanconi anemia (FA) core complex. Required for the normal activation of the FA pathway, leading to monoubiquitination of the FANCI-FANCD2 complex in response to DNA damage, cellular resistance to DNA cross-linking drugs, and prevention of chromosomal breakage. In complex with CENPS and CENPX, binds double-stranded DNA (dsDNA), fork-structured DNA (fsDNA) and Holliday junction substrates. Its ATP-dependent DNA branch migration activity can process branched DNA structures such as a movable replication fork. This activity is strongly stimulated in the presence of CENPS and CENPX. In complex with FAAP24, efficiently binds to single-strand DNA (ssDNA), splayed-arm DNA, and 3'-flap substrates. In vitro, on its own, strongly binds ssDNA oligomers and weakly fsDNA, but does not bind to dsDNA.

References:

[1]. Alberto Ciccia, et al. Identification of FAAP24, a Fanconi anemia core complex protein that interacts with FANCM. Mol Cell. 2007 Feb 9;25(3):331-43. [Content Brief]

[2]. Baptiste Fouquet, et al. A homozygous FANCM mutation underlies a familial case of non-syndromic primary ovarian insufficiency. Elife. 2017 Dec 12;6:e30490. [Content Brief]

[3]. Zhijiang Yan, et al. A histone-fold complex and FANCM form a conserved DNA-remodeling complex to maintain genome stability. Mol Cell. 2010 Mar 26;37(6):865-78. [Content Brief]

[4]. Georgina Mosedale, et al. The vertebrate Hef ortholog is a component of the Fanconi anemia tumor-suppressor pathway. Nat Struct Mol Biol. 2005 Sep;12(9):763-71. [Content Brief]

[5]. Amom Ruhikanta Meetei, et al. A human ortholog of archaeal DNA repair protein Hef is defective in Fanconi anemia complementation group M. Nat Genet. 2005 Sep;37(9):958-63. [Content Brief]

[6]. Thiyam Ramsing Singh, et al. MHF1-MHF2, a histone-fold-containing protein complex, participates in the Fanconi anemia pathway via FANCM. Mol Cell. 2010 Mar 26;37(6):879-86. [Content Brief]

[7]. Thiyam Ramsing Singh, et al. Impaired FANCD2 monoubiquitination and hypersensitivity to camptothecin uniquely characterize Fanconi anemia complementation group M. Blood. 2009 Jul 2;114(1):174-80. [Content Brief]

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