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FLASH GENE
Symbol SETMAR contributors: mct - updated : 20-01-2017
HGNC name SET domain and mariner transposase fusion gene
HGNC id 10762
Location 3p26.1      Physical location : 4.344.987 - 4.358.948
Synonym symbol(s) METNASE, Mar1
EC.number 2.1.1.43
DNA
TYPE functioning gene
STRUCTURE 17.35 kb     3 Exon(s)
10 Kb 5' upstream gene genomic sequence study
MAPPING cloned Y linked N status provisional
RNA
TRANSCRIPTS type messenger
identificationnb exonstypebpproduct
ProteinkDaAAspecific expressionYearPubmed
3 - 2157 - 684 - 2007 17877369
4 - 1740 - 545 - 2007 17877369
4 - 1720 - 428 - 2007 17877369
3 - 1408 - 406 - 2007 17877369
2 - 1293 - 396 - 2007 17877369
2 - 1775 - 365 - 2007 17877369
EXPRESSION
Type widely
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Digestiveliver    
Nervousbrain    
Reproductivemale systemprostate   
Urinarybladder    
Visualeye    
tissue
SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
Muscular    
cell lineage
cell lines
fluid/secretion
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • a SET histone methylase domain , SET domain necessary for the recovery from DNA damage at the replication forks following hydroxyurea (HU) treatment
  • a transposase domain essential for SETMAR function in DNA repair
  • a DDN catalytic motif required for SETMAR functions in non-homologous end joining (NHEJ) repair and replication restart
  • HOMOLOGY
    interspecies homolog to murine Setmar
    Homologene
    FAMILY
    CATEGORY enzyme
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,nucleus,chromatin/chromosome
    basic FUNCTION
  • histone-lysine N-methyltransferase activity
  • methylates histone H3 lysines 4 and 36, which are associated with open chromatin )
  • its DNA cleavage activity, unlike those of other eukaryotic transposases, is not coupled to its sequence-specific DNA binding
  • SET and transposase domain protein that methylates histone H3 and promotes DNA double-strand break repair
  • enhances TOP2A decatenation, and this activity is repressed by automethylation
  • key factor that promotes restar t of stalled replication forks, implicated in the repair of collapsed forks
  • promotes cell proliferation, but it does not alter cell cycle distributions, or replication fork progression
  • fusion of a histone methylase and transposase protein that arose specifically in primates
  • having a potential function opposing transposases and may thus play a key role in suppressing translocations that underlie oncogenicity
  • DNA repair protein, localized to an induced double-strand break (DSB) and directly mediated the formation of H3K36me2 near the induced DSB
  • SET-transposase fusion protein that promotes nonhomologous end joining (NHEJ) repair
  • potential role for its endonuclease activity in promoting the joining of noncompatible ends
  • SET and transposase domain protein that promotes both DNA double-strand break (DSB) repair and restart of stalled replication forks
  • while both SETMAR and DCLRE1C are biochemically capable of resolving a variety of damaged DNA ends for the repair of complex double-strand breaks, DCLRE1C appears to act more efficiently in the context of other nonhomologous end joining proteins
  • chimeric SET-transposase protein that plays essential role(s) in non-homologous end joining (NHEJ) repair and replication fork restart
  • CELLULAR PROCESS nucleotide, transcription, regulation
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA binding
    RNA
    small molecule metal binding,
    ion zn2+
    protein
  • interacting with PRPF19 (is necessary to bring SETMAR to the DSB sites for its function(s) in DNA repair)
  • physically interacts and co-localizes with TOP2A (Topo IIalpha), the key chromosome decatenating enzyme
  • interacts with DNA Ligase IV (LIG4) and promotes nonhomologous end-joining (NHEJ) DNA repair
  • with DBN1, and HILPDA, SETMAR, is a direct target of the SOX11 protein (are direct transcriptional targets of the SOX11 protein)
  • SETMAR decreases CHEK1 interaction with DDB1, and decreases CHEK1 ubiquitination
  • SETMAR enhances EXO1-mediated exonuclease activity on the lagging-strand DNA by facilitating EXO1 loading onto a single-strand gap at the stalled replication fork
  • cell & other
    REGULATION
    Phosphorylated by CHEK1 (phosphorylation of SETMAR enhances DNA repair but inhibits replication fork restart)
    ASSOCIATED DISORDERS
    ANIMAL & CELL MODELS