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FLASH GENE
Symbol SIX4 contributors: mct - updated : 22-01-2014
HGNC name sine oculis homeobox homolog 4 (Drosophila)
HGNC id 10890
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • a six domain
  • a helix-turn-helix (homeo) DNA binding domain
  • an intervening region of unknown function
  • a transactivation domain
    • HOMOLOGY
    interspecies homolog to Drosophila sine oculis homeo box SIX4
    ortholog to rattus Six 4 predicted
    ortholog to murine Six4
    Homologene
    FAMILY
  • SIX/Sine oculis homeobox family
    • CATEGORY transcription factor
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,nucleus
    basic FUNCTION
  • putatively involved in differentiation or maturation of neuronal cells and retinal development
  • SIX1 and SIX4 regulate SLC12A2
  • SIX1 and SIX4 may act synergistically to mediate olfactory placode specification and patterning through FGF and BMP signaling pathways
  • SIX1 and SIX4 are essential global regulators of muscle gene expression, as well as a central switch to drive the skeletal muscle fast phenotype during fetal development
  • SIX1 and SIX4 function synergistically to form gustatory papillae during development of the tongue
  • SMARCD3-SIX4 transcriptional complex inducing DEPTOR and mediating activation of AKT1 and glycolytic metabolism by SMARCD3 in a cell-autonomous manner
  • SIX1 and SIX4 are required for male gonadal differentiation
  • combinatorial expression of SIX1, SIX2, and SIX4 is required for the molecular programs governing craniofacial and cerebral development
    • CELLULAR PROCESS nucleotide, transcription, regulation
    PHYSIOLOGICAL PROCESS development
    text
  • morphogenesis
  • eye development
    • PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA binding
    RNA
    small molecule
    protein
  • SIX4 cooperates with SIX1 in the metanephric mesenchyme to regulate the level of GDNF expression
    • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS
  • Six1/Six4-deficient mice exhibited more severe kidney phenotypes than the Six1-deficient mice