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FLASH GENE
Symbol DEPTOR contributors: mct/npt/pgu - updated : 13-04-2016
HGNC name DEP domain containing 6
HGNC id 22953
Location 8q24.12      Physical location : -
Synonym name
  • DEP domain containing mTOR interacting protein
  • Synonym symbol(s) DEP.6, FLJ12428, FLJ13854, FLJ12341, DKFZp564B1778, DEPDC6
    DNA
    TYPE functioning gene
    STRUCTURE 177.26 kb     9 Exon(s)
    MAPPING cloned Y linked N status provisional
    RNA
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    9 - 2631 46.2 409 - 2000 11256614
    DEPDC6 variant 1
    7 - 2333 - 308 - -
    EXPRESSION
    Type widely
       expressed in (based on citations)
    organ(s)
    SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
    Endocrineadrenal gland   highly
    Respiratoryrespiratory tracttrachea  highly
    tissue
    SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
    Connectiveadipose  highly
    cell lineage
    cell lines
    fluid/secretion
    at STAGE
    PROTEIN
    PHYSICAL PROPERTIES
    STRUCTURE
    motifs/domains
  • tandem N-terminal DEP (dishevelled, egl-10, pleckstrin) domains
  • a C-terminal PDZ (postsynaptic density 95, discs large, zonula occludens-1) domain, mediating its interaction with MTOR
  • HOMOLOGY
    Homologene
    FAMILY
    CATEGORY regulatory
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm
    basic FUNCTION
  • within cells is an inhibitor of MTORC1 and MTORC2 activities (its phosphorylation is necessary to reverse the inhibitory effects of DEPDC6 on MTORC2 activity)
  • accumulates upon glucose deprivation and MTOR inhibition to induce autophagy
  • plays a pivotal role in the development and progression of human malignances, which could in part be mediated through its inhibitory role toward MTOR
  • as a new regulator of adipogenesis (pMID: 22883231)
  • is a critical upstream regulator of endothelial cells (ECs) activation responses, suggesting that it plays an important role in endogenous mechanisms of anti-inflammation and pro-resolution
  • SMARCD3 expression and expression of DEPTOR was downregulated in skeletal muscle in obesity, accompanied by extracellular signal-related kinase (ERK) activation
  • plays a key role in maintaining stem cell pluripotency by limiting MTOR activity in undifferentiated embryonic stem cells (ESCs)
  • is a novel stemness factor that promotes pluripotency and self-renewal in ESCs by inhibiting MTOR signaling
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
  • SMARCD3/DEPTOR pathway is a target of proinflammatory signaling in skeletal muscle that may link meta-inflammation to skeletal myofiber metabolism and insulin resistance
  • plays a key role in maintaining stem cell pluripotency by limiting MTOR activity in undifferentiated embryonic stem cells (ESCs)
  • a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • MTOR-interacting protein, that normally functions to inhibit the MTORC1 and MTORC2 pathways
  • interacts with a C-terminal portion of MTOR (AA1483
  • 2000) that is upstream of its kinase domain and does not encompass the mLST8/G
    L binding site (AA 2001
    2549)
  • inhibitor of the MTOR kinase that is highly regulated at the posttranslational level
  • CRTC2 modulated negatively by interaction with DEPTOR and positively by the TSC1-TSC2 protein complex
  • BTRC regulates cell growth and autophagy by controlling the ubiquitination and destruction of DEPTOR, an endogenous mammalian target of rapamycin inhibitor, in a phosphorylation-dependent manner
  • through DEPTOR stabilization, AMBRA1 establishes a feedback loop that ensures the rapid onset of autophagy by enhancing MTOR inactivation
  • inhibitor of MTOR and CRTC2
  • CUL1 promoted MTOR activity and cap-dependent translation by enhancing the ubiquitination and degradation of DEPTOR
  • RNF7 is an E3 ligase that promotes ubiquitylation and degradation of PHLPP1 and DEPTOR, leading to activation of the PI3K/AKT/MTOR axis, whereas RNF7 knockdown caused their accumulation
  • cell & other
    REGULATION
    induced by the SMARCD3-SIX4 transcriptional complex and mediates activation of AKT1 and glycolytic metabolism by SMARCD3 in a cell-autonomous manner
    Other degraded via ubiquitin-proteasome pathway by an unknown E3 ubiquitin ligase
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --over  
    in a subset of multiple myelomas harboring cyclin D1/D3 or c-MAF/MAFB translocations
    constitutional     --low  
    in cases of AD compared to healthy controls can lead to an augmentation of MTOR signalling, leading to APP accumulation
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target pharmacologically induced reduction in DEPDC6 expression or disruption of the DEPDC6-MTOR interaction could have therapeutic benefits for the treatment of multiple myeloma
    ANIMAL & CELL MODELS