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FLASH GENE
Symbol STK38 contributors: mct - updated : 31-05-2014
HGNC name serine/threonine kinase 38
HGNC id 17847
EXPRESSION
Type ubiquitous
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Digestivemouthtongue  highly
 stomach   highly
Lymphoid/Immunespleen   highly
 thymus   highly
Reproductivefemale systemuterus  highly
Urinarybladder   highly
tissue
SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
Connectivebone   
cells
SystemCellPubmedSpeciesStageRna symbol
Blood/Hematopoieticleukocyte
cell lineage
cell lines
fluid/secretion blood
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • twelve protein kinase catalytic subdomains
  • a potential bipartite nuclear localization signal
  • conjugated PhosphoP
    HOMOLOGY
    interspecies ortholog to murine Stk38
    homolog to Drosophila trc
    homolog to C. elegans sax-1
    ortholog to xenopus trc-prov1
    Homologene
    FAMILY
  • protein kinase superfamily
  • nuclear-Dbf2-related (NDR) family of Ser/Thr kinases
  • CATEGORY enzyme
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm
    intracellular,nucleus
    text low levels present in the cytoplasm
    basic FUNCTION
  • protein amino acid phosphorylation
  • protein kinase cascade
  • implicated in cell proliferation and/or tumor progression
  • might play a role in the HIV-1 life cycle
  • with STK38L, are proapoptotic kinases and key members of the RASSF1/STK4 signaling cascade
  • required for accurate chromosome alignment at metaphase
  • its kinase activity increased in early mitotic phase and was dependent on FRY and STK3
  • STK38/STK38L have been implicated in controlling centrosome duplication and mitotic chromosome alignment downstream of the HIPPO kinase homologs MST1 and STK3
  • its activation is required to prevent cell death in response to oxidative stress
  • implicated to function in centrosome duplication, control of cell cycle and apoptosis
  • novel role of STK38 in NFKB activation
  • CELLULAR PROCESS cell life, proliferation/growth
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
  • STK24-STK38/STK38L-CDKN1A axis is an important regulator of G(1)/S progression of mammalian cells
  • INTERACTION
    DNA
    RNA
    small molecule metal binding, cofactor, nucleotide,
  • ATP
  • Mg2+
  • protein
  • MOBKL1B
  • homodimeric S100B
  • HCCA2 and STK38L (this association dramatically stimulates STK38 and STK38L catalytic activity)
  • MOBKL1A
  • STK24-STK38-CDKN1A axis is an important regulator of G(1)/S progression of mammalian cells
  • MICAL1 is a binding partner of NDR (nuclear Dbf2-related) kinases, STK4, and STK38
  • regulates MYC protein stability and turnover in a kinase activity-dependent manner
  • novel function of CCND1 in promoting cell cycle progression by enhancing STK38/STK38L kinase activity independent of CDK4
  • STK38-mediated phosphorylation of CDC25A at Ser-76 and the subsequent degradation of CDC25A are required to promote DNA damage-induced G2/M checkpoint activation
  • cell & other
    REGULATION
    activated by binding of S100B
    the binding of MOB1/MOBKL1A and MOB2/HCCA2 to the N-terminal of STK38 (autoinhibition released)
    inhibited by MOB2(negatively regulated by increased MOB2 expression)
    GSK3B, that inhibits STK38 full activation
    Other
  • STK3-, FRY-, and MOB2-mediated activation of STK38 is crucial for the fidelity of mitotic chromosome alignment in mammalian cells
  • ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --over  
    resulted in centrosome overduplication in a kinase-activity-dependent manner, while expression of kinase-dead STK38/STK38L or depletion of STK38/STK38L by small interfering RNA (siRNA) negatively affected centrosome duplication
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    cancerhemopathy 
    STK38 kinase inactivation abrogates apoptosis following B-cell receptor activation, whereas its silencing significantly decreases MYC levels and increases apoptosis, thus providing a novel viable target for treating B-cell lymphomas
    ANIMAL & CELL MODELS