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FLASH GENE
Symbol STK25 contributors: mct - updated : 27-03-2018
HGNC name serine/threonine kinase 25 (STE20 homolog, yeast)
HGNC id 11404
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
kinase domain in N terminus
HOMOLOGY
interspecies homolog to C.elegans f14h12.4
Homologene
FAMILY
  • serine/threonine kinase family, GCK III subfamily
  • Ste20 superfamily of kinases
    • CATEGORY enzyme
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,organelle,membrane
    intracellular,cytoplasm,organelle,Golgi
    basic FUNCTION
  • functioning in a signaling pathway required for cell migration and polarization
  • play distinctly different roles in stressed versus non-stressed cells, regulating cell death in the former
  • can induce cell death entering the nucleus, but this is not necessarily the only way it can kill a cell
  • RELN and STK25 have opposing roles in neuronal polarization and dendritic Golgi deployment
  • STK25 regulates lipid partitioning in human liver cells by controlling triacylglycerol (TAG) synthesis as well as lipolytic activity
  • is a critical regulator of ectopic lipid deposition, systemic glucose, and insulin homeostasis
  • multiple roles of STK25 in nonalcoholic steatohepatitis (NASH) pathogenesis
  • is a critical regulator of liver steatosis, hepatic lipid metabolism and whole body glucose and insulin homeostasis
  • STK25 emerges as a new regulator of the complex interplay between lipid storage, mitochondrial energetics and insulin action in skeletal muscle
  • is a critical regulator of ectopic fat storage, meta-inflammation, and fibrosis in liver and skeletal muscle
  • is a critical regulator of energy homeostasis and Nonalcoholic fatty liver disease (NAFLD) progression
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
  • PDCD10 can heterodimerize with GCKIII kinases (STK24, MST4, and STK25) to regulate cardiovascular development
    • INTERACTION
    DNA
    RNA
    small molecule
    protein
  • activated by the Golgi matrix protein GOLGA2 and plays a role in cell migration through its substrate YWHAZ
  • STK25 regulates neuronal polarization and Golgi morphology in an antagonistic manner to DAB1
  • PDCD10 interacts with STK25, an oxidant stress response kinase related to sterile-20 (Ste20) that is activated by oxidative stress and induces apoptotic cell death
    • CCM2 can be phosphorylated by STK25, and the kinase activity of STK25 is required for death signaling
  • STK26 and STK25 belong to the Ste20-like kinases and interact with PDCD10 which is closely linked to cancer diseases
  • STK25 as the kinase component of STRIPAK can inhibit the function of the STRIPAK inhibitor SAV1
    • cell & other
    REGULATION
    activated by oxidant stress and by autophosphorylation
    not activated by growth factors,alkylating agents,cytokines or environmental stress
    chemical anoxia in a caspase-independent manner, something that has not been described for any other of the GCKIII family members
    ASSOCIATED DISORDERS
    corresponding disease(s) DEL2Q37
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --over  
    in conditions of excess dietary fuels associates with a shift in the metabolic balance in peripheral tissues from lipid oxidation to storage, leading to a systemic insulin resistance
    tumoral     --over  
    in prostate cancer
    Susceptibility
    Variant & Polymorphism
    Candidate gene pseudopseudohypoparathyroidism (PPHP)
    for brachymetaphalangism and/or obesity in the del2q37 syndrome
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    diabete  
    reducing STK25 function may provide a new strategy for the treatment of patients with type 2 diabetes
    digestiveliver 
    reducing STK25 function may provide a new strategy for the treatment of patients with Nonalcoholic fatty liver disease (NAFLD)
    metabolism  
    potential drug target for metabolic disease
    ANIMAL & CELL MODELS
  • Stk25-/- mice are protected against methionine and choline-deficient (MCD) diet-induced NASH, as evidenced by repressed liver steatosis, oxidative damage, inflammation, and fibrosis, whereas Stk25 transgenic mice developed a more severe nonalcoholic steatohepatitis (NASH) phenotype, compared with corresponding wild-type littermates
  • transgenic mice overexpressing STK25, when challenged with a high-fat diet, develop reduced glucose tolerance and insulin sensitivity compared to wild-type siblings