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FLASH GENE
Symbol DOK3 contributors: mct/npt - updated : 03-05-2016
HGNC name docking protein 3
HGNC id 24583
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • a pleckstrin homology (PH) domain generally acting as a lipid/protein-interacting module and necessary for the tyrosine phosphorylation of Dok proteins and their negative functions in T cells (Guittard 2009)
  • HOMOLOGY
    Homologene
    FAMILY
  • Dok family of adaptors
  • CATEGORY adaptor
    SUBCELLULAR LOCALIZATION     plasma membrane
        intracellular
    intracellular,cytoplasm
    basic FUNCTION
  • negatively regulates mitogen-activated protein kinase Erk downstream of protein-tyrosine kinases (PTKs)(Honma 2006)
  • sequesters GRB2 from Shc and inhibits the Ras-Erk pathway downstream of PTKs (Honma 2006)
  • plays a distinct and nonredundant role in the negative regulation of B-cell receptor (BCR) signaling
  • adaptor protein that function in feedback loops to modulate tyrosine kinase signaling (Berger 2010)
  • function in negative-feedback signaling loops that tightly modulate the duration and intensity of growth factor signaling (Berger 2010)
  • is a negative regulator of TLR signaling by limiting LPS-induced ERK activation and cytokine responses in macrophages
  • plays a role in TLR signaling during both na
  • ve and endotoxin-induced tolerant conditions
  • DOK1, DOK2, and DOK3 cooperatively play critical anti-inflammatory roles in lung homeostasis
  • functions as a negative regulator and attenuates B-cell receptor-mediated calcium signaling
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
  • DOK3/GRB2 modulates the balance between activatory and inhibitory LYN functions with the aim to adjust BCR signaling efficiency
  • INTERACTION
    DNA
    RNA
    small molecule
    protein
  • interacting with GRB2, through the GRB2 SH2 domain (GRB2 is a DOK3-binding protein upon its tyrosine phosphorylation) (Honma 2006)
  • DOK3 physically associated with the ITAM of TYROBP through its phosphotyrosine-binding domain
  • DOK3 was shown to bind TRAF3, and the binding of TRAF3 and TBK1 to DOK3 required the tyrosine-rich C-terminal domain of DOK3
  • DOK3 is a nonredundant regulator of plasma cell (PC) differentiation by up-regulating CD274 expression through the attenuation of calcium signaling
  • TRAF6-mediated degradation of DOK3 is required for production of IL6 and TNF in TLR9 signaling
  • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS
  • Dok3-deficient mice had increased susceptibility to challenge with a sublethal dose of lipopolysaccharide (LPS) and produced increased serum concentrations of the inflammatory cytokine tumor necrosis factor
  • Dok3(-/-) mice have increased populations of T follicular-helper (Tfh) and germinal center (GC) B cells upon immunization with a T-cell-dependent antigen