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FLASH GENE
Symbol INPP5J contributors: mct/pgu - updated : 05-05-2020
HGNC name inositol polyphosphate-5-phosphatase J
HGNC id 8956
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • two distinct regions, an anionic head group and a pair of fatty acid tails
  • SKICH domain mediating plasma membrane ruffle localization
  • binds at an interface between the transmembrane domain (TMD) and the cytoplasmic domain (CTD), and this binding site consists of a conserved non-specific phospholipid-binding region in the TMD and a specific phosphatidylinositol-binding region in the CTD
  • C-terminal growth cone-targeting domain
  • HOMOLOGY
    Homologene
    FAMILY
  • inositol-1,4,5-trisphosphate 5- phosphatase type II family
  • CATEGORY enzyme
    SUBCELLULAR LOCALIZATION     plasma membrane
        intracellular
    intracellular,cytoplasm,cytosolic
    text
  • localized at the inner leaflet of the plasma membrane
  • basic FUNCTION
  • regulator of phosphoinositide 3-kinase-dependent neurite elongation
  • INPP5J and DPYSL2 exert opposing roles in promoting axon selection and neurite elongation and the complex between these proteins serves to regulate the localization of effectors that promote neurite extension
  • negative regulator of PI3K/Akt signaling
  • can control the resting membrane potential through a specific ion-channel-receptor-ligand interaction that brings about a large conformational change, analogous to neurotransmitter activation of ion channels at synapses
  • a key signalling molecule that regulates dendritic outgrowth through activation of small GTPase signalling via interaction between FRMPD4 and ARHGEF7
  • is not involved in the regulation of KCNT1, KCNT2 by cell volume
  • role of INPP5J in regulating EHD2 plasma membrane localization
  • is a suppressor of oncogenic PI3K/AKT signaling in breast cancer
  • minor phospholipid component of cell membranes, having previously been shown to directly bind TRP channels and to play a unique role in modulating receptor function
  • putative tumour suppressor in melanoma and breast cancer
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component DPYSL22·INPP5J complex is likely to dynamically regulate both neurite outgrowth and axon polarity in the normal brain
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • tonically associated with TRPV1 (is now believed to be a TRPV1 agonist, potentiating activation by chemical and thermal stimuli)
  • ABCC8 controls KCNJ11 gating by modulating KCNJ11 interactions with INPP5J
  • interacting with DPYSL2 (its C-terminal growth cone-targeting domain facilitates its interaction with DPYSL2)
  • association between INPP5J and DPYSL2 does not require DPYSL2 phosphorylation, rather this complex significantly reduces when GSK3B is active, conditions under which PI3K/Akt signaling is not activated
  • is in addition a novel regulator of the activity of KCNT1 and KCNT2 channels
  • BASP1 myristoylation and association with INPP5J are required for the interaction of BASP1 with HDAC1, which mediates the recruitment of HDAC1 to the promoter and elicits transcriptional repression
  • feedback mechanism that replenishes Plasma membrane (PM) INPP5J during receptor-induced Ca(2+) signaling via the Ca(2+) effector ESYT1 and the PITPNM1 at ER-PM junctions
  • INPP5J-binding alters VCL structure to direct higher-order oligomerization and suggests that INPP5J and F-actin binding to VCL are mutually permissive
  • S100A1 competes with CALM1 and INPP5J for binding site on the C-terminus of the TPRV1 receptor
  • PLCB3, INPP5J interact with N-terminus region of TRPM4 channel
  • binding of INPP5J at the N-terminus of the TRPM1 receptor
  • PTEN, INPP5J and INPP4B distinctly regulate PtdIns(3,4,5)P3 signalling downstream of PI3K and dysregulation of these phosphatases affects cancer outcomes
  • KCNQ1/KCNE1 channel does not require INPP5J or PI(4)P for anterograde trafficking, but is heavily reliant on INPP5J for channel function once at the plasma membrane (PM)
  • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --low  
    accelerates oncogene-driven breast cancer tumor growth, but paradoxically reduces metastasis by regulating AKT1-dependent tumor cell migration
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS