Gene interactions and pathways from curated databases and text-mining

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ARF6 — SLC2A4

Pathways - manually collected, often from reviews:

  • NCI Pathway Database Arf6 trafficking events: GLUT4 (SLC2A4) → ARF6/GTP complex (ARF6) (modification, collaborate) Li et al., J Cell Biol 2007*
    Evidence: mutant phenotype, physical interaction, other species
  • NCI Pathway Database Arf6 trafficking events: ARF6/GTP complex (ARF6) → GLUT4/clathrin heavy chain/ACAP1 complex (ACAP1-CLTC-SLC2A4) (modification, activates)
    Li et al., J Cell Biol 2007*
    Evidence: mutant phenotype, physical interaction, other species
  • WikiPathways Insulin Signaling: STXBP2/CYTH3/KIF5B/EHD2/ARF6/RAB4A/CAP1/STXBP1/CRK/STXBP4/TBC1D4/SH2B2/EHD1/ARHGAP33/STX4/SNAP25/RHOQ/SNAP23/CBLB/STXBP3/CBL/FLOT2/CBLC/MYO1C/RHOJ/SORBS1/ARF1/RAPGEF1/VAMP2/FLOT1/KIF3A → SLC2A4 (activation)

Text-mined interactions from Literome

Millar et al., J Biol Chem 1999 : These data suggest an important role for ARF6 in regulating cell surface levels of GLUT4 in adipocytes, and argue for a role for both ARF5 and ARF6 in the regulation of membrane trafficking to the plasma membrane
Bose et al., Mol Cell Biol 2001 : Remarkably, expression of a dominant inhibitory form of the actin-regulatory GTPase ARF6 [ ARF6 ( T27N ) ] in cultured adipocytes selectively inhibited both F-actin formation and GLUT4 translocation in response to endothelin 1 but not insulin
Lawrence et al., Mol Cell Biol 2001 : However, the same ARF6 inhibitory mutant blocked the stimulation of hexose uptake and GLUT4 translocation in response to either endothelin 1 or an activated form of Galphaq, Galphaq ( Q209L )