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SLC2A4 — STX4
Pathways - manually collected, often from reviews:
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NCI Pathway Database Insulin-mediated glucose transport:
SNARE/Synip complex (VAMP2-STX4-STXBP4)
→
Insulin responsive Vesicles complex (SLC2A4-LNPEP-VAMP2)
(translocation, activates)
Min et al., Mol Cell 1999, Baumann et al., Nature 2000, Ramm et al., Mol Biol Cell 2000, Chiang et al., Nature 2001, Liu et al., Mol Cell Biol 2002, Malide et al., J Histochem Cytochem 1997
Evidence: mutant phenotype, assay
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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
St-Denis et al., J Basic Clin Physiol Pharmacol 1998
(Diabetes Mellitus, Type 2) :
Furthermore, recent studies have demonstrated that VAMP2/3,
syntaxin 4 , SNAP-23, and NSF are functionally
involved in insulin stimulated
GLUT4 translocation in adipose cells and thus are likely to be involved in the Gs- and Gi-mediated modulation of the glucose transport response to insulin as well
Chen et al., J Biol Chem 1997
:
The docking/fusion of GLUT4 vesicles with the plasma membrane appeared to utilize a similar mechanism, since expression of a dominant interfering mutant of
syntaxin-4 prevented both insulin- and osmotic shock induced
GLUT4 translocation