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AKT1 — SNAP25
Pathways - manually collected, often from reviews:
-
WikiPathways Insulin Signaling:
GSK3B/AKT2/AKT1/SGK3/SGK1/GSK3A/PDPK1/SGK2
→
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
(activation)
Text-mined interactions from Literome
Kawasaki et al., Mol Cell Biol 2003
(Ischemia...) :
Both GSNO and
SNAP increased
Akt phosphorylation and activity, which were blocked by cotreatment with the PI3 kinase inhibitor wortmannin
Culmsee et al., Mol Pharmacol 2005
(MAP Kinase Signaling System) :
Analysis of the major signaling pathways downstream of TrkA revealed that both
SNAP and DPN
enhanced phosphorylation of
Akt and the mitogen activated kinases ( MAPK ) Erk1/2 ... It was striking that inhibition of the soluble guanylyl cyclase ( sGC ) by 1H- [ 1,2,4 ] oxadiazolo [ 4,3-a ] quinoxalin-1-one ( ODQ ) or protein kinase G ( PKG ) inhibition by ( 9S,10R,12R ) -2,3,9,10,11,12-hexahydro-10-methoxy-2,9-dimethyl-1-oxo-9,12-epoxy-1H-diindolo- [ 1,2,3-fg : 3',2',1'-kl ] pyrrolo [ 3,4-i ] [ 1,6 ] benzodiazocine-10-carboxylic acid methyl ester ( KT5823 ) also blocked the neuroprotective effect of the NO donors, and ODQ clearly attenuated
SNAP induced phosphorylation of TrkA,
Akt , and MAPK
Størling et al., Diabetologia 2005
:
The constitutive level of active, Ser473 phosphorylated
Akt in INS-1 cells was
suppressed by
SNAP
Dillon et al., J Clin Endocrinol Metab 2009
:
Basal IGF-I protein expression
increased in
SUP after 3 months ( P = 0.05 ), with no changes in androgen receptor or total and phosphorylated
Akt , mammalian target of rapamycin, S6 kinase, and 4E-binding protein
Zrelli et al., Planta Med 2011
:
HT as well as the NO donor
SNAP reduced the phosphorylation levels of
Akt , suggesting that HT inactivates Akt via NO production with subsequent apoptosis of VSMCs
Ponnusamy et al., American journal of physiology. Renal physiology 2012
(Necrosis) :
Necrotic
RPTC-Sup induced phosphorylation of extracellular signal regulated kinases ( ERK1/2 ), p38, c-Jun NH ( 2 ) -terminal kinases ( JNKs ), and
AKT
Cheng et al., Proc Natl Acad Sci U S A 2012
(Diabetes Mellitus, Type 2) :
APPL1 potentiates insulin secretion in pancreatic ß cells by enhancing protein kinase
Akt dependent expression of
SNARE proteins in mice