◀ Back to PIK3R1
CXCL12 — PIK3R1
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Hwang et al., Int J Hematol 2006
:
IFN-gamma did not enhance
SDF-1 induced activation of
PI3K/Akt or up-regulate the expression of CXCR4 or its function in bone marrow CD34+ cells
Smith et al., Cell Signal 2007
:
Use of second generation inhibitors that can discriminate between individual PI3K isoforms, revealed that PI3Kgamma was the major contributor to
CXCL12 induced migration and
PI3K/Akt signaling ( as assessed by S6 phosphorylation )
Lin et al., J Biol Chem 2011
:
Thrombin induced IL-8/CXCL8 release and
IL-8/CXCL8-luciferase activity were
attenuated by a
PI3K inhibitor ( LY294002 ), an Akt inhibitor ( 1-L-6-hydroxymethyl-chiro-inositol-2- ( ( R ) -2-O-methyl-3-O-octadecylcarbonate ) ), and the dominant negative mutants of Rac1 ( RacN17 ) and Akt ( AktDN )
Wang et al., World J Gastroenterol 2011
(Colonic Neoplasms) :
SDF-1 induced significant phosphorylation of
PI3K/AKT and ß-catenin
Chen et al., J Biol Chem 2012
(Stomach Neoplasms) :
Moreover, CXCR4 immunoprecipitated by anti-p110ß antibody increased after CXCL12 stimulation and G ( i ) protein inhibitor pertussis toxin abrogated
CXCL12 induced activation of
PI3K
Li et al., Am J Transplant 2012
(Arteriosclerosis) :
Conditioned media from Ltv-p53 transferred SMCs activated
PI3K/Akt/mTOR and MAPK/Erk signaling in a
SDF-1a dependent manner and thereby promoted mesenchymal stem cell (MSC) migration and proliferation