◀ Back to HSPG2
HSPG2 — PIK3R1
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Reistad et al., Toxicological sciences : an official journal of the Society of Toxicology 2005
:
We suggest that tyrosine kinase mediated activation of
PI3K could
result in enhanced activation of calcium dependent PKC by enhanced
PLC activity, followed by intracellular calcium release leading to ROS formation in neutrophil granulocytes
Yadav et al., J Immunol 2006
(Mycobacterium Infections) :
This cPKC and
PI3K activation was
dependent on SPK and
PI-PLC
Massheimer et al., Steroids 2006
:
However,
PLC activation was
dependent on
PI3K since presence of LY 294002 in the incubation medium abolished estrone induced DAG increment
Irino et al., J Neurosci Res 2008
:
These results indicate that Akt activation is dependent on the
PI3K pathway and a
PLC mediated
increase in intracellular calcium and suggest that Akt activation is involved in ADP induced microglial chemotaxis
Wang et al., J Am Chem Soc 2008
:
To explore the specificity of these types of molecules, we have synthesized D-3-deoxydioctanoylphosphatidylinositol ( D-3-deoxy-diC8PI ), D-3,5-dideoxy-diC8PI, and D-3-deoxy-diC8PI-5-phosphate and their enantiomers, characterized their aggregate formation by novel high-resolution field cycling ( 31 ) P NMR, and examined their susceptibility to
phospholipase C (PLC) , their
effects on the catalytic activities of
PI3K and PTEN against diC8PI and diC8PI-3-phosphate substrates, respectively, and their ability to induce the death of U937 human leukemic monocyte lymphoma cells
Liao et al., J Cell Physiol 2011
(Inflammation) :
In conclusion, MSF-2 opposes fMLP mediated neutrophil activation and inflammation by inhibiting
PI3K activation and subsequent
activation of AKT and
PLC?2
Cao et al., PLoS Biol 2013
(Angelman Syndrome) :
In Ube3A deficient mice, the BDNF induced recruitment of PSD-95, as well as PLC? and Grb2 associated binder 1 (Gab1) with TrkB receptors was attenuated, resulting in reduced activation of
PLC?-a-calcium/calmodulin dependent protein kinase II ( CaMKII ) and
PI3K-Akt , but leaving the extracellular signal regulated kinase ( Erk ) pathway intact
Schmid et al., PloS one 2013
(Inflammation...) :
We show here that
PI3K? activates
PLC? , leading to RasGrp/CalDAG-GEF-I & II mediated, Rap1a dependent activation of integrin a4ß1, extravasation of monocytes and granulocytes, and inflammation associated tumor progression ... Genetic depletion of
PLC? , CalDAG-GEFI or II, Rap1a, or the Rap1 effector RIAM was
sufficient to prevent integrin a4 activation by chemoattractants or activated
PI3K? ( p110?CAAX ), while activated Rap ( RapV12 ) promoted constitutive integrin activation and cell adhesion that could only be blocked by inhibition of RIAM or integrin a4ß1