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HSPG2 — NOS1
Text-mined interactions from Literome
Freye et al., Anasthesiol Intensivmed Notfallmed Schmerzther 2003
(Chronic Disease...) :
Another and more relevant mechanism of long-term opioid binding is that of subsequent protein kinase C ( PKC ),
phospholipase C (PLC) translocation and
activation of
nitric oxide synthetase (NOS)
Jaureguiberry et al., Peptides 2004
:
The stimulatory effect of ETs on
NOS activity was inhibited in the
presence of
PLC , PKC, PKA and CaMK-II inhibitors ( U-73122, GF-109203X, H-89 and KN-62, respectively ), and the IP3 receptor selective antagonist, 2-APB
Furlán et al., Cell Physiol Biochem 2005
:
In addition, the beta3 adrenoceptor dependent increase in cGMP and activation of
NOS were
blocked by the inhibition of
phospholipase C (PLC) , calcium/calmodulin (CaM), endothelial NOS activity and cGMP accumulation
Sterin-Borda et al., Int Endod J 2007
:
Inhibitors of
phospholipase C (PLC) , protein kinase C ( PKC ) and calcium/calmodulin (CaM)
prevented the pilocarpine dependent increase in n-nos and e-nos mRNA levels and
NOS activity