◀ Back to NOS2
NOS2 — SYT1
Text-mined interactions from Literome
Nakashima et al., J Am Soc Nephrol 1999
:
It can be concluded that ( 1 )
iNOS can be induced without active NF-kappaB ; ( 2 ) Dex, acetylsalicylic acid, and PDTC
inhibit only
p65 ; and ( 3 ) JAK2 is involved in iNOS induction, and the contribution of JAK2 to nitrite production is greater than that of NF-kappaB
Teng et al., Gen Pharmacol 2000
:
In conclusion, a p50 and
p65 NF-kappaB heterodimer binds to a reverse-NF-kappaB site on the rat iNOS promoter and
contributes to
iNOS induction by IL-1beta and IFN-gamma in RASMCs
Majano et al., Hepatology 2001
:
In conclusion, cytoplasmic location of HBx protein is essential for the transcriptional
activation of the
iNOS gene through the nuclear translocation of
p50-p65 heterodimers
Qi et al., Microsurgery 2004
(Reperfusion Injury) :
NF-kappaB
p65 involves in reperfusion injury and
iNOS gene regulation in skeletal muscle
Shih et al., Stroke 2006
(Subarachnoid Hemorrhage) :
E ( 2 )
inhibits the SAH induced increase of
iNOS by increasing the association of
p65/ER , which in turn inhibits the binding of p65 to iNOS DNA
Saha et al., J Immunol 2007
(Inflammation) :
The combination of IL-1beta and IFN-gamma, previously shown to strongly
induce inducible NO synthase in human primary astrocytes, induced p38 dependent phosphorylation of acetyltransferase coactivator p300, but not p65, and subsequent association of p300 with
p65
Bhaskaran et al., Int J Mol Med 2010
:
Chamomile : an anti-inflammatory agent
inhibits inducible
nitric oxide synthase expression by blocking
RelA/p65 activity ... These results demonstrate that chamomile
inhibits NO production and
iNOS gene expression by inhibiting
RelA/p65 activation and supports the utilization of chamomile as an effective anti-inflammatory agent