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CALML3 — NOS2

Pathways - manually collected, often from reviews:

• KEGG Calcium signaling pathway: CALM1/CALM2/CALM3/CALML3/CALML5/CALML6 → NOS1/NOS2/NOS3 (protein-protein, binding/association)

Text-mined interactions from Literome

Hauser et al., Shock 2001 (Sepsis) : CLP resulted in suppression of the pressor effect of norepinephrine ( NE ) in vivo ( measured by changes in blood pressure in response to NE boluses ) and ex vivo ( changes in contraction force in isolated mesenteric arteries in response to NE concentrations ), and in the expression of iNOS protein
Nishina et al., Anesth Analg 2001 (Respiration Disorders...) : CLP increased plasma nitrite/nitrate ( NOx ; stable NO metabolites ), and diaphragm malondialdehyde ( MDA ; a product of lipid peroxidation ), positive immunostaining for nitrotyrosine ( peroxynitrite footprint ), and iNOS activity
Eum et al., Nitric Oxide 2007 (Sepsis) : The level of iNOS and HO-1 mRNA expression were increased by CLP , which was prevented by both AG and L-NAME
Overhaus et al., Shock 2009 (Disease Models, Animal...) : Cecal ligation and puncture and simultaneous HS + CLP caused significant inflammatory messenger RNA induction of IL-6, iNOS , IL-10, and heme oxygenase 1 compared with control and HS, and these responses were significantly suppressed in HS + delayed CLP colonic muscularis extracts
Zhang et al., Exp Toxicol Pathol 2011 (Disease Models, Animal...) : Moreover, AS inhibited CLP induced the activation of mitogen activated protein kinases ( MAPKs ) and nuclear factor-?B ( NF-?B ), the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) protein in lung tissues, and the production of serum tumor necrosis factor ( TNF-a ) and interleukin-6 (IL-6)
Vromen et al., Shock 1996 (Shock, Septic) : CLP resulted in increased plasma nitrite/nitrate levels ( up to 59 microM at 24 h ) and increased pulmonary iNOS activity ( up to 71 fmoles/mg/min at 12 h ) and caused a significant vascular hyporeactivity at 18 h