PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
23220724-3	2013	We hypothesize that aldosterone enhances O(2)(-) production in the MD mediated by protein kinase C (PKC), which buffers the effect of NO in control of TGF response.	Superoxides	41-45	protein kinase C, alpha	Mus musculus	100-103	
23220724-9	2013	To determine if PKC is involved in aldosterone-induced O(2)(-) production, we exposed the O(2)(-) cells to a nonselective PKC inhibitor chelerythrine chloride, a specific PKCalpha inhibitor Go6976, or a PKCalpha siRNA, and the aldosterone-induced increase in O(2)(-) production was blocked.	Superoxides	55-62	protein kinase C, alpha	Mus musculus	16-19	
23220724-9	2013	To determine if PKC is involved in aldosterone-induced O(2)(-) production, we exposed the O(2)(-) cells to a nonselective PKC inhibitor chelerythrine chloride, a specific PKCalpha inhibitor Go6976, or a PKCalpha siRNA, and the aldosterone-induced increase in O(2)(-) production was blocked.	Superoxides	55-59	protein kinase C, alpha	Mus musculus	16-19	
23220724-10	2013	These data indicate that aldosterone-stimulated O(2)(-) production in the MD buffers the effect of NO in control of TGF response, an effect that was mediated by PKCalpha.	Superoxides	48-52	protein kinase C, alpha	Mus musculus	161-169