PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19275680-4	2009	Patients with insulin resistance and/or type 2 diabetes have high levels of plasma free fatty acids, inflammatory cytokines, and/or glucose, and over-activation of the cardiovascular renin-angiotensin system, all are capable of activating p38 MAPK.	Fatty Acids, Nonesterified	83-99	mitogen-activated protein kinase 14	Homo sapiens	239-242	
16803882-0	2006	p38 Mitogen-activated protein kinase mediates free fatty acid-induced gluconeogenesis in hepatocytes.	Fatty Acids, Nonesterified	46-61	mitogen-activated protein kinase 14	Homo sapiens	0-3	
34118488-10	2021	Notably, inhibition of p38 mitogen-activated protein kinase (MAPK) could block YAP activation in FFA-treated Huh7 cells.	Fatty Acids, Nonesterified	97-100	mitogen-activated protein kinase 14	Homo sapiens	23-59	
17384440-2	2007	We have recently reported that FFA can induce gluconeogenesis in hepatocytes through p38 mitogen-activated protein kinase (p38).	Fatty Acids, Nonesterified	31-34	mitogen-activated protein kinase 14	Homo sapiens	85-88	
17384440-2	2007	We have recently reported that FFA can induce gluconeogenesis in hepatocytes through p38 mitogen-activated protein kinase (p38).	Fatty Acids, Nonesterified	31-34	mitogen-activated protein kinase 14	Homo sapiens	123-126	
12372842-4	2002	Thus, we propose a unifying hypothesis whereby hyperglycemia and FFA-induced activation of the nuclear factor-kappaB, p38 MAPK, and NH2-terminal Jun kinases/stress-activated protein kinases stress pathways, along with the activation of the advanced glycosylation end-products/receptor for advanced glycosylation end-products, protein kinase C, and sorbitol stress pathways, plays a key role in causing late complications in type 1 and type 2 diabetes, along with insulin resistance and impaired insulin secretion in type 2 diabetes.	Fatty Acids, Nonesterified	65-68	mitogen-activated protein kinase 14	Homo sapiens	118-121