PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28601556-6	2017	Mechanistically, we found that cannabidiol regulated melanogenesis by upregulating MITF through phosphorylation of p38 mitogen-activated protein kinase (MAPK) and p42/44 MAPK, independent of cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling.	Cannabidiol	31-42	mitogen-activated protein kinase 14	Homo sapiens	115-151	
34576119-8	2021	Application of CBD partially attenuated these effects of UVB irradiation both in healthy and psoriatic keratinocytes, reducing the levels of 15-d-PGJ2, p-p38 and caspase 8 while increasing Bcl2 expression.	Cannabidiol	15-18	mitogen-activated protein kinase 14	Homo sapiens	154-157	
32656944-7	2020	Mechanistically, cannabidiol-regulated osteoblastic differentiation in U2OS and MG-63 by strengthen the protein-protein interaction among RUNX2, OSX, or the phosphorylated p38 mitogen-activated protein kinase (MAPK).	Cannabidiol	17-28	mitogen-activated protein kinase 14	Homo sapiens	172-208	
29088769-4	2017	We emphasized three main aspects of signaling mechanisms induced by CBD treatment (alone or in combination with gamma-irradiation) in human GBM that govern cell death: 1) CBD significantly upregulated the active (phosphorylated) JNK1/2 and MAPK p38 levels with the subsequent downregulation of the active phospho-ERK1/2 and phospho-AKT1 levels.	Cannabidiol	68-71	mitogen-activated protein kinase 14	Homo sapiens	245-248	
29088769-5	2017	MAPK p38 was one of the main drivers of CBD-induced cell death, while death levels after combined treatment of CBD and radiation were dependent on both MAPK p38 and JNK.	Cannabidiol	40-43	mitogen-activated protein kinase 14	Homo sapiens	5-8	
29088769-5	2017	MAPK p38 was one of the main drivers of CBD-induced cell death, while death levels after combined treatment of CBD and radiation were dependent on both MAPK p38 and JNK.	Cannabidiol	111-114	mitogen-activated protein kinase 14	Homo sapiens	157-160