PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34601745-1	2022	BACKGROUND: The administration of L-glutamine (Gln) suppresses allergic airway inflammation via the rapid upregulation of MAPK phosphatase (MKP)-1, which functions as a negative regulator of inflammation by deactivating p38 and JNK mitogen-activated protein kinases (MAPKs).	Glutamine	34-45	dual specificity phosphatase 1	Mus musculus	122-146	
34601745-1	2022	BACKGROUND: The administration of L-glutamine (Gln) suppresses allergic airway inflammation via the rapid upregulation of MAPK phosphatase (MKP)-1, which functions as a negative regulator of inflammation by deactivating p38 and JNK mitogen-activated protein kinases (MAPKs).	Glutamine	47-50	dual specificity phosphatase 1	Mus musculus	122-146	
34601745-3	2022	Therefore, we investigated the mechanism by which endogenous Gln regulates MKP-1 induction and allergic airway inflammation in an ovalbumin-based murine asthma model.	Glutamine	61-64	dual specificity phosphatase 1	Mus musculus	75-80	
34601745-9	2022	Importantly, homeostatic MKP-1 induction did not occur at all, which resulted in prolonged p38 MAPK and cytosolic phospholipase A2 (cPLA2 ) phosphorylation in Gln-deficient mice.	Glutamine	159-162	dual specificity phosphatase 1	Mus musculus	25-30	
34601745-12	2022	CONCLUSION: Gln deficiency leads to the impairment of MKP-1 induction and activation of p38 MAPK and cPLA2 , resulting in the augmentation of neutrophilic, more so than eosinophilic, airway inflammation.	Glutamine	12-15	dual specificity phosphatase 1	Mus musculus	54-59