PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
12821717-4	2003	Here, we show that RANKL mRNA induction and ERK activation, when treated with synthetic lipid A (an active center of LPS), were markedly reduced in mouse osteoblasts lacking Cot/Tpl2, which was recently recognized as an essential kinase for the induction of TNF-alpha by LPS in macrophages.	Lipid A	88-95	mitogen-activated protein kinase 1	Mus musculus	44-47	
17496062-12	2007	MPO was also comparable in vehicle-treated or C3H/HeJ mice treated with LPS or lipid A at 6 and 24 h. Phospho-ERK activation was pronounced at 6 and 24 h after lipid A but not LPS treatment.	Lipid A	160-167	mitogen-activated protein kinase 1	Mus musculus	110-113	
17496062-13	2007	In vitro studies confirmed the relationship between phospho-ERK activation and cytokine expression in macrophage stimulated with either LPS or lipid A.	Lipid A	143-150	mitogen-activated protein kinase 1	Mus musculus	60-63	
17496062-14	2007	Compared with whole LPS, the lipid A fraction is associated with amplified whole lung MPO and ERK activation 6 h after intratracheal instillation in mice.	Lipid A	29-36	mitogen-activated protein kinase 1	Mus musculus	94-97	
10354505-9	1999	Although a monosaccharide lipid A analog, GLA-58, was able to stimulate macrophages to activate ERK proteins without cytokine production, pretreatment of macrophages with this compound suppressed both LPS-stimulated activation of ERK and cytokine production.	Lipid A	26-33	mitogen-activated protein kinase 1	Mus musculus	96-99	
31241993-2	2019	Pretreatment with the nontoxic immunomodulator monophosphoryl lipid A (MPLA) prevents inhibition by LPS through activation of a TLR4-TIR-domain-containing adaptor-inducing interferon-beta (TRIF)-phosphatidylinositol 3-kinase (PI3K) pathway that prevents LPS-induced ERK activation.	Lipid A	62-69	mitogen-activated protein kinase 1	Mus musculus	266-269