PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28587938-11	2017	Furthermore, etidronate inhibited the translocation of NF-kappaB but not p38 MAPK in J774.1 cells stimulated with Pam3CSK4 or lipid A.	Lipid A	126-133	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	55-64	
26235132-7	2015	Moreover, the RNA interference (RNAi) of NFkappaB suppressed the expression of iNOS induced by lipid A.	Lipid A	95-102	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	41-49	
26235132-8	2015	We demonstrated that lipid A-induced iNOS expression in ECPC-4 cells was mainly regulated by the activation of NFkappaB-IkappaB intracellular signaling pathway.	Lipid A	21-28	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	111-119	
21152039-0	2010	ATF3 plays a key role in Kdo2-lipid A-induced TLR4-dependent gene expression via NF-kappaB activation.	Lipid A	30-37	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	81-90	
14529784-2	2003	This study examines whether lipid A may directly modulate the radioresponse of tumor cells by activating inducible nitric oxide synthase (iNOS) or cyclooxygenase-2 (COX-2) through nuclear factor-kappaB (NF-kappaB) signaling.	Lipid A	28-35	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	180-201	
14529784-2	2003	This study examines whether lipid A may directly modulate the radioresponse of tumor cells by activating inducible nitric oxide synthase (iNOS) or cyclooxygenase-2 (COX-2) through nuclear factor-kappaB (NF-kappaB) signaling.	Lipid A	28-35	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	203-212	
12717385-8	2003	Lipid A induces NF-kappaB activation in HSCs from TLR4-sufficient (C3H/OuJ) mice but not from TLR4-deficient (C3H/HeJ) mice.	Lipid A	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	16-25	
10064907-9	1999	LPS stimulation of p38 phosphorylation, NF-kappaB activation, and surface IgM expression were all blocked completely by lipid A-like endotoxin antagonists whether or not CD14 was present.	Lipid A	120-127	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	40-49	
10064907-11	1999	Our data support the hypothesis that lipid A-mediated activation of cells requires stimulation of a putative lipid A sensor that is downstream of CD14, but upstream of p38 and NF-kappaB.	Lipid A	37-44	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	176-185	
25837580-7	2015	The afterglow exposure also results in a reduction of the lipid A proinflammatory activity, assessed by the net decrease of the redox-sensitive NFkappaB transcription factor nuclear translocation in murine aortic endothelial cells stimulated with control vs afterglow-treated (pure and extracted) lipid A.	Lipid A	58-65	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	144-152	
24686069-6	2014	We also demonstrated that lptA mutant bacteria were more susceptible to human and murine cathelicidins due to increased binding by these peptides and that the differential induction of NF-kappaB by wild-type and unmodified lipid A was more pronounced in the presence of CAMPs.	Lipid A	223-230	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	185-194