PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29269727-3	2017	Here, we show that palmitate-stimulated CD11b+F4/80low hepatic infiltrating macrophages, but not CD11b+F4/80high Kupffer cells, generate ROS via dynamin-mediated endocytosis of TLR4 and NOX2, independently from MyD88 and TRIF.	Palmitates	19-28	myeloid differentiation primary response gene 88	Mus musculus	211-216	
19666548-7	2009	Islets from mice deficient in IL-1beta or MyD88 challenged with glucose and palmitate in vitro also produced significantly less IL-6 and chemokines.	Palmitates	76-85	myeloid differentiation primary response gene 88	Mus musculus	42-47	
34953038-8	2022	Subsequently, it leads to inactivation of PA-caused myeloid differentiation factor 88 (MyD88)-dependent nuclear factor-kappaB (NF-kappaB) cascade.	Palmitates	42-44	myeloid differentiation primary response gene 88	Mus musculus	52-85	
34953038-8	2022	Subsequently, it leads to inactivation of PA-caused myeloid differentiation factor 88 (MyD88)-dependent nuclear factor-kappaB (NF-kappaB) cascade.	Palmitates	42-44	myeloid differentiation primary response gene 88	Mus musculus	87-92	
23968977-6	2013	We also found that palmitate induced the expression of proinflammatory genes via a novel toll-like receptor 4/myeloid differentiation primary response 88/nuclear factor-kappaB/NADPH oxidase 1/reactive oxygen species signaling pathway: nuclear factor-kappaB was activated by palmitate via toll-like receptor 4 and its adapter, MyD88, and once active, it transactivated Nox1, encoding NADPH oxidase 1, a major reactive oxygen species generator in SMCs.	Palmitates	19-28	myeloid differentiation primary response gene 88	Mus musculus	326-331	
23968977-8	2013	More importantly, Myd88 knockout mice were resistant to palmitate-induced exacerbation of neointima formation.	Palmitates	56-65	myeloid differentiation primary response gene 88	Mus musculus	18-23	
19808018-4	2009	Compared to control mice, MyD88(DeltaCNS) mice are protected from high-fat diet (HFD)-induced weight gain, from the development of HFD-induced leptin resistance, and from the induction of leptin resistance by acute central application of palmitate.	Palmitates	238-247	myeloid differentiation primary response gene 88	Mus musculus	26-31	
16798732-4	2006	Treatment with palmitate rapidly induced the association of myeloid differentiation factor 88 (MyD88) with the TLR2 receptor, activated the stress-linked kinases p38, JNK, and protein kinase C, induced degradation of IkappaBalpha, and increased NF-kappaB DNA binding.	Palmitates	15-24	myeloid differentiation primary response gene 88	Mus musculus	60-93	
16798732-4	2006	Treatment with palmitate rapidly induced the association of myeloid differentiation factor 88 (MyD88) with the TLR2 receptor, activated the stress-linked kinases p38, JNK, and protein kinase C, induced degradation of IkappaBalpha, and increased NF-kappaB DNA binding.	Palmitates	15-24	myeloid differentiation primary response gene 88	Mus musculus	95-100	
16798732-8	2006	RNA interference-mediated inhibition of TLR2 and MyD88 expression in C2C12 muscle cells resulted in a near complete inhibition of palmitate-induced insulin resistance and IL-6 production.	Palmitates	130-139	myeloid differentiation primary response gene 88	Mus musculus	49-54