PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19468685-4	2009	The IRE1/XBP1 branch of the UPR is activated by high dietary carbohydrates and controls the expression of genes involved in fatty acid and cholesterol biosynthesis.	Fatty Acids	124-134	X-box binding protein 1	Homo sapiens	9-13	
22023201-8	2012	Another recently identified pathway in IBD, namely endoplasmic stress/XBP1, regulates fatty acid synthesis and facilitates adipogenesis and adipocyte differentiataion.	Fatty Acids	86-96	X-box binding protein 1	Homo sapiens	70-74	
33277471-5	2020	Functionally, we show that Xbp1 ablation significantly reduces cellular membrane fluidity and impairs lipid homeostasis via rate-limiting metabolic processes in fatty acid monounsaturated and phospholipid remodeling pathways.	Fatty Acids	161-171	X-box binding protein 1	Homo sapiens	27-31	
30111834-7	2018	In addition, XBP1s abolished palmitate-induced insulin resistance in adipocytes by increasing adiponectin secretion, repressing the secretion of pro-inflammatory adipokines such as leptin, monocyte chemoattractant protein 1, and tumor necrosis factor alpha, and decreasing fatty acid release.	Fatty Acids	273-283	X-box binding protein 1	Homo sapiens	13-17	
19751410-2	2009	We have recently discovered that the transcription factor XBP1, best known as a key regulator of the unfolded protein response (UPR), is required for de novo fatty acid synthesis in the liver, a function unrelated to its role in the UPR.	Fatty Acids	158-168	X-box binding protein 1	Homo sapiens	58-62	
19751410-3	2009	(1) XBP1 protein expression is induced in the liver by a high carbohydrate diet and directly controls the induction of critical genes involved in fatty acid synthesis.	Fatty Acids	146-156	X-box binding protein 1	Homo sapiens	4-8	
19751410-8	2009	A more complete understanding of the mechanisms by which XBP1 accelerates de novo fatty acid synthesis in the liver while preserving normal hepatic lipid composition is highly relevant to the treatment of diseases such as atherosclerosis and metabolic syndrome that are associated with dyslipidemia.	Fatty Acids	82-92	X-box binding protein 1	Homo sapiens	57-61	
19751410-9	2009	Since excess fat accumulation in the liver could result from increased hepatic fatty acid synthesis, compounds that inhibit XBP1 activation may also be useful therapeutics for the treatment of human alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD), increasingly common causes of morbidity and mortality in the United States.	Fatty Acids	79-89	X-box binding protein 1	Homo sapiens	124-128