PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
35362022-0	2022	Sphingolipid changes in Parkinson L444P GBA mutation fibroblasts promote alpha-synuclein aggregation.	Sphingolipids	0-12	glucosylceramidase beta	Homo sapiens	40-43	
34811369-8	2021	We then used the ratio of glucosylceramide to sphingomyelin (the GlcCer/SM ratio) to explore whether these two sphingolipid fractions altered in GBA-PD were useful for stratifying idiopathic PD patients.	Sphingolipids	111-123	glucosylceramidase beta	Homo sapiens	145-148	
34213307-1	2021	A major risk factor for Gaucher"s disease is loss of function mutations in the GBA1 gene that encodes lysosomal beta-glucocerebrosidase, resulting in accumulation of glucosylceramide (GlcCer), a key lysosomal sphingolipid.	Sphingolipids	209-221	glucosylceramidase beta	Homo sapiens	79-83	
35362022-16	2022	This treatment restored glucocerebrosidase activity and sphingolipid levels and composition of PD-GBA cells.	Sphingolipids	56-68	glucosylceramidase beta	Homo sapiens	98-101	
30315684-2	2019	In the biallelic state (homozygous or compound heterozygous) mutations in the glucocerebrosidase gene (GBA) may cause GD, in which glucosylceramide, the sphingolipid substrate of the glucocerebrosidase enzyme (GCase), accumulates in visceral organs leading to a number of clinical phenotypes.	Sphingolipids	153-165	glucosylceramidase beta	Homo sapiens	103-106	
28847804-3	2017	We propose that glucosylsphingosine, a sphingolipid accumulating in GD, mediates PD pathology in GBA-associated PD.	Sphingolipids	39-51	glucosylceramidase beta	Homo sapiens	97-100	
23118351-1	2013	Gaucher"s disease (GD) is caused by mutations in the GBA1 gene, which encodes acid-beta-glucosidase, an enzyme involved in the degradation of complex sphingolipids.	Sphingolipids	150-163	glucosylceramidase beta	Homo sapiens	53-57	
23118351-1	2013	Gaucher"s disease (GD) is caused by mutations in the GBA1 gene, which encodes acid-beta-glucosidase, an enzyme involved in the degradation of complex sphingolipids.	Sphingolipids	150-163	glucosylceramidase beta	Homo sapiens	78-99	
22337770-7	2012	These studies identified PI4KIIIbeta and PI4KIIalpha as important regulators of lysosomal delivery of GBA, revealing a new element of control to sphingolipid homeostasis by phosphoinositides.	Sphingolipids	145-157	glucosylceramidase beta	Homo sapiens	102-105	
25933391-11	2015	A significant increase and accumulation of several species for the lipid classes, ceramides and sphingolipids, was observed in LBD brains carrying GBA mutations compared to controls (p range: p<0.05-p<0.01).	Sphingolipids	96-109	glucosylceramidase beta	Homo sapiens	147-150	
21221911-1	2010	Gaucher disease is a genetic disorder of sphingolipid metabolism resulting from dysfunction of the lysosomal membrane-associated glycoprotein glucocerebrosidase (GBA) and resulting in intracellular accumulation of glucosylceramide and other glycolipids.	Sphingolipids	41-53	glucosylceramidase beta	Homo sapiens	162-165	
19374450-1	2009	Human lysosomal enzymes acid-beta-glucosidase (GCase) and acid-alpha-galactosidase (alpha-Gal A) hydrolyze the sphingolipids glucosyl- and globotriaosylceramide, respectively, and mutations in these enzymes lead to the lipid metabolism disorders Gaucher and Fabry disease, respectively.	Sphingolipids	111-124	glucosylceramidase beta	Homo sapiens	24-45	
19374450-1	2009	Human lysosomal enzymes acid-beta-glucosidase (GCase) and acid-alpha-galactosidase (alpha-Gal A) hydrolyze the sphingolipids glucosyl- and globotriaosylceramide, respectively, and mutations in these enzymes lead to the lipid metabolism disorders Gaucher and Fabry disease, respectively.	Sphingolipids	111-124	glucosylceramidase beta	Homo sapiens	47-52