PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34320345-4	2021	Agxt deletion in apolipoprotein E-deficient (Apoe-/-) mice decreases the glycine/oxalate ratio and increases atherosclerosis with induction of hepatic pro-atherogenic pathways, predominantly cytokine/chemokine signaling and dysregulated redox homeostasis.	Oxalates	81-88	alanine-glyoxylate aminotransferase	Mus musculus	0-4	
34433051-3	2021	Downregulation and hypermethylation of alanine-glyoxylate aminotransferase (Agxt), which detoxifies glyoxylate, preventing excessive oxalate accumulation, is accompanied by increased oxalate formation after metabolism of the precursor hydroxyproline.	Oxalates	133-140	alanine-glyoxylate aminotransferase	Mus musculus	76-80	
34433051-4	2021	Viral-mediated Agxt transfer or inhibiting hydroxyproline catabolism rescues excessive oxalate release.	Oxalates	87-94	alanine-glyoxylate aminotransferase	Mus musculus	15-19	
34320345-8	2021	Conversely, AGXT overexpression in Apoe-/- mice increases the glycine/oxalate ratio and decreases aortic superoxide, CCL5, and atherosclerosis.	Oxalates	70-77	alanine-glyoxylate aminotransferase	Mus musculus	12-16	
30676254-2	2019	Loss of alanine glyoxylate aminotransferase (AGT) function to convert intermediate metabolite glyoxylate to glycine causes the accumulation and reduction of glyoxylate to glycolate, which eventually is oxidized to oxalate.	Oxalates	214-221	alanine-glyoxylate aminotransferase	Mus musculus	8-43	
34267881-5	2021	Dual inhibitor 7 demonstrated an IC50 of 88 nM for oxalate reduction in an Agxt-knockdown mouse hepatocyte assay.	Oxalates	51-58	alanine-glyoxylate aminotransferase	Mus musculus	75-79	
33002578-2	2021	Alanine glyoxylate aminotransferase (AGT), deficient in PH type 1, is a key enzyme in limiting glyoxylate oxidation to oxalate.	Oxalates	119-126	alanine-glyoxylate aminotransferase	Mus musculus	0-35	
33002578-2	2021	Alanine glyoxylate aminotransferase (AGT), deficient in PH type 1, is a key enzyme in limiting glyoxylate oxidation to oxalate.	Oxalates	119-126	alanine-glyoxylate aminotransferase	Mus musculus	37-40	
30676254-2	2019	Loss of alanine glyoxylate aminotransferase (AGT) function to convert intermediate metabolite glyoxylate to glycine causes the accumulation and reduction of glyoxylate to glycolate, which eventually is oxidized to oxalate.	Oxalates	214-221	alanine-glyoxylate aminotransferase	Mus musculus	45-48	
30676254-9	2019	Repeat dosing in Agxt-/- mice resulted in a 40% reduction in urinary oxalate, suggesting therapeutic benefit.	Oxalates	69-76	alanine-glyoxylate aminotransferase	Mus musculus	17-21	
30676254-10	2019	These studies suggest that mRNA encoding AGT led to increased expression and activity of the AGT enzyme in liver that translated into decrease in urinary oxalate levels.	Oxalates	154-161	alanine-glyoxylate aminotransferase	Mus musculus	41-44	
30676254-10	2019	These studies suggest that mRNA encoding AGT led to increased expression and activity of the AGT enzyme in liver that translated into decrease in urinary oxalate levels.	Oxalates	154-161	alanine-glyoxylate aminotransferase	Mus musculus	93-96	
26689264-5	2016	Next, we produced double KO mice (Agxt1(-/-) Hao1(-/-)) that showed low levels of oxalate excretion compared with hyperoxaluric mice model (Agxt1(-/-)).	Oxalates	82-89	alanine-glyoxylate aminotransferase	Mus musculus	34-39	
18698135-2	2009	We tested an oral therapy with a crystalline, cross-linked formulation of oxalate-decarboxylase (OxDc-CLEC) on the reduction of urinary oxalate and decrease in the severity of kidney injury in two models: AGT1 knockout mice (AGT1KO) in which hyperoxaluria is the result of an Agxt gene deficiency, and in AGT1KO mice challenged with ethylene glycol (EG).	Oxalates	74-81	alanine-glyoxylate aminotransferase	Mus musculus	205-209	
18475180-9	2008	RESULTS: The procedure resulted in progressive replacement of the mutant host hepatocytes with the AGT-competent hepatocytes, leading to correction of urinary oxalate excretion.	Oxalates	159-166	alanine-glyoxylate aminotransferase	Mus musculus	99-102	
21163900-7	2011	Our results demonstrate that the cecum and distal colon contribute significantly to enteric oxalate excretion in Oxalobacter-colonized Agxt and WT mice.	Oxalates	92-99	alanine-glyoxylate aminotransferase	Mus musculus	135-139	
21163900-8	2011	In colonized Agxt mice, urinary oxalate excretion was reduced 50% (to within the normal range observed for WT mice).	Oxalates	32-39	alanine-glyoxylate aminotransferase	Mus musculus	13-17	
21163900-9	2011	Moreover, plasma oxalate concentrations in Agxt mice were also normalized (reduced 50%).	Oxalates	17-24	alanine-glyoxylate aminotransferase	Mus musculus	43-47	
17110443-1	2006	Mutations in the alanine-glyoxylate amino transferase gene (AGXT) are responsible for primary hyperoxaluria type I, a rare disease characterized by excessive hepatic oxalate production that leads to renal failure.	Oxalates	166-173	alanine-glyoxylate aminotransferase	Mus musculus	60-64