PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
11912240-11	2002	There is considerable evidence for a GDH shunt to return the carbon in amino acids back into reactions of carbon metabolism and the tri-carboxylic acid cycle.	Tricarboxylic Acids	132-151	glutamate dehydrogenase 1	Homo sapiens	37-40	
20194501-10	2010	Astrocytes and Sertoli cells are known to support neurons and germ cells, respectively, providing them with lactate that largely derives from the tricarboxylic acid cycle via conversion of glutamate to alpha-ketoglutarate (GDH reaction).	Tricarboxylic Acids	146-164	glutamate dehydrogenase 1	Homo sapiens	223-226	
20194501-11	2010	As hGDH2 is not subject to GTP control, the enzyme is able to metabolize glutamate even when the tricarboxylic acid cycle generates GTP amounts sufficient to inactivate the housekeeping hGDH1 protein.	Tricarboxylic Acids	97-115	glutamate dehydrogenase 1	Homo sapiens	186-191	
15273247-8	2004	We propose that GDH is one target of action of sulfite, leading to a decrease in alpha-ketoglutarate and a diminished flux through the tricarboxylic acid cycle accompanied by a decrease in NADH through the mitochondrial electron transport chain, a decreased MMP, and a decrease in ATP synthesis.	Tricarboxylic Acids	135-153	glutamate dehydrogenase 1	Homo sapiens	16-19	
23535601-5	2013	Whereas most cells use glutamate dehydrogenase (GLUD1) to convert glutamine-derived glutamate into alpha-ketoglutarate in the mitochondria to fuel the tricarboxylic acid cycle, PDAC relies on a distinct pathway in which glutamine-derived aspartate is transported into the cytoplasm where it can be converted into oxaloacetate by aspartate transaminase (GOT1).	Tricarboxylic Acids	151-169	glutamate dehydrogenase 1	Homo sapiens	48-53	
34829892-4	2021	GDH1 function may be relevant in cancer cells (or HCC) to drive the glutamine catabolism from L-glutamate towards the synthesis of alpha-ketoglutarate (alpha-KG), thus supplying key tricarboxylic acid cycle (TCA cycle) metabolites.	Tricarboxylic Acids	182-200	glutamate dehydrogenase 1	Homo sapiens	0-4	
28032919-1	2017	A key enzyme in brain glutamate homeostasis is glutamate dehydrogenase (GDH) which links carbohydrate and amino acid metabolism mediating glutamate degradation to CO2 and expanding tricarboxylic acid (TCA) cycle capacity with intermediates, i.e. anaplerosis.	Tricarboxylic Acids	181-199	glutamate dehydrogenase 1	Homo sapiens	47-70	
28032919-1	2017	A key enzyme in brain glutamate homeostasis is glutamate dehydrogenase (GDH) which links carbohydrate and amino acid metabolism mediating glutamate degradation to CO2 and expanding tricarboxylic acid (TCA) cycle capacity with intermediates, i.e. anaplerosis.	Tricarboxylic Acids	181-199	glutamate dehydrogenase 1	Homo sapiens	72-75	
28032919-1	2017	A key enzyme in brain glutamate homeostasis is glutamate dehydrogenase (GDH) which links carbohydrate and amino acid metabolism mediating glutamate degradation to CO2 and expanding tricarboxylic acid (TCA) cycle capacity with intermediates, i.e. anaplerosis.	Tricarboxylic Acids	201-204	glutamate dehydrogenase 1	Homo sapiens	47-70	
28032919-1	2017	A key enzyme in brain glutamate homeostasis is glutamate dehydrogenase (GDH) which links carbohydrate and amino acid metabolism mediating glutamate degradation to CO2 and expanding tricarboxylic acid (TCA) cycle capacity with intermediates, i.e. anaplerosis.	Tricarboxylic Acids	201-204	glutamate dehydrogenase 1	Homo sapiens	72-75	
28032919-0	2017	Expression of the human isoform of glutamate dehydrogenase, hGDH2, augments TCA cycle capacity and oxidative metabolism of glutamate during glucose deprivation in astrocytes.	Tricarboxylic Acids	76-79	glutamate dehydrogenase 1	Homo sapiens	35-58	
25220053-3	2014	Activation of the mTORC1 pathway has been shown previously to promote the anaplerotic entry of glutamine to the TCA cycle via GDH.	Tricarboxylic Acids	112-115	glutamate dehydrogenase 1	Homo sapiens	126-129