PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26213322-9	2015	Of importance, RT-PCR and Western blotting demonstrated that high glucose inhibited DNA-damage-inducible transcript 4 (DDIT4) and TSC1/TSC2, up-regulated Rheb/mTOR/p70S6K and enhanced expression of the apoptosis regulating proteins, such as phospho-Bcl-2, cytochrome C and cleaved caspase.	Glucose	66-73	TSC complex subunit 1	Homo sapiens	130-134	
27362797-2	2016	We previously showed that constitutive activation of the mammalian target of rapamycin complex 1 (mTORC1), by loss of its negative regulator the tuberous sclerosis complex protein 1 (Tsc1; also known as Hamartin), was sufficient to promote robust survival of nutrient-stressed cones in two mouse models of RP by improving glucose uptake and utilization.	Glucose	322-329	TSC complex subunit 1	Homo sapiens	183-187	
27362797-2	2016	We previously showed that constitutive activation of the mammalian target of rapamycin complex 1 (mTORC1), by loss of its negative regulator the tuberous sclerosis complex protein 1 (Tsc1; also known as Hamartin), was sufficient to promote robust survival of nutrient-stressed cones in two mouse models of RP by improving glucose uptake and utilization.	Glucose	322-329	TSC complex subunit 1	Homo sapiens	203-211	
22544327-8	2012	Herein, we also demonstrate that deletion of Tsc1 in pancreatic beta cells results in improved glucose tolerance, hyperinsulinemia and expansion of beta-cell mass that persists with aging.	Glucose	95-102	TSC complex subunit 1	Homo sapiens	45-49	
25298408-3	2015	In TSC-deficient cells, metabolic wiring is extensively disrupted and rerouted as a consequence of mTORC1 hyperactivation, leading to multiple vulnerabilities, including "addiction" to glutamine, glucose, and autophagy.	Glucose	196-203	TSC complex subunit 1	Homo sapiens	3-6	
23142078-2	2013	We show that glucose and glutamine, by supplying carbons to the TCA cycle to produce ATP, positively feed back to mTORC1 through an AMPK-, TSC1/2-, and Rag-independent mechanism by regulating mTORC1 assembly and its lysosomal localization.	Glucose	13-20	TSC complex subunit 1	Homo sapiens	139-143	
24275666-6	2014	Interestingly, glucose starvation-induced autophagy, but not amino acid starvation-induced autophagy, was increased significantly in Tsc1-null tumor cells.	Glucose	15-22	TSC complex subunit 1	Homo sapiens	133-137	
22018140-2	2011	For example, in tuberous sclerosis complex (TSC)-related tumors, the loss of TSC1/2 function causes constitutive mTORC1 activity, which stimulates glycolysis, resulting in glucose addiction in vitro.	Glucose	172-179	TSC complex subunit 1	Homo sapiens	44-47	
22018140-2	2011	For example, in tuberous sclerosis complex (TSC)-related tumors, the loss of TSC1/2 function causes constitutive mTORC1 activity, which stimulates glycolysis, resulting in glucose addiction in vitro.	Glucose	172-179	TSC complex subunit 1	Homo sapiens	77-83	
31235817-4	2019	In this study, we investigated the effects of TSC1 on high glucose (HG)-induced EMT of human proximal tubular epithelial HK-2 cells in vitro and renal fibrosis in TSC1-/- and db/db mice.	Glucose	59-66	TSC complex subunit 1	Homo sapiens	46-50	
31761686-6	2019	As TSC is potentially caused by a disruption of the mechanistic target of rapamycin (mTOR) pathway, a main integrator of metabolic information and intracellular signaling, we aimed to examine the impact of different glucose concentrations in the culture media on cellular phenotypes implicated in tuber characteristics.	Glucose	216-223	TSC complex subunit 1	Homo sapiens	3-6	
20427478-0	2010	Role of the TSC1-TSC2 complex in the integration of insulin and glucose signaling involved in pancreatic beta-cell proliferation.	Glucose	64-71	TSC complex subunit 1	Homo sapiens	12-16	
20513425-3	2010	Thus, TSC1/2-/- cells are hypersensitive to glucose deprivation, and this has been linked to increased p53 translation and activation of apoptosis.	Glucose	44-51	TSC complex subunit 1	Homo sapiens	6-10