The Utilization of Extracellular Proteins as Nutrients Is Suppressed by mTORC1.
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Novel drugs that target the metabolic reprogramming in renal cell cancerFundamentals of cancer metabolismAmino Acid Sensing by mTORC1: Intracellular Transporters Mark the SpotKRAS Mutant Pancreatic Cancer: No Lone Path to an Effective TreatmentGenetics and biology of pancreatic ductal adenocarcinomaLipid metabolic reprogramming in cancer cellsGrowth factor signaling to mTORC1 by amino acid-laden macropinosomes.Macropinocytosis Exploitation by Cancers and Cancer TherapeuticsThe Mechanistic Target of Rapamycin: The Grand ConducTOR of Metabolism and AgingTargeting carbonic anhydrase IX improves the anti-cancer efficacy of mTOR inhibitorsStarved epithelial cells uptake extracellular matrix for survival.From Krebs to clinic: glutamine metabolism to cancer therapy.Autophagic Mechanism in Anti-Cancer Immunity: Its Pros and Cons for Cancer Therapy.Collagen-derived proline promotes pancreatic ductal adenocarcinoma cell survival under nutrient limited conditions.Attacking the supply wagons to starve cancer cells to death.mTORC1 maintains metabolic balance.The Hippo pathway effectors YAP and TAZ promote cell growth by modulating amino acid signaling to mTORC1.Cancer's Fuel Choice: New Flavors for a Picky EaterThe Emerging Hallmarks of Cancer MetabolismCatabolic pathways regulated by mTORC1 are pivotal for survival and growth of cancer cells expressing mutant Ras.Cathepsin B modulates lysosomal biogenesis and host defense against Francisella novicida infection.Coordinate regulation of autophagy and the ubiquitin proteasome system by MTOR.Targeting cancer metabolism by simultaneously disrupting parallel nutrient access pathways.MicroRNAs-103/107 coordinately regulate macropinocytosis and autophagy.mTORC1 inhibition in cancer cells protects from glutaminolysis-mediated apoptosis during nutrient limitationResistance to mTORC1 Inhibitors in Cancer Therapy: From Kinase Mutations to Intratumoral Heterogeneity of Kinase ActivityGlutamine at focus: versatile roles in cancer.Glutamine fuels proliferation but not migration of endothelial cells.Targeting metabolic reprogramming in KRAS-driven cancers.Direct evidence for cancer-cell-autonomous extracellular protein catabolism in pancreatic tumors.PIKfyve Regulates Vacuole Maturation and Nutrient Recovery following Engulfment.mTOR Signaling in Growth, Metabolism, and Disease.Hypoxia and cellular metabolism in tumour pathophysiology.O-GlcNAcylation in Cancer Biology: Linking Metabolism and Signaling.Metabolic scavenging by cancer cells: when the going gets tough, the tough keep eating.mTORC1 and mTORC2 in cancer and the tumor microenvironment.PLK1 (polo like kinase 1) inhibits MTOR complex 1 and promotes autophagy.Understanding the Intersections between Metabolism and Cancer Biology.Glutamine Metabolism in Cancer: Understanding the Heterogeneity.mTORC1 signaling and the metabolic control of cell growth.
P2860
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P2860
The Utilization of Extracellular Proteins as Nutrients Is Suppressed by mTORC1.
description
2015 nî lūn-bûn
@nan
2015年の論文
@ja
2015年論文
@yue
2015年論文
@zh-hant
2015年論文
@zh-hk
2015年論文
@zh-mo
2015年論文
@zh-tw
2015年论文
@wuu
2015年论文
@zh
2015年论文
@zh-cn
name
The Utilization of Extracellular Proteins as Nutrients Is Suppressed by mTORC1.
@en
type
label
The Utilization of Extracellular Proteins as Nutrients Is Suppressed by mTORC1.
@en
prefLabel
The Utilization of Extracellular Proteins as Nutrients Is Suppressed by mTORC1.
@en
P2093
P2860
P1433
P1476
The Utilization of Extracellular Proteins as Nutrients Is Suppressed by mTORC1
@en
P2093
Craig B Thompson
Kevin Wright
Wilhelm Palm
Youngkyu Park
P2860
P304
P356
10.1016/J.CELL.2015.06.017
P407
P577
2015-07-02T00:00:00Z