Results 21 to 30 of about 66,391 (264)

Spatiotemporal feedforward between PKM2 tetramers and mTORC1 prompts mTORC1 activation

open access: yesPhysical Biology, 2022
Abstract Most mammalian cells couple glucose availability to anabolic processes via the mTORC1 pathway. However, the mechanism by which fluctuations in glucose availability are rapidly translated into mTORC1 signals remains elusive. Here, we show that cells rapidly respond to changes in glucose availability through the spatial coupling ...
Yu Xia   +3 more
openaire   +2 more sources

PIP4kγ is a substrate for mTORC1 that maintains basal mTORC1 signaling during starvation [PDF]

open access: yesScience Signaling, 2014
A feedback loop involving PIP4kγ and mTORC1 maintains basal mTORC1 activity under nutrient-deprived conditions.
Ashley M, Mackey   +4 more
openaire   +2 more sources

mTORC1 as the main gateway to autophagy [PDF]

open access: yesEssays in Biochemistry, 2017
Cells and organisms must coordinate their metabolic activity with changes in their environment to ensure their growth only when conditions are favourable. In order to maintain cellular homoeostasis, a tight regulation between the synthesis and degradation of cellular components is essential.
Rabanal-Ruiz, Yoana   +2 more
openaire   +2 more sources

Rapamycin inhibits mTORC1, but not completely [PDF]

open access: yesAutophagy, 2009
Rapamycin is widely used as a complete inhibitor of the mTORC1 nutrient-sensitive signaling complex. Using a novel ATP-competitive inhibitor named Torin1, we have found that many mTORC1 functions that regulate cap-dependent translation and autophagy are resistant to inhibition by rapamycin.
Thoreen, Carson C, Sabatini, David
openaire   +4 more sources

PIKFYVE-dependent regulation of MTORC1 and TFEB

open access: yesAutophagy Reports, 2022
TFEB (transcription factor EB) is essential for the upregulation of gene expression required for macroautophagy/autophagy and lysosomal function. Under nutrient-rich conditions, TFEB is inactivated by MTOR (mechanistic target of rapamycin kinase) complex
Junya Hasegawa   +2 more
doaj   +1 more source

p38 regulates the tumor suppressor PDCD4 via the TSC-mTORC1 pathway

open access: yesCell Stress, 2021
Programmed cell death protein 4 (PDCD4) exerts critical functions as tumor suppressor and in immune cells to regulate inflammatory pro-cesses. The phosphoinositide 3-kinase (PI3K) promotes degradation of PDCD4 via mammalian target of rapamycin complex 1 (
Clarissa Braun   +6 more
doaj   +1 more source

p16: cycling off the beaten path

open access: yesMolecular & Cellular Oncology, 2019
p16INK4A (hereafter called p16) is a faithful cellular ally in the fight against tumorigenesis. Although its canonical pathway through retinoblastoma (RB) is well delineated, RB-independent functions for p16 are beginning to emerge. Here we summarize non-
Raquel Buj, Katherine M. Aird
doaj   +1 more source

A Novel Combination Therapy Approach Targeting STAT3 and Autophagy in Glioblastoma

open access: yesAutophagy Reports, 2022
The aggressive brain cancer glioblastoma (GBM) is notoriously resistant to radiotherapy and chemotherapy, which drives tumor recurrence and relapse. GBM cells are highly addicted to STAT3 (signal transducer and activator of transcription 3) and STAT3 ...
Sujoy Bhattacharya   +2 more
doaj   +1 more source

Nutrient regulation of mTORC1 at a glance [PDF]

open access: yesJournal of Cell Science, 2019
ABSTRACT The mechanistic target of rapamycin (mTOR) signaling pathway coordinates environmental and intracellular cues to control eukaryotic cell growth. As a pivot point between anabolic and catabolic processes, mTOR complex 1 (mTORC1) signaling has established roles in regulating metabolism, translation and autophagy.
Kendall J. Condon, David M. Sabatini
openaire   +2 more sources

Autophagy Function and Regulation in Kidney Disease

open access: yesBiomolecules, 2020
Autophagy is a dynamic process by which intracellular damaged macromolecules and organelles are degraded and recycled for the synthesis of new cellular components.
Gur P. Kaushal   +3 more
doaj   +1 more source

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