Results 61 to 70 of about 102,812 (293)

TARDBP/TDP-43 regulates autophagy in both MTORC1-dependent and MTORC1-independent manners [PDF]

open access: yesAutophagy, 2016
In a recent paper we addressed the mechanism by which defective autophagy contributes to TARDBP/TDP-43-mediated neurodegenerative disorders. We demonstrated that TARDBP regulates MTORC1-TFEB signaling by targeting RPTOR/raptor, a key component and an adaptor protein of MTORC1.
Zheng, Ying   +6 more
openaire   +2 more sources

Research advances of cell autophagy in focal segmental glomerulosclerosis

open access: yesLinchuang shenzangbing zazhi
As a clinical pathological syndrome, focal segmental glomerulosclerosis (FSGS) is characterized by focal glomerulosclerosis, disappearance of podocyte processes and massive proteinuria. Current researches have confirmed that foot cell injury is a central
Min Zhang, Yan Mi, Cai-li Wang
doaj   +1 more source

mTOR hyperactivity mediates lysosomal dysfunction in Gaucher's disease iPSC-neuronal cells

open access: yesDisease Models & Mechanisms, 2019
Bi-allelic GBA1 mutations cause Gaucher's disease (GD), the most common lysosomal storage disorder. Neuronopathic manifestations in GD include neurodegeneration, which can be severe and rapidly progressive.
Robert A. Brown   +8 more
doaj   +1 more source

Influenza virus differentially activates mTORC1 and mTORC2 signaling to maximize late stage replication. [PDF]

open access: yesPLoS Pathogens, 2017
Influenza A virus usurps host signaling factors to regulate its replication. One example is mTOR, a cellular regulator of protein synthesis, growth and motility.
Sharon K Kuss-Duerkop   +13 more
doaj   +1 more source

Bipartite binding and partial inhibition links DEPTOR and mTOR in a mutually antagonistic embrace

open access: yeseLife, 2021
The mTORC1 kinase complex regulates cell growth, proliferation, and survival. Because mis-regulation of DEPTOR, an endogenous mTORC1 inhibitor, is associated with some cancers, we reconstituted mTORC1 with DEPTOR to understand its function.
Maren Heimhalt   +15 more
doaj   +1 more source

Mammalian EAK-7 activates alternative mTOR signaling to regulate cell proliferation and migration. [PDF]

open access: yes, 2018
Nematode EAK-7 (enhancer-of-akt-1-7) regulates dauer formation and controls life span; however, the function of the human ortholog mammalian EAK-7 (mEAK-7) is unknown.
Fox, Alexandra Lucienne   +5 more
core   +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

Folliculin promotes substrate-selective mTORC1 activity by activating RagC to recruit TFE3.

open access: yesPLoS Biology, 2022
Mechanistic target of rapamycin complex I (mTORC1) is central to cellular metabolic regulation. mTORC1 phosphorylates a myriad of substrates, but how different substrate specificity is conferred on mTORC1 by different conditions remains poorly defined ...
Kristina Li   +5 more
doaj   +1 more source

Dual targeting of RET and SRC synergizes in RET fusion‐positive cancer cells

open access: yesMolecular Oncology, EarlyView.
Despite the strong activity of selective RET tyrosine kinase inhibitors (TKIs), resistance of RET fusion‐positive (RET+) lung cancer and thyroid cancer frequently occurs and is mainly driven by RET‐independent bypass mechanisms. Son et al. show that SRC TKIs significantly inhibit PAK and AKT survival signaling and enhance the efficacy of RET TKIs in ...
Juhyeon Son   +13 more
wiley   +1 more source

The yin yang of sunitinib: One drug, two doses, and multiple outcomes

open access: yesMolecular & Cellular Oncology, 2017
Our recent work showed that sunitinib exerts dual effect on cancer cells in different dose ranges. In clinically relevant doses, cancer cells tolerate sunitinb cytotoxicity by upregulating pro-survival MCL-1 and activating mTORC1 signaling. Inhibition of
Mohamed Elgendy
doaj   +1 more source

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