Results 71 to 80 of about 66,500 (291)

PRAS40 suppresses atherogenesis through inhibition of mTORC1-dependent pro-inflammatory signaling in endothelial cells [PDF]

open access: yes, 2019
Endothelial pro-inflammatory activation plays a pivotal role in atherosclerosis, and many pro-inflammatory and atherogenic signals converge upon mechanistic target of rapamycin (mTOR).
Althoff, Till F.   +14 more
core   +1 more source

RhoA regulates the mechanistic target of rapamycin complex 1 (mTORC1)

open access: yesThe FASEB Journal, 2013
The mTORC1 signaling pathway plays a vital role in integrating signals generated by hormones and nutrients to control cell growth and metabolism. The point of integration of many of the input signals from hormones is the GTPase activating protein complex TSC1/2 that acts to repress the mTORC1‐stimulatory activity of the small GTPase Rheb.
Bradley S. Gordon   +5 more
openaire   +1 more source

Thioredoxin-1 maintains mechanistic target of rapamycin (mTOR) function during oxidative stress in cardiomyocytes [PDF]

open access: yes, 2017
Thioredoxin 1 (Trx1) is a 12-kDa oxidoreductase that catalyzes thiol-disulfide exchange reactions to reduce proteins with disulfide bonds. As such, Trx1 helps protect the heart against stresses, such as ischemia and pressure overload.
Bhat, Santosh   +16 more
core   +1 more source

The crosstalk between MYC and mTORC1 during osteoclastogenesis

open access: yesFrontiers in Cell and Developmental Biology, 2022
Osteoclasts are bone-resorbing cells that undergo extensive changes in morphology throughout their differentiation. Altered osteoclast differentiation and activity lead to changes in pathological bone resorption.
Seyeon Bae   +10 more
doaj   +1 more source

Loss of ATF3 exacerbates liver damage through the activation of mTOR/p70S6K/ HIF-1α signaling pathway in liver inflammatory injury. [PDF]

open access: yes, 2018
Activating transcription factor 3 (ATF3) is a stress-induced transcription factor that plays important roles in regulating immune and metabolic homeostasis.
Jiang, Bin   +9 more
core   +2 more sources

Targeting carbonic anhydrase IX improves the anti-cancer efficacy of mTOR inhibitors. [PDF]

open access: yes, 2016
The inhibition of the mechanistic target of rapamycin complex 1 (mTORC1) by chemical inhibitors, such as rapamycin, has demonstrated anti-cancer activity in preclinical and clinical trials.
Datta, D.   +11 more
core   +1 more source

Insights from yeast into whether the rapamycin inhibition of heat shock transcription factor (Hsf1) can prevent the Hsf1 activation that results from treatment with an Hsp90 inhibitor [PDF]

open access: yes, 2014
In human cells TORC1 mTOR (target of rapamycin) protein kinase complex renders heat shock transcription factor 1 (Hsf1) competent for stress activation. In such cells, as well as in yeast, the selective TORC1 inhibitor rapamycin blocks this activation in
Atkins   +51 more
core   +3 more sources

Identification of regions critical for the integrity of the TSC1-TSC2-TBC1D7 complex [PDF]

open access: yes, 2014
The TSC1-TSC2-TBC1D7 complex is an important negative regulator of the mechanistic target of rapamycin complex 1 that controls cell growth in response to environmental cues.
Halley, D.J.J. (Dicky)   +7 more
core   +1 more source

Insulin potentiates essential amino acids effects on mechanistic target of rapamycin complex 1 signaling in MAC-T cells [PDF]

open access: yesJournal of Dairy Science, 2020
Different models of lactation offer conflicting evidence as to whether insulin signaling is required for AA to stimulate mechanistic target of rapamycin complex 1 (mTORC1) activity. We hypothesized that insulin potentiates essential AA stimulation of mTORC1 activity in the MAC-T mammary epithelial cell line.
Virginia L. Pszczolkowski   +6 more
openaire   +2 more sources

Deletion of Tsc2 in nociceptors reduces target innervation, ion channel expression, and sensitivity to heat [PDF]

open access: yes, 2018
The mechanistic target of rapamycin complex 1 (mTORC1) is known to regulate cellular growth pathways, and its genetic activation is sufficient to enhance regenerative axon growth following injury to the central or peripheral nervous systems.
Carlin, Dan   +6 more
core   +2 more sources

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