Merck
Search Within
Applied Filters:
Keyword:'sml0382'
Showing 1-11 of 11 results for "

sml0382

" within Papers
Sort by Relevance
Ku-0063794 is a specific inhibitor of the mammalian target of rapamycin (mTOR)
Garcaa-Martanez JM, et al.
The Biochemical Journal, 421(1), 29-42 (2009)
Glenn R Bantug et al.
Immunity, 48(3), 542-555 (2018-03-11)
Glycolysis is linked to the rapid response of memory CD8+ T cells, but the molecular and subcellular structural elements enabling enhanced glucose metabolism in nascent activated memory CD8+ T cells are unknown. We found that rapid activation of protein kinase B (PKB
Fang Hao et al.
Molecular cancer research : MCR, 15(7), 929-941 (2017-04-01)
We examined the impact of crosstalk between the insulin receptor and G protein-coupled receptor (GPCR) signaling pathways on the regulation of Yes-associated protein (YAP) localization, phosphorylation, and transcriptional activity in the context of human pancreatic ductal adenocarcinoma (PDAC). Stimulation of
Quantifying autophagy using novel LC3B and p62 TR-FRET assays
Bresciani A, et al.
PLoS ONE, 13(3) (2018)
Xiaosa Li et al.
Theranostics, 7(19), 4671-4688 (2017-12-01)
Rationale: Postmenopausal atherosclerosis (AS) has for decades been attributed to estrogen deficiency. Although the follicular stimulating hormone (FSH) levels rise sharply in parallel, the direct effect of FSH on AS has never been investigated. In this study, we explored the
Follicular stimulating hormone accelerates atherogenesis by increasing endothelial VCAM-1 expression
Li X, et al.
Theranostics, 7(19), 4671-4671 (2017)
Alberto Bresciani et al.
PloS one, 13(3), e0194423-e0194423 (2018-03-20)
Autophagy is a cellular mechanism that can generate energy for cells or clear misfolded or aggregated proteins, and upregulating this process has been proposed as a therapeutic approach for neurodegenerative diseases. Here we describe a novel set of LC3B-II and
Eyal Amiel et al.
Journal of immunology (Baltimore, Md. : 1950), 193(6), 2821-2830 (2014-08-12)
TLR-mediated activation of dendritic cells (DCs) is associated with a metabolic transition in which mitochondrial oxidative phosphorylation is inhibited by endogenously synthesized NO and the cells become committed to glucose and aerobic glycolysis for survival. We show that inhibition of
Mitochondria-endoplasmic reticulum contact sites function as immunometabolic hubs that orchestrate the rapid recall response of memory CD8+ T cells
Bantug GR, et al.
Immunity, 48(3), 542-555 (2018)
Quantifying autophagy using novel LC3B and p62 TR-FRET assays
Bresciani A, et al.
Testing, 13(3) (2018)
Juan M García-Martínez et al.
The Biochemical journal, 421(1), 29-42 (2009-05-01)
mTOR (mammalian target of rapamycin) stimulates cell growth by phosphorylating and promoting activation of AGC (protein kinase A/protein kinase G/protein kinase C) family kinases such as Akt (protein kinase B), S6K (p70 ribosomal S6 kinase) and SGK (serum and glucocorticoid
Page 1 of 1
Page 1 of 1