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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)

Mitochondria-Endoplasmic Reticulum Contact Sites Function as Immunometabolic Hubs that Orchestrate the Rapid Recall Response of Memory CD8+ T Cells.

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

Insulin Receptor and GPCR Crosstalk Stimulates YAP via PI3K and PKD in Pancreatic Cancer Cells.

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)

Follicular Stimulating Hormone Accelerates Atherogenesis by Increasing Endothelial VCAM-1 Expression.

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)

Quantifying autophagy using novel LC3B and p62 TR-FRET assays.

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

Mechanistic target of rapamycin inhibition extends cellular lifespan in dendritic cells by preserving mitochondrial function.

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)

Ku-0063794 is a specific inhibitor of the mammalian target of rapamycin (mTOR).

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

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