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https://pubmed.ncbi.nlm.nih.gov/11740206/
Western blot analysis showed a significant increase of phospho-Akt 4 hours after focal cerebral ischemia in the cortex, whereas phospho-Akt was decreased in the ischemic core. Double staining with phospho-Akt and TUNEL showed different cellular distributions of phospho-Akt and TUNEL-positive staining.Cited by: 334
https://pubmed.ncbi.nlm.nih.gov/30074018/
RESULTS p-Akt was activated during early cerebral I/R at 0.5 hours, and reached the highest levels at 4 hours, then gradually decreased from 6 hours, and reached and maintained the lowest levels at 12-24 hours. Bax expression was gradually increased from 6 hours and reached the highest level at 24 hours.Cited by: 12
https://pubmed.ncbi.nlm.nih.gov/12373512/
BDNF and NMDA increased Akt phosphorylation within 5 minutes but maximal activation by NMDA was observed at 3 hours. Akt phosphorylation was completely blocked by the PI-3 kinase inhibitor LY294002. NMDA-mediated activation of Akt was completely blocked by MK-801 and partially blocked by the TrkB receptor inhibitor, K252a, indicating the ...Cited by: 55
https://cancerres.aacrjournals.org/content/79/6/1019
2019-3-15 · However, this compound causes dephosphorylation of AKT (Thr308) for only a short time and hyperphosphorylation occurs again with continuous exposure. INK128, an mTOR inhibitor, also caused dephosphorylation of S6K1 and AKT (Ser 473) for 1 hour, but AKT was again phosphorylated at both Ser and Thr residues again by 24 hours.Cited by: 172
https://www.nature.com/articles/srep35660/
2016-10-20 · AKT phosphorylation and activity status. (a) H9 hESCs grown on Matrigel were starved for 6 hours with KSR/bFGF-free DMEM/F12 cell culture medium and …Cited by: 31
https://www.cisbio.com/phospho-akt1-2-3-ser473-cellular-kit-40548
Phosphorylated AKT was measured after 3.5 hours using the two-plate assay protocol. Total AKT used to control the phosphorylation status of AKT (Ser473). HEK293 cells (100,000 cells/well) were activated with IGF-1 for 10 min, using the two-plate assay protocol of the …
https://www.sciencedirect.com/science/article/pii/S0085253815479001
2001-8-1 · To examine whether hyperosmolality stimulates the phosphorylation of Akt in MDCK cells, the cells were exposed to hyperosmotic media (600 mOsm/kg H 2 O final osmolality) prepared by adding NaCl, urea, or raffinose for 1, 3, 6, 12, 24, and 48 hours. Densitometric analysis showed that exposure to hyperosmolar media caused two peaks of phosphorylation of Akt.Cited by: 113
https://cancerdiscovery.aacrjournals.org/content/candisc/1/3/248.full.pdf
AZD8055 for up to 24 hours. We found that AKT kinase ac-tivity declines within 1 hour of addition of the drug, reaches a nadir of 15% of baseline at 8 hours, and then rises to 60% of baseline by 24 hours after addition of the drug (Fig. 2C). and will therefore prevent feedback induction of AKT, which
https://www.sciencedirect.com/science/article/pii/S2451945619303964
2020-1-16 · Introduction. The serine/threonine kinase AKT is a central component of the phosphoinositide 3-kinase (PI3K) signaling cascade and is a key regulator of critical cellular processes, including proliferation, survival, and metabolism (Manning and Toker, 2017).The AKT protein kinase family comprises three highly homologous isoforms, AKT1, AKT2, and AKT3, that possess both …Cited by: 26
https://cancerres.aacrjournals.org/content/73/7/2189
2013-4-1 · Neuroblastoma is a pediatric tumor of the peripheral sympathetic nervous system with a highly variable prognosis. Activation of the phosphoinositide 3-kinase (PI3K)/AKT pathway in neuroblastoma is correlated with poor patient prognosis, but the precise downstream effectors mediating this effect have not been determined. Here we identify the forkhead transcription factor FOXO3a as a key target ...Cited by: 130
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