|1.||Mills, Gordon B: 30 articles (10/2015 - 04/2003)|
|2.||Evers, B Mark: 14 articles (09/2012 - 09/2002)|
|3.||Yamori, Takao: 12 articles (02/2015 - 04/2006)|
|4.||Lu, Yiling: 10 articles (11/2012 - 04/2003)|
|5.||Hennessy, Bryan T: 9 articles (10/2015 - 08/2008)|
|6.||Wang, Jing: 8 articles (08/2015 - 05/2005)|
|7.||Maira, Sauveur-Michel: 8 articles (01/2014 - 07/2008)|
|8.||McCubrey, James A: 8 articles (08/2013 - 09/2008)|
|9.||Vogt, Peter K: 8 articles (07/2010 - 01/2005)|
|10.||Dan, Shingo: 7 articles (02/2015 - 04/2010)|
02/01/2015 - "Although pharmacological inhibition of phosphatidylinositol 3-kinase (PI3K) is an attractive therapeutic strategy for cancer therapy, molecular determinants for efficacy of PI3K inhibitors (PI3Kis) remain unclear. "
12/01/2015 - "There are numerous studies that demonstrate the anti-neoplastic activity of phosphatidylinositol 3-kinase (PI3K) inhibitors and the mechanisms of inducing autophagy in cancer cells. "
11/01/2012 - "Recent studies have reported that ADM protected tumor cells against apoptotic cell death via the upregulation of Bcl-2 or the activation of the phosphatidylinositol 3-kinase/Akt pathway. "
11/01/2011 - "Recent studies indicate that unregulated activation of the Phosphatidylinositol 3-kinase (PI3K)/Akt pathway is a prominent feature of many human cancers and Akt is overexpressed or activated in all major cancers. "
11/01/2010 - "In this study, we investigated whether this activation is both maintained by a wild-type Ras/phosphatidylinositol 3-kinase (PI3K)/Akt-positive feedback loop in endothelial cells and affects tumor angiogenesis. "
05/01/2007 - "The phosphatidylinositol 3-kinase signaling pathway exerts protective effects during sepsis by controlling C5a-mediated activation of innate immune functions."
01/01/2016 - "In addition, activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway has been reported to be beneficial in sepsis. "
09/01/2015 - "Apelin attenuates postburn sepsis via a phosphatidylinositol 3-kinase/protein kinase B dependent mechanism: A randomized animal study."
10/01/2009 - "In sepsis, skeletal muscle GLUT4 translocation is impaired as a result of the reduced phosphatidylinositol 3-kinase/Akt pathway associated with insulin receptor substrate down-regulation through nuclear factor-kappaB activation."
05/26/2006 - "Interleukin-1beta enhances GABAA receptor cell-surface expression by a phosphatidylinositol 3-kinase/Akt pathway: relevance to sepsis-associated encephalopathy."
03/01/2009 - "Our results suggest that AM pretreatment could enhance HT-induced myocardial Akt phosphorylation and subsequent HSP72 expression in a phosphatidylinositol 3-kinase-dependent manner, in association with tolerance against ischemia/reperfusion injury. "
07/01/2004 - "2. The phosphatidylinositol 3-kinase/akt pathway is one such pathway that is partially regulated via oxidative state and, in an oxidative stress paradigm such as ischaemic-reperfusion injury, may be inactivated, which can lead to exacerbation of cell death. "
10/26/2004 - "We demonstrate that (i) primary cultures of cortical neurons from Rai-/- mice are more sensitive to apoptosis induced by hypoxia or oxidative stress; (ii) in Rai-/- mice, ischemia/reperfusion injury induces severe neurological deficits, increased apoptosis and size of the infarct area, and significantly higher mortality; and (iii) Rai functions as a stress-response gene that increases phosphatidylinositol 3-kinase activation and Akt phosphorylation after hypoxic or oxidation insults. "
02/01/2010 - "Rosiglitazone-induced myocardial protection against ischaemia-reperfusion injury is mediated via a phosphatidylinositol 3-kinase/Akt-dependent pathway."
02/01/2013 - "Although PKG signaling in PoCo has been proposed to depend on the activation of the phosphatidylinositol 3-kinase (PI3K)/Akt cascade, recent data bring into question a causal role of reperfusion injury signaling kinase (RISK) in PoCo protection. "
01/01/2007 - "Blocking Akt activation using a phosphatidylinositol 3-kinase inhibitor, LY294002 (20 muM), or expressing dominant negative (inactive) Akt increased DCVC-induced RPTC necrosis to 42%. "
08/01/1999 - "These data suggest that neuroprotective effects of natural gangliosides may preferentially reflect reduction of neuronal apoptosis rather than necrosis, and be mediated through mechanisms involving activation of phosphatidylinositol 3-kinase."
01/01/2006 - "Differential regulation of interleukin-12 and tumour necrosis factor-alpha by phosphatidylinositol 3-kinase and ERK 1/2 pathways during Mycobacterium tuberculosis infection."
12/15/2006 - "A scavenger of reactive oxygen species, as well as inhibitors of phosphatidylinositol 3-kinase, ERK, JNK1, and NOS, also blocked PKGIalpha-mediated protection against necrosis and apoptosis. "
01/12/2006 - "In vitro, LMP1 activates numerous signaling pathways including p38, c-Jun N terminal kinase (JNK), phosphatidylinositol 3 kinase (PI3K)/Akt, and NF-kappaB through interactions with tumor necrosis receptor-associated factors (TRAFs). "
|5.||Breast Neoplasms (Breast Cancer)
08/01/2013 - "Recent studies showed that basal-like breast cancer is frequently associated with an increased activity of the phosphatidylinositol 3-kinase (PI3K) pathway, which is critical for cell growth, survival, and angiogenesis. "
07/31/2013 - "Activating mutations of the PIK3CA gene occur frequently in breast cancer, and inhibitors that are specific for phosphatidylinositol 3-kinase (PI3K) p110α, such as BYL719, are being investigated in clinical trials. "
01/01/2005 - "The hypothesis of this study was that erbB2 confers resistance to radiation-induced apoptosis in breast cancer cells through the phosphatidylinositol 3-kinase (PI3-K)/Akt signalling pathway. "
01/01/2015 - "Activation of the phosphatidylinositol 3-kinase (PI3K)/AKT/mTOR pathway is common in breast cancer. "
10/10/2014 - "Phosphatidylinositol 3-kinase (PI3K)/AKT pathway aberrations are common in breast cancer, with mutations in PIK3CA being the most common. "
|1.||Proto-Oncogene Proteins c-akt (Protein Kinase B)
|3.||Epidermal Growth Factor Receptor (EGF Receptor)
|6.||Reactive Oxygen Species (Oxygen Radicals)
|8.||Protein Kinases (Protein Kinase)
|1.||Drug Therapy (Chemotherapy)