Phosphatidylinositol 3-Kinases

Phosphotransferases that catalyzes the conversion of 1-phosphatidylinositol to 1-phosphatidylinositol 3-phosphate. Many members of this enzyme class are involved in RECEPTOR MEDIATED SIGNAL TRANSDUCTION and regulation of vesicular transport with the cell. Phosphatidylinositol 3-Kinases have been classified both according to their substrate specificity and their mode of action within the cell.

Also Known As:

Networked: 715 relevant articles (12 outcomes, 59 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Draznin, Boris: 8 articles (03/2009 - 01/2002)
2.	Durden, Donald L: 5 articles (09/2014 - 01/2010)
3.	Asano, Tomoichiro: 4 articles (07/2014 - 12/2002)
4.	Ye, Keqiang: 4 articles (03/2010 - 12/2004)
5.	Leitner, J Wayne: 4 articles (03/2009 - 08/2004)
6.	Klippel, Anke: 4 articles (06/2006 - 06/2002)
7.	Sasaoka, T: 4 articles (02/2005 - 08/2001)
8.	Vanhaesebroeck, Bart: 3 articles (12/2014 - 04/2013)
9.	Katagiri, Hideki: 3 articles (07/2014 - 12/2002)
10.	Ono, Hiraku: 3 articles (07/2014 - 12/2002)

Related Diseases

1.	Neoplasms (Cancer) 04/01/2004 - "Improved insight into the regulation of PTEN is leading to a richer understanding of the contribution of PTEN and the PI-3 kinase pathway to human tumors. " 01/01/2011 - "In this study we experimentally assessed the role of the PI3-kinase pathway and its regulator PIK3CA, which is frequently altered in cervical cancer, in HPV-induced transformation. " 01/01/2008 - "Recent studies reported that the p110alpha (PIK3CA), catalytic subunit of PI3-kinase is somatically mutated in human cancers. " 04/01/2006 - "Recent studies have shown that the PIK3CA gene, which encodes the p110alpha catalytic subunit of phosphatidylinositol 3-kinases, is mutated in human cancers. " 07/20/2001 - "The present study shows that PTEN, a tumor suppressor that inhibits PI 3-kinase function, impairs TNF activation of Akt and the IKK complex in 293 cells. "
2.	Ischemia 03/01/2004 - "These results suggest that eNOS expression is up-regulated in the endothelium via PI-3K pathways after transient forebrain ischemia, and that preconditioning-induced eNOS expression plays an important role in neuroprotection in the ischemic tolerance." 10/01/2003 - "We conclude that PI 3-kinase and Akt are activated after renal ischemia/reperfusion and that Akt phosphorylation leads to phosphorylation of FKHR and FKHRL1, which may affect epithelial cell fate in acute renal failure." 05/01/2015 - "Thus, we investigated the effects of sevoflurane on intestinal IRI with sevoflurane given before, during or after intestinal ischemia, and the role of phosphatidylinositol 3 kinases (PI3K)/Akt pathway in these effects. " 02/09/2006 - "Western blotting showed that ischemia-related changes of GDNF and PI-3 kinase protein levels were similar to the immunohistochemical changes after ischemia. " 01/01/2003 - "The results suggest that sustained increases in tyrosine phosphorylation and increased interaction of NR2B with the SH2 domain of PI3-kinase may contribute to altered signal transduction in the CA3/dentate gyrus after transient ischemia."
3.	Reperfusion Injury 03/01/2006 - "Post-ischemic interventions that activate phosphatidylinositol-3-OH kinase (PI3K)-Akt or ERK1/2 pro-survival kinases (the so-called "reperfusion injury signalling kinase (RISK) pathway") during the first few minutes of reperfusion protect against lethal reperfusion-induced injury. " 05/01/2012 - "[Effect of ischemic postconditioning on phosphatidylinositol-3-OH kinase and extracellular signal-regulated protein kinase in rats with hepatic ischemia-reperfusion injury]." 06/01/2006 - "PI3-kinase inhibitor wortmannin imposes a deleterious effect on serum blood urea nitrogen level, renal function after renal ischaemia/reperfusion injury in mice. " 12/01/2007 - "Activation of the Reperfusion Injury Salvage Kinase (RISK) pathway, which incorporates phosphatidylinositol-3-OH kinase (PI3K)-Akt/protein kinase B (PKB) and p44/42 mitogen-activated protein kinase (MAPK), underlies protection against ischemia-reperfusion (I/R) injury. " 11/01/2007 - "Protection against myocardial ischemia-reperfusion (I/R) injury involves activation of phosphatidylinositol-3-OH kinase (PI3K)- Akt/protein kinase B and p44/42 mitogen-activated protein kinase (MAPK), components of the reperfusion injury salvage kinase (RISK) pathway. "
4.	Insulin Resistance 06/01/2007 - "The objective of this study was to assess the role of the p85alpha subunit of PI 3-kinase and PI 3-kinase signaling in GH-mediated insulin resistance in adipose tissue. " 03/01/2009 - "We recently reported that rs361072, a promoter C/T variant of p110beta, the catalytic subunit of PI3-kinase, was associated with a protection from insulin resistance (IR) in Caucasian adolescents in proportion of their body mass. " 01/01/2008 - "[Induction of insulin resistance induced by PI-3K inhibitor in porcine granulosa cells]." 09/01/2006 - "However, the effects of chronic oxidative stress appear rather different, particularly a proposed role for nitrosylation of Akt and other targets leading to inhibition of PI 3-kinase signaling during diabetic insulin resistance in muscle. " 11/20/2003 - "These findings suggest that the change of C to G at position -9 of the PTEN gene is associated with the insulin resistance of type 2 diabetes due possibly to a potentiated hydrolysis of the PI3-kinase product."
5.	Infection 02/01/2003 - "Our studies show that inhibition of the PI3-kinase signaling pathway suppresses virus infection post-viral entry and post-reverse transcription but prior to HIV gene expression. " 09/01/2008 - "Both PI3-kinase and PKC-alpha were activated during ES entry into HBMEC between 15 min and 30 min of infection. " 11/04/2005 - "Infection of 16HBE14o- human bronchial epithelial cells with RV39 induced rapid activation of PI 3-kinase and phosphorylation of Akt, a downstream effector of PI 3-kinase. " 11/01/2004 - "Furthermore, apoptosis of melanocytes induced by deprivation of iTbI was prevented almost completely by infection with an adenovirus vector encoding a constitutively active mutant of either PI 3-kinase or Akt. " 08/17/2001 - "We used an adenoviral infection system to test the possibility that activation of PI 3-kinase or Akt alone is sufficient to stimulate NHE3 activity. "

Related Drugs and Biologics

1.	Phosphotransferases (Kinase)
2.	Protein Kinases (Protein Kinase)
3.	Proto-Oncogene Proteins c-akt (Protein Kinase B)
4.	Insulin (Novolin)
5.	Phosphatidylinositols (Phosphatidylinositol)
6.	DNA (Deoxyribonucleic Acid)
7.	Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)
8.	lysyl- arginyl- alanyl- lysyl- alanyl- lysyl- threonyl- threonyl- lysyl- lysyl- arginine (PKCS)
9.	DNA-Activated Protein Kinase
10.	Serine (L-Serine)

Related Therapies and Procedures

1.	Drug Therapy (Chemotherapy)
2.	Heterologous Transplantation (Xenotransplantation)
3.	Ischemic Postconditioning
4.	Chemoprevention
5.	Therapeutics