Gene interactions and pathways from curated databases and text-mining

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Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Dickson et al., Am J Physiol Endocrinol Metab 2004 (Diabetes Mellitus, Type 2...) : Pancreatic beta-cell growth and survival in the onset of type 2 diabetes : a role for protein kinase B in the Akt ?
Creighton , Oncogene 2007 (Breast Neoplasms...) : The subset of genes both upregulated by Akt and dependent on mTOR activity were associated with estrogen receptor negative status, higher grade, increasing tumor size and poor prognosis in multiple patient cohorts ; these associations were either not present or not as strong for the Akt induced , mTOR independent genes or for AKT1 expression alone
Peng et al., Genes Dev 2003 (Abnormalities, Multiple...) : Specifically, Akt1 and Akt2 are required for the induced expression of PPARgamma, the master regulator of adipogenesis, establishing a new essential role for Akt in adipocyte differentiation ... These functions of Akt were uncovered despite the observed lower level of Akt activity mediated by Akt3 in Akt1/Akt2 DKO cells, suggesting that a critical threshold level of Akt activity is required to maintain normal cell proliferation, growth, and differentiation
Osman et al., Cancer 2006 (Disease Progression...) : Loss of neutral endopeptidase and activation of protein kinase B ( Akt ) is associated with prostate cancer progression
Mutiara et al., Mol Cell Endocrinol 2008 : Akt/PKB activation by GnRH and IGF-1 was completely eliminated in the presence of the PI3-kinase inhibitor, LY 294002, but not in the presence of an Akt/PKB inhibitor
Tokuda et al., Hum Mol Genet 2011 (Disease Susceptibility...) : An in vitro kinase assay revealed that Akt3 ( Nmf350 ) confers higher enzymatic activity, suggesting that Akt3 ( Nmf350 ) might enhance AKT signaling in the brain
Lengyel et al., Steroids 2007 : In response to E2, phosphorylation of Akt/PKB on Ser473 and FOXO1 on Ser256 and Thr24 residues increased but with distinct kinetics, regulating the activation and inactivation of Akt and FOXO1 proteins, respectively
Fukuda et al., J Cell Biol 2003 : Thus, CH-ILKBP is an important component of the prosurvival signaling pathway functioning primarily by facilitating the membrane translocation of PKB/Akt and consequently the activation of PKB/Akt in response to extracellular survival signals
Nomura et al., Mol Carcinog 2003 (Cell Transformation, Neoplastic) : The expression of DNM-Akt1 also suppressed EGF induced p70 S6K activation as well as Akt activation
Culig et al., Endocr Relat Cancer 2005 (Neoplasms, Hormone-Dependent...) : Similarly, activation of the AR by phosphorylated protein kinase B , Akt , has also been reported in prostate cancer
Dai et al., PloS one 2012 (Acute Disease...) : Here, we demonstrate for the first time that acute ECM results in significantly reduced activation of protein kinase B ( PKB or Akt ) leading to decreased Akt phosphorylation and inhibition of the glycogen kinase synthase ( GSK3ß ) in the brains of mice infected with Plasmodium berghei ANKA ( PbA ) compared to uninfected controls and to mice infected with the non-neurotrophic P. berghei NK65 ( PbN )
Fisher et al., Am J Physiol Endocrinol Metab 2005 : We hypothesized that AMP activated protein kinase related kinase 5 ( ARK5 ) /novel kinase family 1 ( NUAK1 ), an AMP activated protein kinase (AMPK) related kinase that has been found to be stimulated by protein kinase B ( Akt ), would be expressed in rat skeletal muscle and activated by electrically elicited contractions, 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside ( AICAR ), or insulin
Segrelles et al., Mol Biol Cell 2008 (Nails, Malformed...) : Here we report the developmental consequences of deregulated Akt activity in the basal layer of stratified epithelia, mediated by the expression of a constitutively active Akt1 ( myrAkt ) in transgenic mice
Ritchie et al., Biochem J 2010 : Insulin stimulates endothelial NO ( nitric oxide ) synthesis via PKB ( protein kinase B ) /Akt mediated phosphorylation and activation of eNOS ( endothelial NO synthase ) at Ser-1177
Kang et al., J Exp Med 2007 (Pulmonary Fibrosis) : TGF-beta(1) and bleomycin also activated phosphatidylinositol 3-kinase (PI3K) and protein kinase B (PKB)/AKT via SEMA 7A-dependent mechanisms, and PKB/AKT inhibition diminished TGF-beta(1) induced fibrosis
Stojanovic et al., J Biol Chem 2006 : Agonist induced elevation of NO and cGMP was inhibited by Akt inhibitors and reduced in Akt-1 knock-out platelets
Tirosh et al., J Biol Chem 1999 : The effect of this finding on the downstream insulin signal was demonstrated by a 90 % reduction in insulin stimulated protein kinase B (PKB) serine 473 phosphorylation and impaired activation of PKBalpha and PKBgamma
Lee et al., Int J Oncol 2004 (Stomach Neoplasms) : In contrast, PKB/Akt regulation by TGF-beta1 was not different in suspension or in adhesion, and Smad7, but not the other Smads, activated PKB/Akt phosphorylation on TGF-beta1 treatment, indicating a specificity of Smad2 mediated and cell adhesion status dependent activation of Erk1/2 activity
Oehler-Jänne et al., Biochem Biophys Res Commun 2008 : Down-regulation of p-Ser ( 473 ) -PKB/Akt was reversible and re-exposure to physiological temperature resulted in increased p-Ser ( 473 ) -PKB/Akt phosphorylation levels
Tiganis et al., J Biol Chem 1999 : We find that the integrin mediated activation of PKB/Akt in COS1 cells is abrogated by the specific EGF receptor protein-tyrosine kinase inhibitor tyrphostin AG1478, and that TC45 and TC45-D182A can inhibit activation of PKB/Akt following the attachment of COS1 cells to fibronectin
Dang et al., J Neurosci Res 2005 (Neurofibromatoses) : Although the c-Kit ligand stem cell factor (SCF) induces the phosphorylation of protein kinase B ( or Akt ) and prevents apoptosis in Schwann cells, SCF has no effect on the proliferation or differentiation of Schwann cells
Subramanyam et al., J Biol Chem 2010 : Thus, it is concluded that in human epithelial cells, shrinkage induced activation of Akt1 is involved in the RVI process and that apoptotic inhibition of RVI is caused by inhibition of Akt activation, which results from ROS mediated activation of ASK1
Moore et al., J Biol Chem 2011 (MAP Kinase Signaling System) : mTORC2 protein complex mediated Akt ( Protein Kinase B ) Serine 473 Phosphorylation is not required for Akt1 activity in human platelets [ corrected ]
Wang et al., Cell Res 2005 : We found that arsenic trioxide induced the expression and the phosphorylation of Akt/PKB and it inhibited the interaction between Akt/PKB and PPARgamma
Sun et al., Neuroscience 2007 (Pain) : The PKB/Akt inhibitor, Akt inhibitor IV, has the same effect
Sedding et al., Circ Res 2005 : Previously, we demonstrated a mechanosensitive activation of phosphoinositide 3-kinase (PI3-K)/protein kinase B ( Akt ) resulting in p27Kip1 transcriptional downregulation and cell cycle entry of vascular smooth muscle cells ( VSMC )
Fukazawa et al., J Mol Cell Cardiol 2003 : NRG-1beta treatment induced rapid activation of Akt/PKB that was inhibited by wortmannin, and adenoviral mediated overexpression of a dominant negative Akt prevented the protective effect of NRG-1beta
Hanrahan et al., Cancer Discov 2012 (Cystadenocarcinoma, Serous...) : Inhibition of AKT1 caused growth arrest in a subset of ovarian cell lines, but not in those with AKT3 expression, which required pan-AKT inhibition
Brognard et al., Cancer Res 2001 (Carcinoma, Non-Small-Cell Lung...) : Akt/PKB activation was phosphatidylinositol 3-kinase dependent and promoted survival because the phosphatidylinositol 3 inhibitors LY294002 and wortmannin inhibited Akt/PKB phosphorylation, Akt/PKB activity, and increased apoptosis only in cells with active Akt/PKB
Huang et al., Cardiovasc Drugs Ther 2011 (Disease Models, Animal...) : LV-IS-reduction induced by esmolol + milrinone was eliminated in the presence of protein kinase A-(PKA)-inhibitor ( Rp-cAMPS ) or Akt-inhibitor ( AKT 1/2 kinase inhibitor )
Stoeltzing et al., Cancer Cell 2006 (Neoplasms...) : In this issue of Cancer Cell, Phung and coworkers demonstrate that sustained endothelial activation of Akt by expression of constitutively activated Akt1 ( myrAkt1 ) leads to blood vessels that essentially recapitulate the complex structural and functional abnormalities of tumor vessels