Gene interactions and pathways from curated databases and text-mining

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ABL1 — AKT1

Text-mined interactions from Literome

Gross et al., Mol Cell Biol 1999 (Cell Transformation, Neoplastic...) : In addition, we found that DeltaSH3 c-Abl induced less activation of Akt and STAT5 than did Bcr-Abl, suggesting that activation of these pathways plays a critical role in inducing a CML-like disease
Voss et al., Oncogene 2000 (MAP Kinase Signaling System...) : The mitogenic MAPK/Erk kinases as well as Akt/PKB , a kinase implicated to negatively regulate apoptosis, were also constitutively activated by both Bcr-Abl and Tel-Abl
Tang et al., J Biol Chem 2000 : Transfection of cells with a dominant negative PKB reduces both the Abl stimulated PKB activity and the survival effect conferred by activation of this oncogene
Nieborowska-Skorska et al., Oncogene 2000 (Leukemia, Myeloid) : We show here that the defect in activation of PI-3k/Akt by BCR/ABL DeltaSH2 mutant ( SH2 domain deleted ) and of STAT5 by BCR/ABL DeltaSH3+DeltaSH2 mutant ( SH3 and SH2 domains deleted ) is not permanent and both Akt and STAT5 could be ` re-activated ' by in vitro culture
van der Kuip et al., Blood 2001 : Thus, cooperative activation of PI-3K/AKT by Bcr-Abl and integrins causes synergistic protection of Bcr-Abl+ cells from DNA damage induced apoptosis
Tseng et al., Blood 2005 : As protein kinase B ( Akt ) plays a pivotal role in Abl oncogene mediated cell survival, we hypothesize that concurrent inhibition of Akt will sensitize resistant cells to the residual apoptotic activity of imatinib mesylate, thereby overcoming the resistance
Barnes et al., Oncogene 2005 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : Both IL-3 treatment and expression of Bcr-Abl led to enhanced phosphorylation of Akt ( protein kinase B )
Chu et al., Cancer Res 2007 (Cell Transformation, Neoplastic...) : BCR/ABL expression results in enhanced Ras and Akt activity but reduced mitogen activated protein kinase activity in human hematopoietic cells, which is reversed by BCR/ABL-Y177 mutation
Weisberg et al., Blood 2008 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive...) : BAG956 was shown to block AKT phosphorylation induced by BCR-ABL- , and induce apoptosis of BCR-ABL expressing cell lines and patient bone marrow cells at concentrations that also inhibit PI3K signaling
Hirano et al., J Biol Chem 2009 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : Thus, Bcr-Abl represses the expression of PHLPP1 and PHLPP2 and continuously activates Akt1 , -2, and -3 via phosphorylation on Ser-473, resulting in the proliferation of CML cells
Ghosh-Choudhury et al., J Biol Chem 2013 : Remarkably, inhibition of c-Abl significantly suppressed BMP-2 stimulated PI 3-kinase activity and its downstream Akt phosphorylation