Gene interactions and pathways from curated databases and text-mining

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Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Kimura et al., Blood 2005 (Leukemia) : Although several Src inhibitors are more effective than imatinib and simultaneously inhibit Lyn , whose overexpression is associated with imatinib resistance, these inhibitors are less specific than imatinib
Chang et al., Am J Physiol Lung Cell Mol Physiol 2008 : We found that hPMVEC express Fyn, Yes, c-Src , Lyn, and Blk and that the protein expression of Fyn, Yes, c-Src, and Lyn could be inhibited with specific siRNA
Mahon et al., Cancer Res 2008 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : In contrast, dasatinib, a dual Bcr-Abl and Src kinase inhibitor, inhibited the phosphorylation of both BCR-ABL and Lyn , and induced apoptosis of the Bcr-Abl cell line overexpressing p53/56 Lyn
Suzuki-Inoue et al., J Biol Chem 2001 : In vitro kinase assays and Western blotting of GPIa immunoprecipitates revealed that Src and Lyn constitutively associate with GPIa/IIa and that Src activity increases transiently after rhodocytin stimulation
Fiskus et al., Clin Cancer Res 2006 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : Treatment with dasatinib attenuated the levels of autophosphorylated Bcr-Abl, p-CrkL, phospho-signal transducer and activator of transcription 5 ( p-STAT5 ), p-c-Src , and p-Lyn ; inhibited the activity of Lyn and c-Src ; and induced apoptosis of the cultured CML cells
Congleton et al., Leukemia 2012 (Leukemia, Myeloid) : Src inhibitors, PP2 and dasatinib, increase retinoic acid induced association of Lyn and c-Raf ( S259 ) and enhance MAPK dependent differentiation of myeloid leukemia cells