FOXO3-dependent BCL2L11 gene expression

Stable Identifier
Reaction [omitted]
Homo sapiens
Locations in the PathwayBrowser
SVG |   | PPTX  | SBGN
Click the image above or here to open this reaction in the Pathway Browser
The layout of this reaction may differ from that in the pathway view due to the constraints in pathway layout
BCL2L11 (also known as BIM) is a pro-apoptotic factor whose expression is downregulated by FLT3 signaling as a consequence of AKT-dependent FOXO3 phosphorylation and nuclear export (Brandts et al, 2005; Scheijen et al, 2004; reviewed in Kazi and Ronnstrand, 2019; Yadav et al, 2018).. Downregulation of BCL2L11 may contribute to evasion of apoptosis and promote cellular survival downstream of FLT3 and FLT3 ITD signaling (Nordigarden et al, 2009).
Literature References
PubMed ID Title Journal Year
29309929 FoxO transcription factors in cancer metabolism

Zhuang, L, Yadav, RK, Chauhan, AS, Gan, B

Semin. Cancer Biol. 2018
14981546 FLT3 receptors with internal tandem duplications promote cell viability and proliferation by signaling through Foxo proteins

Griffin, JD, Scheijen, B, Kang, H, Ngo, HT

Oncogene 2004
19064725 BH3-only protein Bim more critical than Puma in tyrosine kinase inhibitor-induced apoptosis of human leukemic cells and transduced hematopoietic progenitors carrying oncogenic FLT3

Villunger, A, Lam, EW, Kraft, M, Jönsson, JI, Eliasson, P, Labi, V, Nordigården, A

Blood 2009
16266983 Constitutive activation of Akt by Flt3 internal tandem duplications is necessary for increased survival, proliferation, and myeloid transformation

Berdel, WE, Serve, H, Rode, M, Brandts, CH, Sargin, B, Buerger, H, McMahon, M, Choudhary, C, Biermann, C, Lindtner, B, Müller-Tidow, C, Schwäble, J

Cancer Res. 2005
This event is regulated
Positively by
Cite Us!