Gene interactions and pathways from curated databases and text-mining

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BCL10 — EPO

Text-mined interactions from Literome

Pircher et al., J Biol Chem 2001 : In FDCER cell lines, which express endogenous c-Kit, the signaling capacities of such minimal Epo receptor forms ( ER-HY343 and ER-HY343F ) have been dissected to reveal : 1 ) that Epo dependent mitogenesis, survival, and bcl-x gene expression via ER-HY343 depend upon the intactness of the Tyr-343 STAT5 binding site ; 2 ) that ER-HY343 dependent bcl-x ( L ) gene transcription is enhanced markedly via c-Kit ; 3 ) that socs-3, plfap, dpp-1, and cacy-bp gene transcription is induced via ER-HY343, whereas dpp-1 and cacy-bp gene expression is also supported by ER-HY343F ; 4 ) that ectopically expressed SOCS-3 suppresses proliferative signaling by not only ER-HY343 but also c-Kit ; and 5 ) that in FDCER and primary erythroid cells, c-Kit appears to provide the primary route to MAPK activation
Sola et al., Pediatr Res 2005 (Brain Ischemia...) : The most effective dose after FCI was 1000 U/kg for 3 d. Immunoanalyses showed that Epo induced a significant increase in phosphorylated Janus kinase 2 and signal transducer and activator of transcription-5 expressions at 1 and 3 d and up-regulated Bcl-xL expression by 24 h after FCI but did not affect Epo receptor or NF-kappaB expression
Diwan et al., Apoptosis 2008 (Anemia...) : Previously, we found that BH3-only proapoptotic factor, Nix, opposed erythroblast-survival signaling by erythropoietin induced Bcl-xl during normal erythrocyte formation
Okazaki et al., Neoplasia (New York, N.Y.) 2008 (Neovascularization, Pathologic) : Erythropoietin activated the extracellular signal regulated kinase signaling pathway and up-regulated the expression of the downstream antiapoptotic protein Bcl-xL in HMVECs