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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