Block of C/EBP alpha function by phosphorylation in acute myeloid leukemia with FLT3 activating mutations.
Block of C/EBP alpha function by phosphorylation in acute myeloid leukemia with FLT3 activating mutations.
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DOI:
10.1084/jem.20052242
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发表时间:
2006-02-20
影响因子:
15.3
通讯作者:
Tenen, DG
中科院分区:
文献类型:
--
作者:
Radomska, HS;Bassères, DS;Zheng, R;Zhang, P;Dayaram, T;Yamamoto, Y;Sternberg, DW;Lokker, N;Giese, NA;Bohlander, SK;Schnittger, S;Delmotte, MH;Davis, RJ;Small, D;Hiddemann, W;Gilliland, DG;Tenen, DG
Mutations constitutively activating FLT3 kinase are detected in ∼30% of acute myelogenous leukemia (AML) patients and affect downstream pathways such as extracellular signal–regulated kinase (ERK)1/2. We found that activation of FLT3 in human AML inhibits CCAAT/enhancer binding protein α (C/EBPα) function by ERK1/2-mediated phosphorylation, which may explain the differentiation block of leukemic blasts. In MV4;11 cells, pharmacological inhibition of either FLT3 or MEK1 leads to granulocytic differentiation. Differentiation of MV4;11 cells was also observed when C/EBPα mutated at serine 21 to alanine (S21A) was stably expressed. In contrast, there was no effect when serine 21 was mutated to aspartate (S21D), which mimics phosphorylation of C/EBPα. Thus, our results suggest that therapies targeting the MEK/ERK cascade or development of protein therapies based on transduction of constitutively active C/EBPα may prove effective in treatment of FLT3 mutant leukemias resistant to the FLT3 inhibitor therapies.
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影响因子:
20.3
作者:
Kottaridis, PD;Gale, RE;Linch, DC
通讯作者:
Linch, DC
影响因子:
20.3
作者:
D'Alo, F;Johansen, LM;Tenen, DG
通讯作者:
Tenen, DG
DOI:
10.1073/pnas.0404731101
发表时间:
2004-09-07
影响因子:
11.1
作者:
Helbling, D;Mueller, BU;Pabst, T
通讯作者:
Pabst, T
影响因子:
11.4
作者:
Kaeferstein, A;Krug, U;Verbeek, W
通讯作者:
Verbeek, W
影响因子:
50.3
作者:
Kelly, LM;Yu, JC;Giese, NA
通讯作者:
Giese, NA