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STAT3beta does not interfere with granulocyte colony-stimulating factor-induced neutrophilic differentiation
J P de Koning1, A C Ward, E Caldenhoven
1Institute of Hematology, Erasmus University, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands.
Summary
STAT3beta does not inhibit granulocyte colony-stimulating factor (G-CSF)-induced myeloid cell differentiation or p27 expression. This splice variant does not act as a negative regulator in this process.
Area of Science:
- Cell Biology
- Molecular Biology
- Hematopoiesis
Background:
- Signal transducer and activator of transcription 3 (STAT3) activation is key for G-CSF-mediated neutrophilic differentiation.
- STAT3-induced cell cycle exit involves upregulation of p27(Kip1).
- STAT3beta, a splice variant, may inhibit STAT3 transcriptional activity, but its role in hematopoietic differentiation is unclear.
Purpose of the Study:
- To investigate the role of STAT3beta in G-CSF-mediated myeloid differentiation.
- To determine if STAT3beta inhibits G-CSF-induced p27(Kip1) expression.
Main Methods:
- Ectopic expression of STAT3beta in 32D cells with wild-type G-CSF receptors.
- Assessment of G-CSF-mediated neutrophilic differentiation and p27 induction.
- Analysis of p27(Kip1) promoter activity in the presence of STAT3beta.
Main Results:
- STAT3beta overexpression did not affect the rate of G-CSF-induced neutrophilic differentiation.
- STAT3beta did not inhibit G-CSF-induced p27(Kip1) expression.
- STAT3beta alleviated inhibition of p27 transactivation by a dominant-negative STAT3 mutant.
Conclusions:
- STAT3beta does not function as a negative regulator of G-CSF-induced p27 expression.
- STAT3beta does not inhibit G-CSF-mediated myeloid differentiation.