PMID- 10336453
OWN - NLM
STAT- MEDLINE
DCOM- 19990629
LR  - 20210209
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 274
IP  - 22
DP  - 1999 May 28
TI  - The role of STAT3 in granulocyte colony-stimulating factor-induced enhancement of
      neutrophilic differentiation of Me2SO-treated HL-60 cells. GM-CSF inhibits the
      nuclear translocation of tyrosine-phosphorylated STAT3.
PG  - 15575-81
AB  - The role of granulocyte colony-stimulating factor (G-CSF) on neutrophilic
      differentiation of Me2SO-treated HL-60 cells was studied. G-CSF augmented the
      functional maturation of Me2SO-treated HL-60 cells in terms of both
      O-2-generating ability and expression of the
      formyl-methionyl-leucyl-phenylalanine receptor. G-CSF induced enhancement of cell
      growth in Me2SO-treated HL-60 cells. These results indicate that G-CSF is a
      potent enhancer for the differentiation and proliferation of Me2SO-treated HL-60 
      cells. G-CSF caused the activation of p70 S6 kinase but not mitogen-activated
      protein (MAP) kinase. On the other hand, G-CSF rapidly induced tyrosine
      phosphorylation of signal transducers and activators of transcription-3 (STAT3), 
      but did not induce serine727 phosphorylation. From the analysis of confocal laser
      scanning fluorescence microscopy and differential centrifugation, it was clearly 
      demonstrated that G-CSF induced nuclear translocation of tyrosine-phosphorylated 
      STAT3. The G-CSF-dependent enhancement of neutrophilic differentiation in
      Me2SO-HL-60 cells was reversely inhibited by granulocyte-macrophage
      colony-stimulating factor (GM-CSF). Notably, in the presence of GM-CSF, G-CSF
      induced the tyrosine phosphorylation of STAT3 but failed to induce the nuclear
      translocation of tyrosine-phosphorylated STAT3. GM-CSF induced activation of not 
      only p70 S6 kinase, but also of MAP kinase. Furthermore, GM-CSF caused the rapid 
      serine727 phosphorylation of STAT3, both in the presence and absence of G-CSF.
      PD98059, an MEK1 inhibitor, inhibited the G-CSF-dependent serine727
      phosphorylation of STAT3 and blocked the inhibitory effect of GM-CSF on
      G-CSF-dependent nuclear translocation of STAT3. These results suggest that
      G-CSF-dependent nuclear translocation of STAT3 coordinates with the promotion of 
      neutrophilic differentiation in Me2SO-treated HL-60 cells.
FAU - Yamaguchi, T
AU  - Yamaguchi T
AD  - Department of Biological Chemistry and Biologicals, National Institute of Health 
      Sciences, Kamiyoga 1-18-1, Setagaya-ku, Tokyo 158-8501, Japan.
FAU - Mukasa, T
AU  - Mukasa T
FAU - Uchida, E
AU  - Uchida E
FAU - Kanayasu-Toyoda, T
AU  - Kanayasu-Toyoda T
FAU - Hayakawa, T
AU  - Hayakawa T
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Flavonoids)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (STAT3 protein, human)
RN  - 0 (Trans-Activators)
RN  - 143011-72-7 (Granulocyte Colony-Stimulating Factor)
RN  - 21820-51-9 (Phosphotyrosine)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - EC 2.7.11.1 (Ribosomal Protein S6 Kinases)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
RN  - SJE1IO5E3I (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one)
RN  - YOW8V9698H (Dimethyl Sulfoxide)
SB  - IM
MH  - Calcium-Calmodulin-Dependent Protein Kinases/metabolism
MH  - Cell Differentiation/drug effects
MH  - Cell Division/drug effects
MH  - DNA-Binding Proteins/*metabolism
MH  - Dimethyl Sulfoxide
MH  - Enzyme Activation/drug effects
MH  - Flavonoids/pharmacology
MH  - Fluorescent Antibody Technique
MH  - Granulocyte Colony-Stimulating Factor/*pharmacology
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/*pharmacology
MH  - HL-60 Cells/*drug effects
MH  - Humans
MH  - Phosphotyrosine/analysis
MH  - Ribosomal Protein S6 Kinases/metabolism
MH  - STAT3 Transcription Factor
MH  - Signal Transduction/drug effects
MH  - Trans-Activators/*metabolism
EDAT- 1999/05/21 00:00
MHDA- 1999/05/21 00:01
CRDT- 1999/05/21 00:00
PHST- 1999/05/21 00:00 [pubmed]
PHST- 1999/05/21 00:01 [medline]
PHST- 1999/05/21 00:00 [entrez]
AID - 10.1074/jbc.274.22.15575 [doi]
AID - S0021-9258(19)73062-2 [pii]
PST - ppublish
SO  - J Biol Chem. 1999 May 28;274(22):15575-81. doi: 10.1074/jbc.274.22.15575.