Abstract
Leukocyte alkaline phosphatase (LAP) is synergistically induced by the combination of all-trans retinoic acid (ATRA) and granulocyte-colony-stimulating factor (G-CSF) in acute promyelocytic leukemia (APL) cells (Gianni′ M. et al., Blood 83: 1909-1921, 1994). The role of cAMP and tyrosine kinases in the induction of LAP was investigated. In the APL cell line NB4, adenosine-3′: 5′-monophosphothioate, cyclic, Rp isomer, a reversible inhibitor of cAMP-dependent protein kinase (PKA), has no effect on the induction of LAP enzymatic activity and mRNA triggered by ATRA + G-CSF, in conditions where this compound completely blocks the upregulation of LAP transcript caused by the combination of the PKA agonist, dibutyryl-cAMP (db-cAMP), and ATRA. Challenge of NB4 cells with G-CSF, dbcAMP and ATRA causes a much higher induction of LAP relative to that observed in the presence of ATRA + G-CSF or ATRA + dbcAMP. Treatment of NB4 with ATRA and G-CSF results in increases in tile tyrosine phosphorylation of several proteins. In the presence of the cytokine and the retinoid, tyrosine kinase inhibitors decrease LAP enzymatic activity and mRNA.
| Original language | English |
|---|---|
| Pages (from-to) | 846-854 |
| Number of pages | 9 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 208 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Mar 17 1995 |
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ASJC Scopus subject areas
- Molecular Biology
- Cell Biology
- Biophysics
- Biochemistry
Cite this
Tyrosine Kinases but Not cAMP-Dependent Protein Kinase Mediate the Induction of Leukocyte Alkaline Phosphatase by Granulocyte-Colony-Stimulating Factor and Retinoic Acid in Acute Promyelocytic Leukemia Cells. / Gianni, M.; Calzi, M. L.; Terao, M.; Rambaldi, A.; Garattini, E.
In: Biochemical and Biophysical Research Communications, Vol. 208, No. 2, 17.03.1995, p. 846-854.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Tyrosine Kinases but Not cAMP-Dependent Protein Kinase Mediate the Induction of Leukocyte Alkaline Phosphatase by Granulocyte-Colony-Stimulating Factor and Retinoic Acid in Acute Promyelocytic Leukemia Cells
AU - Gianni, M.
AU - Calzi, M. L.
AU - Terao, M.
AU - Rambaldi, A.
AU - Garattini, E.
PY - 1995/3/17
Y1 - 1995/3/17
N2 - Leukocyte alkaline phosphatase (LAP) is synergistically induced by the combination of all-trans retinoic acid (ATRA) and granulocyte-colony-stimulating factor (G-CSF) in acute promyelocytic leukemia (APL) cells (Gianni′ M. et al., Blood 83: 1909-1921, 1994). The role of cAMP and tyrosine kinases in the induction of LAP was investigated. In the APL cell line NB4, adenosine-3′: 5′-monophosphothioate, cyclic, Rp isomer, a reversible inhibitor of cAMP-dependent protein kinase (PKA), has no effect on the induction of LAP enzymatic activity and mRNA triggered by ATRA + G-CSF, in conditions where this compound completely blocks the upregulation of LAP transcript caused by the combination of the PKA agonist, dibutyryl-cAMP (db-cAMP), and ATRA. Challenge of NB4 cells with G-CSF, dbcAMP and ATRA causes a much higher induction of LAP relative to that observed in the presence of ATRA + G-CSF or ATRA + dbcAMP. Treatment of NB4 with ATRA and G-CSF results in increases in tile tyrosine phosphorylation of several proteins. In the presence of the cytokine and the retinoid, tyrosine kinase inhibitors decrease LAP enzymatic activity and mRNA.
AB - Leukocyte alkaline phosphatase (LAP) is synergistically induced by the combination of all-trans retinoic acid (ATRA) and granulocyte-colony-stimulating factor (G-CSF) in acute promyelocytic leukemia (APL) cells (Gianni′ M. et al., Blood 83: 1909-1921, 1994). The role of cAMP and tyrosine kinases in the induction of LAP was investigated. In the APL cell line NB4, adenosine-3′: 5′-monophosphothioate, cyclic, Rp isomer, a reversible inhibitor of cAMP-dependent protein kinase (PKA), has no effect on the induction of LAP enzymatic activity and mRNA triggered by ATRA + G-CSF, in conditions where this compound completely blocks the upregulation of LAP transcript caused by the combination of the PKA agonist, dibutyryl-cAMP (db-cAMP), and ATRA. Challenge of NB4 cells with G-CSF, dbcAMP and ATRA causes a much higher induction of LAP relative to that observed in the presence of ATRA + G-CSF or ATRA + dbcAMP. Treatment of NB4 with ATRA and G-CSF results in increases in tile tyrosine phosphorylation of several proteins. In the presence of the cytokine and the retinoid, tyrosine kinase inhibitors decrease LAP enzymatic activity and mRNA.
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U2 - 10.1006/bbrc.1995.1413
DO - 10.1006/bbrc.1995.1413
M3 - Article
VL - 208
SP - 846
EP - 854
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 2
ER -