PMID- 11513742
OWN - NLM
STAT- MEDLINE
DCOM- 20011004
LR  - 20190501
IS  - 0264-6021 (Print)
IS  - 1470-8728 (Electronic)
IS  - 0264-6021 (Linking)
VI  - 358
IP  - Pt 2
DP  - 2001 Sep 1
TI  - Colony-stimulating factor-1 (CSF-1) receptor-mediated macrophage differentiation 
      in myeloid cells: a role for tyrosine 559-dependent protein phosphatase 2A (PP2A) 
      activity.
PG  - 431-6
AB  - M1 myeloid cells transfected with the wild-type (WT) colony-stimulating factor-1 
      (CSF-1) receptor (CSF-1R; M1/WT cells) undergo CSF-1-dependent macrophage 
      differentiation. By mutation studies, we have provided prior evidence that 
      tyrosine 559 in the CSF-1R cytoplasmic domain governs the Src-dependent 
      differentiation pathway. Further components of this pathway were then sought. We 
      report that the extent of CSF-1-mediated tyrosine phosphorylation of protein 
      phosphatase 2A (PP2A), and the associated loss of its activity were reduced in M1 
      cells transfected with the CSF-1R with a tyrosine-to-phenylalanine mutation at 
      position 559 (M1/559 cells), compared with the corresponding responses in 
      CSF-1-treated M1/WT cells. This evidence for an involvement of a reduction in 
      PP2A activity in the differentiation process was supported by the restoration of 
      the defect in the CSF-1-mediated differentiation of M1/559 cells by the addition 
      of the PP2A inhibitor, okadaic acid. It was also found that the degree of 
      activation of extracellular-signal-regulated kinase (ERK) activities by CSF-1 was 
      reduced in M1/559 cells, suggesting their involvement in the differentiation 
      process. These data suggest that PP2A and ERK form part of the Src-dependent 
      signal-transduction cascade governing CSF-1-mediated macrophage differentiation 
      in M1 cells.
FAU - McMahon, K A
AU  - McMahon KA
AD  - Arthritis and Inflammation Research Centre, University of Melbourne, Department 
      of Medicine, Royal Melbourne Hospital, Parkville, Victoria, Australia. 
      kerrie_ann_mcmahon@hotmail.com
FAU - Wilson, N J
AU  - Wilson NJ
FAU - Marks, D C
AU  - Marks DC
FAU - Beecroft, T L
AU  - Beecroft TL
FAU - Whitty, G A
AU  - Whitty GA
FAU - Hamilton, J A
AU  - Hamilton JA
FAU - Csar, X F
AU  - Csar XF
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Biochem J
JT  - The Biochemical journal
JID - 2984726R
RN  - 0 (Enzyme Inhibitors)
RN  - 1W21G5Q4N2 (Okadaic Acid)
RN  - 21820-51-9 (Phosphotyrosine)
RN  - EC 2.7.10.1 (Receptor, Macrophage Colony-Stimulating Factor)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 3.1.3.16 (Phosphoprotein Phosphatases)
RN  - EC 3.1.3.16 (Protein Phosphatase 2)
SB  - IM
MH  - Animals
MH  - Cell Differentiation
MH  - Cell Line
MH  - Enzyme Inhibitors/pharmacology
MH  - Macrophages/cytology/*physiology
MH  - Mice
MH  - Mitogen-Activated Protein Kinase 1/metabolism
MH  - Mitogen-Activated Protein Kinase 3
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - Mutation
MH  - Myeloid Cells/*cytology/drug effects
MH  - Okadaic Acid/pharmacology
MH  - Phosphoprotein Phosphatases/antagonists & inhibitors/*metabolism
MH  - Phosphorylation
MH  - Phosphotyrosine/metabolism
MH  - Protein Phosphatase 2
MH  - Receptor, Macrophage Colony-Stimulating Factor/*chemistry/genetics/*physiology
MH  - Signal Transduction
PMC - PMC1222076
EDAT- 2001/08/22 10:00
MHDA- 2001/10/05 10:01
PMCR- 2002/03/01
CRDT- 2001/08/22 10:00
PHST- 2001/08/22 10:00 [pubmed]
PHST- 2001/10/05 10:01 [medline]
PHST- 2001/08/22 10:00 [entrez]
PHST- 2002/03/01 00:00 [pmc-release]
AID - 10.1042/0264-6021:3580431 [doi]
PST - ppublish
SO  - Biochem J. 2001 Sep 1;358(Pt 2):431-6. doi: 10.1042/0264-6021:3580431.