PMID- 8490168
OWN - NLM
STAT- MEDLINE
DCOM- 19930611
LR  - 20210216
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 81
IP  - 10
DP  - 1993 May 15
TI  - Mechanism of differential inhibition of factor-dependent cell proliferation by 
      transforming growth factor-beta 1: selective uncoupling of FMS from MYC.
PG  - 2539-46
AB  - Transforming growth factor-beta 1 (TGF-beta 1) selectively modulates 
      hematopoietic cell proliferation. The proliferation of FDC-P1 clone MAC-11, a 
      factor-dependent murine myeloid progenitor cell line, was inhibited 
      differentially by TGF-beta 1: strongly in macrophage colony-stimulating factor 
      (M-CSF), mildly in interleukin-3, and not at all in granulocyte-macrophage-CSF 
      (GM-CSF). Flow cytometry and Western blots showed an unexpected increase in 
      expression of FMS, the receptor for M-CSF, in response to TGF-beta 1. Metabolic 
      labeling with 35S-methionine showed that synthesis of FMS protein accelerated in 
      response to TGF-beta 1, whereas its degradation was unaffected. Northern analyses 
      showed a rapid increase in c-fms RNA after the addition of TGF-beta 1. TGF-beta 1 
      did not affect kinase activity, cellular phosphotyrosine response, or 
      internalization of FMS. However, TGF-beta 1 inhibited the induction by M-CSF of 
      c-myc RNA analyzed on Northern blots and protein detected by 
      radioimmuno-precipitation. TGF-beta 1 did not affect induction of c-myc 
      expression by GM-CSF or induction of c-fos or c-jun by M-CSF. Therefore, FMS and 
      the GM-CSF receptor induce c-myc via signal transduction pathways that differ in 
      that only the former is inhibited by TGF-beta 1. This inhibition may account for 
      the selective growth regulation by TGF-beta 1.
FAU - Chen, A R
AU  - Chen AR
AD  - Department of Cell Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 
      98104.
FAU - Rohrschneider, L R
AU  - Rohrschneider LR
LA  - eng
GR  - 5T32CA09351/CA/NCI NIH HHS/United States
GR  - CA20551/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (Actins)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Transforming Growth Factor beta)
RN  - 81627-83-0 (Macrophage Colony-Stimulating Factor)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - 9007-49-2 (DNA)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
SB  - IM
GS  - FMS
GS  - MYC
GS  - c-fos
GS  - c-jun
GS  - c-myc
MH  - Actins/genetics
MH  - Animals
MH  - Blotting, Northern
MH  - Cell Adhesion/drug effects
MH  - Cell Cycle
MH  - Cell Division/drug effects
MH  - Cell Line
MH  - DNA/analysis/metabolism
MH  - *Genes, fms/drug effects
MH  - Genes, fos/drug effects
MH  - Genes, jun/drug effects
MH  - *Genes, myc/drug effects
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology
MH  - Hematopoietic Stem Cells/*cytology/drug effects/physiology
MH  - Humans
MH  - Kinetics
MH  - Macrophage Colony-Stimulating Factor/pharmacology
MH  - Mice
MH  - Protein-Tyrosine Kinases/metabolism
MH  - Recombinant Proteins/pharmacology
MH  - Time Factors
MH  - Transforming Growth Factor beta/*pharmacology
EDAT- 1993/05/15 00:00
MHDA- 1993/05/15 00:01
CRDT- 1993/05/15 00:00
PHST- 1993/05/15 00:00 [pubmed]
PHST- 1993/05/15 00:01 [medline]
PHST- 1993/05/15 00:00 [entrez]
AID - S0006-4971(20)67845-4 [pii]
PST - ppublish
SO  - Blood. 1993 May 15;81(10):2539-46.