PMID- 11802792
OWN - NLM
STAT- MEDLINE
DCOM- 20020312
LR  - 20190501
IS  - 0264-6021 (Print)
IS  - 1470-8728 (Electronic)
IS  - 0264-6021 (Linking)
VI  - 361
IP  - Pt 3
DP  - 2002 Feb 1
TI  - Retinoic acid activation of the ERK pathway is required for embryonic stem cell 
      commitment into the adipocyte lineage.
PG  - 621-7
AB  - Mouse embryonic stem (ES) cells are pluripotent cells that differentiate into 
      multiple cell lineages. The commitment of ES cells into the adipocyte lineage is 
      dependent on an early 3-day treatment with all-trans retinoic acid (RA). To 
      characterize the molecular mechanisms underlying this process, we examined the 
      contribution of the extracellular-signal-regulated kinase (ERK) pathway. 
      Treatment of ES cell-derived embryoid bodies with RA resulted in a prolonged 
      activation of the ERK pathway, but not the c-Jun N-terminal kinase, p38 
      mitogen-activated protein kinase or phosphoinositide 3-kinase pathways. To 
      investigate the role of ERK activation, co-treatment of RA with PD98059, a 
      specific inhibitor of the ERK signalling pathway, prevented both adipocyte 
      formation and expression of the adipogenic markers, adipocyte lipid-binding 
      protein and peroxisome-proliferator-activated receptor gamma. Furthermore, we 
      show that ERK activation is required only during RA treatment. PD98059 does not 
      interfere with the commitment of ES cells into other lineages, such as 
      neurogenesis, myogenesis and cardiomyogenesis. As opposed to the controversial 
      role of the ERK pathway in terminal differentiation, our results clearly 
      demonstrate that this pathway is specifically required at an early stage of 
      adipogenesis, corresponding to the RA-dependent commitment of ES cells.
FAU - Bost, Frederic
AU  - Bost F
AD  - INSERM E9911 and IFR50, Faculte de Medecine, Universite de Nice Sophia Antipolis, 
      Avenue de Valombrose, Nice 06107, France.
FAU - Caron, Leslie
AU  - Caron L
FAU - Marchetti, Irene
AU  - Marchetti I
FAU - Dani, Christian
AU  - Dani C
FAU - Le Marchand-Brustel, Yannick
AU  - Le Marchand-Brustel Y
FAU - Binetruy, Bernard
AU  - Binetruy B
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 (Butadienes)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Flavonoids)
RN  - 0 (Imidazoles)
RN  - 0 (Nitriles)
RN  - 0 (Pyridines)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Transcription Factors)
RN  - 0 (U 0126)
RN  - 5688UTC01R (Tretinoin)
RN  - 63231-63-0 (RNA)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - OU13V1EYWQ (SB 203580)
RN  - SJE1IO5E3I (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one)
SB  - IM
MH  - Adipocytes/*cytology/metabolism
MH  - Animals
MH  - Butadienes/pharmacology
MH  - Cell Lineage
MH  - Embryo, Mammalian/*cytology
MH  - Enzyme Activation
MH  - Enzyme Inhibitors/pharmacology
MH  - Flavonoids/pharmacology
MH  - Imidazoles/pharmacology
MH  - JNK Mitogen-Activated Protein Kinases
MH  - Mice
MH  - Mitogen-Activated Protein Kinases/*metabolism
MH  - Myocardium/cytology
MH  - Neurons/metabolism
MH  - Nitriles/pharmacology
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Protein Binding
MH  - Pyridines/pharmacology
MH  - RNA/metabolism
MH  - Receptors, Cytoplasmic and Nuclear/metabolism
MH  - Signal Transduction
MH  - Stem Cells/*cytology
MH  - Time Factors
MH  - Transcription Factors/metabolism
MH  - Tretinoin/*metabolism/pharmacology
MH  - p38 Mitogen-Activated Protein Kinases
PMC - PMC1222345
EDAT- 2002/01/23 10:00
MHDA- 2002/03/13 10:01
PMCR- 2002/08/01
CRDT- 2002/01/23 10:00
PHST- 2002/01/23 10:00 [pubmed]
PHST- 2002/03/13 10:01 [medline]
PHST- 2002/01/23 10:00 [entrez]
PHST- 2002/08/01 00:00 [pmc-release]
AID - 10.1042/0264-6021:3610621 [doi]
PST - ppublish
SO  - Biochem J. 2002 Feb 1;361(Pt 3):621-7. doi: 10.1042/0264-6021:3610621.