PMID- 11594774
OWN - NLM
STAT- MEDLINE
DCOM- 20011207
LR  - 20211203
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 288
IP  - 1
DP  - 2001 Oct 19
TI  - Insulin, insulin-like growth factor-I, and platelet-derived growth factor 
      activate extracellular signal-regulated kinase by distinct pathways in muscle 
      cells.
PG  - 205-11
AB  - We have investigated the signaling pathways initiated by insulin, insulin-like 
      growth factor-1 (IGF-I), and platelet-derived growth factor (PDGF) leading to 
      activation of the extracellular signal-regulated kinase (ERK) in L6 myotubes. 
      Insulin but not IGF-I or PDGF-induced ERK activation was abrogated by Ras 
      inhibition, either by treatment with the farnesyl transferase inhibitor FTP III, 
      or by actin disassembly by cytochalasin D, previously shown to inhibit Ras 
      activation. The protein kinase C (PKC) inhibitor bisindolylmaleimide abolished 
      PDGF but not IGF-I or insulin-induced ERK activation. ERK activation by insulin, 
      IGF-I, or PDGF was unaffected by the phosphatidylinositol 3-kinase inhibitor 
      wortmannin but was abolished by the MEK inhibitor PD98059. In contrast, 
      activation of the pathway involving phosphatidylinositol 3-kinase (PI3k), protein 
      kinase B, and glycogen synthase kinase 3 (GSK3) was mediated similarly by all 
      three receptors, through a PI 3-kinase-dependent but Ras- and actin-independent 
      pathway. We conclude that ERK activation is mediated by distinct pathways 
      including: (i) a cytoskeleton- and Ras-dependent, PKC-independent, pathway 
      utilized by insulin, (ii) a PKC-dependent, cytoskeleton- and Ras-independent 
      pathway used by PDGF, and (iii) a cytoskeleton-, Ras-, and PKC-independent 
      pathway utilized by IGF-I.
CI  - Copyright 2001 Academic Press.
FAU - Tsakiridis, T
AU  - Tsakiridis T
AD  - Clinical Sciences Division, Department of Medicine, University of Toronto, 1 
      King's College Circle, Toronto, Ontario, Canada M5S 1A8.
FAU - Tsiani, E
AU  - Tsiani E
FAU - Lekas, P
AU  - Lekas P
FAU - Bergman, A
AU  - Bergman A
FAU - Cherepanov, V
AU  - Cherepanov V
FAU - Whiteside, C
AU  - Whiteside C
FAU - Downey, G P
AU  - Downey GP
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (2-(2-oxo-2-((3,7,11-trimethyl-2,6,10-dodecatrienyl)oxy)aminoethyl)phosphonic 
      acid, (2,2-dimethyl-1-oxopropoxy)methyl ester sodium)
RN  - 0 (Actins)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Insulin)
RN  - 0 (Organophosphonates)
RN  - 0 (Platelet-Derived Growth Factor)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 2.7.11.- (Glycogen Synthase Kinases)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.26 (Glycogen Synthase Kinase 3)
RN  - EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
RN  - EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
SB  - IM
MH  - Actins/metabolism
MH  - Animals
MH  - Calcium-Calmodulin-Dependent Protein Kinases/metabolism
MH  - Cell Line
MH  - Cytoskeleton/metabolism
MH  - Enzyme Inhibitors/pharmacology
MH  - Glycogen Synthase Kinase 3
MH  - Glycogen Synthase Kinases
MH  - Insulin/*pharmacology
MH  - Insulin-Like Growth Factor I/*pharmacology
MH  - *MAP Kinase Signaling System
MH  - Mitogen-Activated Protein Kinase Kinases/physiology
MH  - Mitogen-Activated Protein Kinases/*metabolism
MH  - Muscle, Skeletal/drug effects/*enzymology
MH  - Organophosphonates/pharmacology
MH  - Phosphatidylinositol 3-Kinases/physiology
MH  - Phosphorylation
MH  - Platelet-Derived Growth Factor/*pharmacology
MH  - Protein Kinase C/physiology
MH  - *Protein Serine-Threonine Kinases
MH  - Proto-Oncogene Proteins/metabolism
MH  - Proto-Oncogene Proteins c-akt
MH  - Proto-Oncogene Proteins p21(ras)/antagonists & inhibitors/metabolism
EDAT- 2001/10/12 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/10/12 10:00
PHST- 2001/10/12 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/10/12 10:00 [entrez]
AID - S0006-291X(01)95762-6 [pii]
AID - 10.1006/bbrc.2001.5762 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2001 Oct 19;288(1):205-11. doi: 
      10.1006/bbrc.2001.5762.