| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
J Biol Chem, Vol. 275, Issue 18, 13677-13682, May 5, 2000
The 10T1/2-MRF4 fibroblast/myogenic cell system
was used to address the following interrelated questions: whether
distinct signaling pathways underlie myogenic inhibition by basic
fibroblast growth factor (bFGF) and transforming growth factor
(TGF)-
Ras/MEK/ERK Up-regulation of the Fibroblast KCa
Channel FIK Is a Common Mechanism for Basic Fibroblast Growth
Factor and Transforming Growth Factor-
Suppression of
Myogenesis*
; which of these pathways also up-regulates the fibroblast
intermediate conductance calcium-activated potassium channel, FIK, a
positive regulator of cell proliferation; and whether FIK up-regulation underlies some or all myogenic inhibitory signaling events. The results
show that myogenic inhibition in 10T1/2-MRF4 cells, by both bFGF and
TGF-, requires activation of the Ras/mitogen-activated protein (MAP)
kinase/MAP kinase-ERK kinase (MEK)/extracellular signal-regulated
kinase (ERK) pathway, and resultant FIK up-regulation. We show that FIK
is instrumental in MEK-dependent suppression of
acetylcholine receptor channel expression but that MEK activation and
FIK up-regulation are not essential to suppression of myosin heavy
chain and myotube formation. These data indicate that Ras/MEK/ERK induction of FIK is pivotal to regulation of certain myogenic events by
both receptor tyrosine kinases and TGF- receptor, and this is also
the first demonstration of chronic FIK up-regulation by the TGF-
receptor family. Furthermore, the results define the physiologic
signaling requirements for growth factor-stimulated FIK up-regulation,
whereas previous work has concentrated on constitutive FIK
up-regulation in cells stably transfected with oncoprotein signaling
molecules. This study, together with earlier work showing that FIK
positively regulates cell proliferation, establishes this member of the
IK channel family as a multifunctional, growth factor-regulated
signaling molecule.
*
This work was supported by an Indiana Elks grant (to
S. G. R.), National Institutes of Health Grant AR41115 (to
S. F. K.), and a National Institutes of Health NRSA fellowship (to
T. L. P.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Biological
Sciences, Purdue University, West Lafayette, IN 47907, Tel.: 765-494-8191; Fax: 765-494-0876; E-mail:
srane@bilbo.bio.purdue.edu.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  T. A. Baudino, W. Carver, W. Giles, and T. K. Borg Cardiac fibroblasts: friend or foe? Am J Physiol Heart Circ Physiol, September 1, 2006; 291(3): H1015 - H1026. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Pietrangelo, B. Fioretti, R. Mancinelli, L. Catacuzzeno, F. Franciolini, G. Fano, and S. Fulle Extracellular guanosine-5'-triphosphate modulates myogenesis via intermediate Ca2+-activated K+ currents in C2C12 mouse cells J. Physiol., May 1, 2006; 572(3): 721 - 733. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Yang, Y. Chen, Y. Zhang, X. Wang, N. Yang, and D. Zhu Extracellular Signal-Regulated Kinase 1/2 Mitogen-Activated Protein Kinase Pathway Is Involved in Myostatin-Regulated Differentiation Repression Cancer Res., February 1, 2006; 66(3): 1320 - 1326. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Fioretti, T. Pietrangelo, L. Catacuzzeno, and F. Franciolini Intermediate-conductance Ca2+-activated K+ channel is expressed in C2C12 myoblasts and is downregulated during myogenesis Am J Physiol Cell Physiol, July 1, 2005; 289(1): C89 - C96. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Chilton, S. Ohya, D. Freed, E. George, V. Drobic, Y. Shibukawa, K. A. MacCannell, Y. Imaizumi, R. B. Clark, I. M. C. Dixon, et al. K+ currents regulate the resting membrane potential, proliferation, and contractile responses in ventricular fibroblasts and myofibroblasts Am J Physiol Heart Circ Physiol, June 1, 2005; 288(6): H2931 - H2939. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Grgic, I. Eichler, P. Heinau, H. Si, S. Brakemeier, J. Hoyer, and R. Kohler Selective Blockade of the Intermediate-Conductance Ca2+-Activated K+ Channel Suppresses Proliferation of Microvascular and Macrovascular Endothelial Cells and Angiogenesis In Vivo Arterioscler. Thromb. Vasc. Biol., April 1, 2005; 25(4): 704 - 709. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Sorci, F. Riuzzi, C. Arcuri, I. Giambanco, and R. Donato Amphoterin Stimulates Myogenesis and Counteracts the Antimyogenic Factors Basic Fibroblast Growth Factor and S100B via RAGE Binding Mol. Cell. Biol., June 1, 2004; 24(11): 4880 - 4894. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Jager, T. Dreker, A. Buck, K. Giehl, T. Gress, and S. Grissmer Blockage of Intermediate-Conductance Ca2+-Activated K+ Channels Inhibit Human Pancreatic Cancer Cell Growth in Vitro Mol. Pharmacol., March 1, 2004; 65(3): 630 - 638. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Brakemeier, A. Kersten, I. Eichler, I. Grgic, A. Zakrzewicz, H. Hopp, R. Kohler, and J. Hoyer Shear stress-induced up-regulation of the intermediate-conductance Ca2+-activated K+ channel in human endothelium Cardiovasc Res, December 1, 2003; 60(3): 488 - 496. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Kohler, H. Wulff, I. Eichler, M. Kneifel, D. Neumann, A. Knorr, I. Grgic, D. Kampfe, H. Si, J. Wibawa, et al. Blockade of the Intermediate-Conductance Calcium-Activated Potassium Channel as a New Therapeutic Strategy for Restenosis Circulation, September 2, 2003; 108(9): 1119 - 1125. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K A Bowley, M J Morton, M Hunter, and G I Sandle Non-genomic regulation of intermediate conductance potassium channels by aldosterone in human colonic crypt cells Gut, June 1, 2003; 52(6): 854 - 860. [Abstract] [Full Text]
|
|
|
|
 |
|
 D. Sanoudou, J. N. Haslett, A. T. Kho, S. Guo, H. T. Gazda, S. A. Greenberg, H. G. W. Lidov, I. S. Kohane, L. M. Kunkel, and A. H. Beggs Expression profiling reveals altered satellite cell numbers and glycolytic enzyme transcription in nemaline myopathy muscle PNAS, April 15, 2003; 100(8): 4666 - 4671. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Koegel, S. Kaesler, R. Burgstahler, S. Werner, and C. Alzheimer Unexpected Down-regulation of the hIK1 Ca2+-activated K+ Channel by Its Opener 1-Ethyl-2-benzimidazolinone in HaCaT Keratinocytes. INVERSE EFFECTS ON CELL GROWTH AND PROLIFERATION J. Biol. Chem., January 24, 2003; 278(5): 3323 - 3330. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Liu, B. L. Black, and R. Derynck TGF-beta inhibits muscle differentiation through functional repression of myogenic transcription factors by Smad3 Genes & Dev., November 15, 2001; 15(22): 2950 - 2966. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |
