Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Science 1 May 1987:
Vol. 236. no. 4801, pp. 570 - 573
DOI: 10.1126/science.2437651
Prev | Table of Contents | Next

Articles

Science, Vol 236, Issue 4801, 570-573
Copyright © 1987 by American Association for the Advancement of Science

articles

Mitogens and oncogenes can block the induction of specific voltage-gated ion channels

JM Caffrey, AM Brown, and MD Schneider

The mechanisms underlying the ontogeny of voltage-gated ion channels in muscle are unknown. Whether expression of voltage-gated channels is dependent on mitogen withdrawal and growth arrest, as is generally true for the induction of muscle-specific gene products, was investigated in the BC3H1 muscle cell line by patch-clamp techniques. Differentiated BC3H1 myocytes expressed functional Ca2+ and Na+ channels that correspond to those found in T tubules of skeletal muscle. However, Ca2+ and Na+ channels were first detected after about 5 days of mitogen withdrawal. In order to test whether cellular oncogenes, as surrogates for exogenous growth factors, could prevent the expression of ion channels whose induction was contingent on mitogen withdrawal, BC3H1 cells were modified by stable transfection with oncogene expression vectors. Expression vectors containing v-erbB, or c-myc under the control of the SV40 promoter, delayed but did not prevent the appearance of functional Ca2+ and Na+ channels. In contrast, transfection with a Val12 c-H-ras vector, or cotransfection of c-myc together with v-erbB, suppressed the formation of functional Ca2+ and Na+ channels for greater than or equal to 4 weeks. Potassium channels were affected neither by mitogenic medium nor by transfected oncogenes. Thus, the selective effects of certain oncogenes on ion channel induction corresponded to the suppressive effects of mitogenic medium.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Malignant human gliomas express an amiloride-sensitive Na+ conductance.
J. K. Bubien, D. A. Keeton, C. M. Fuller, G. Y. Gillespie, A. T. Reddy, T. B. Mapstone, and D. J. Benos (1999)
Am J Physiol Cell Physiol 276, C1405-C1410
   Abstract »    Full Text »    PDF »
Coordinated Incorporation of Skeletal Muscle Dihydropyridine Receptors and Ryanodine Receptors in Peripheral Couplings of BC3H1 Cells.
F. Protasi, C. Franzini-Armstrong, and B. E. Flucher (1997)
J. Cell Biol. 137, 859-870
   Abstract »    Full Text »    PDF »
Down-regulation of L-type Ca2+ Channel Transcript Levels by 1,25-Dihyroxyvitamin D3. OSTEOBLASTIC CELLS EXPRESS L-TYPE alpha 1C Ca2+ CHANNEL ISOFORMS.
J. G. Meszaros, N. J. Karin, K. Akanbi, and M. C. Farach-Carson (1996)
J. Biol. Chem. 271, 32981-32985
   Abstract »    Full Text »    PDF »
Conditional differentiation of heart- and smooth muscle-derived cells transformed by a temperature-sensitive mutant of SV40 T antigen.
L Jahn, J Sadoshima, A Greene, C Parker, K. Morgan, and S Izumo (1996)
J. Cell Sci. 109, 397-407
   Abstract »    PDF »
Early enhancement of calcium currents by H-ras oncoproteins injected into Hermissenda neurons.
C Collin, A. Papageorge, D. Lowy, and D. Alkon (1990)
Science 250, 1743-1745
   Abstract »    PDF »
A gene with homology to the myc similarity region of MyoD1 is expressed during myogenesis and is sufficient to activate the muscle differentiation program..
D G Edmondson and E N Olson (1989)
Genes & Dev. 3, 628-640
   Abstract »    PDF »


To Advertise     Find Products

Science. ISSN 0036-8075 (print), 1095-9203 (online)