The effects of N-ras oncogene expression on PDGF-BB stimulated responses in cultured mouse myoblasts.

Abstract:

:The role of the ras oncogene in the signalling pathway triggered by platelet-derived growth factor BB (PDGF-BB) has been investigated in a cell line which normally differentiates into myotubes. Following the activation of the N-ras oncogene, however, the cells proliferate and form foci. PDGF-BB stimulated the phosphorylation of tyrosine in several cellular proteins of molecular weight 185, 160, 94, 54, 44, 42 kDa and furthermore Ca2+ was released from internal stores. Activation of the N-ras gene by treatment of cells with dexamethasone (DEX) inhibited these responses to PDGF-BB. On the other hand, both ras-induced and -non induced cells responded to bradykinin (BK), foetal calf serum (FCS) and ionomycin (ION) by releasing Ca2+ from intracellular stores. The inhibition of the response to PDGF-BB in ras-activated cells has been further investigated. The binding of [125I]-PDGF-BB to its receptors was low and western blotting showed a low level of PDGF-BB receptor protein. This was in marked contrast to the receptor number seen in cells grown in growth medium or fusion promoting medium. These results indicate that cells transformed with the N-ras oncogene fail to respond to platelet-derived growth factor and exhibit a very low level of PDGF receptors. This suggests a role for the ras oncogene in the earliest steps of the signalling pathway.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Zeytinoğlu H,Griffiths SL,Dawson AP,Gibson I

doi

10.1016/0898-6568(94)00082-m

subject

Has Abstract

pub_date

1995-03-01 00:00:00

pages

235-46

issue

3

eissn

0898-6568

issn

1873-3913

pii

089865689400082M

journal_volume

7

pub_type

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