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

Zeytinoǧlu H., Griffiths S. L., Dawson A. P., Gibson I.

Cellular Signalling, cilt.7, sa.3, ss.235-246, 1995 (SCI-Expanded) identifier identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 7 Sayı: 3
  • Basım Tarihi: 1995
  • Doi Numarası: 10.1016/0898-6568(94)00082-m
  • Dergi Adı: Cellular Signalling
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.235-246
  • Anahtar Kelimeler: MYOBLAST, RAS, GROWTH FACTOR, CALCIUM, PHOSPHORYLATION, RECEPTORS, SIGNAL TRANSDUCTION, GROWTH-FACTOR RECEPTOR, PROTEIN-KINASE-C, INTRACELLULAR CALCIUM RELEASE, INOSITOL PHOSPHATE PRODUCTION, SIGNAL TRANSDUCTION, TYROSINE PHOSPHORYLATION, HUMAN-FIBROBLASTS, PHOSPHATIDYLINOSITOL TURNOVER, TERMINAL DIFFERENTIATION, BRADYKININ RECEPTORS
  • Anadolu Üniversitesi Adresli: Evet

Özet

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. © 1995.