Previously we showed a rapid and transient inhibition of gap junctional communication (GJC) by platelet-derived growth factor (PDGF) in T51B rat liver epithelial cells expressing wild-type platelet-derived growth factor b receptors (PDGFrb). This action of PDGF correlated with the hyperphosphorylati
โฆ LIBER โฆ
Mitogen-activated protein kinase and phosphorylation of connexin43 are not sufficient for the disruption of gap junctional communication by platelet-derived growth factor and tetradecanoylphorbol acetate
โ Scribed by Mohammad Z. Hossain; Ajit B. Jagdale; Peng Ao; Alton L. Boynton
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 206 KB
- Volume
- 179
- Category
- Article
- ISSN
- 0021-9541
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Gap junctional communication (GJC) between contacting cells has been postulated to be involved in the regulation of cell proliferation. This suggestion stems from numerous studies showing modulation of GJC by agents that influence cellular proliferation. Platelet-derived growth factor (PDGF), a stro