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Synergistic induction of cyclin D1 in oligodendrocyte progenitor cells by IGF‐I and FGF‐2 requires differential stimulation of multiple signaling pathways by Terra J. Frederick; Jungsoo Min; Stefanie C. Altieri; Nina E. Mitchell; Teresa L. Wood is a Neuroscience article available to read on EtoBox.
What is Synergistic induction of cyclin D1 in oligodendrocyte progenitor cells by IGF‐I and FGF‐2 requires differential stimulation of multiple signaling pathways about?
## Abstract D‐type cyclins are direct targets of extracellular signals and critical regulators of G~1~ progression. Our previous data demonstrated that IGF‐I and FGF‐2 synergize to enhance cyclin D1 expression, cyclin E/cdk2 complex activation, and S‐phase entry in OP cells. Here, we provide a mechanistic explanation for how two growth factor signaling pathways converge on a major cell cycle regulator. IGF‐I and FGF‐2 differentially activate signaling pathways to coordinately promote cyclin D1 expression. We show that the p44/p42 MAPK signaling pathway is essential for FGF‐2 induction of cyclin D1 mRNA. In contrast, blocking the PI3‐Kinase pathway results in loss of IGF‐I/FGF‐2 synergistic induction of cyclin D1 protein levels. Moreover, the presence of IGF‐I significantly enhances nuclear localization of cyclin D1, which also requires PI3K signaling. GSK‐3β, a downstream target of the PI3K/Akt pathway, is phosphorylated in the presence of IGF‐I in OPs. Consistent with a known role for GSK‐3β in cyclin D1 degradation, we show that proteasome inhibition in OPs exposed to FGF‐2 increased cyclin D1 levels, equivalent to levels seen in IGF‐I/FGF‐2 treated cells. Thus, we provide a mode
Who reads Synergistic induction of cyclin D1 in oligodendrocyte progenitor cells by IGF‐I and FGF‐2 requires differential stimulation of multiple signaling pathways?
It is typically read by researchers, students, and practitioners in Neuroscience.
- Author
- Terra J. Frederick; Jungsoo Min; Stefanie C. Altieri; Nina E. Mitchell; Teresa L. Wood
- Publisher
- John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley; Research Square (ISSN 0894-1491)
- Published
- 2007
- Language
- EN
- Field
- Neuroscience (Life Sciences)