Publications by authors named "Jeffrey P Miller"
Article Synopsis
- SV40 small t-antigen (ST) works with large T-antigen (LT) and activated rasv12 to drive cancer transformation in immortalized human cells, and other oncogenes can mimic ST's role.
- The exact connection between these oncogenes and the serine-threonine phosphatase protein phosphatase 2A (PP2A) is unclear, prompting an investigation into their interactions.
- The study reveals that p27 is linked to oncogenes that can replace ST and indicates that loss of p27 can facilitate transformation, while modified versions of p27 that resist degradation counteract ST's transforming properties, highlighting p27's significance as a target for PP2A and oncogenes.
Article Synopsis
- Understanding how cell cycle exit relates to differentiation is crucial for studying cancer and tissue development.
- Cancer can develop from stem cells that don't differentiate or from already differentiated cells that start dividing again.
- While it's known that stopping cell division can lead to differentiation, recent findings suggest that cell cycle regulators may also actively reshape the cell's gene expression during this process, indicating their roles go beyond merely causing cells to stop dividing.
Pocket proteins and cyclin-dependent kinase (CDK) inhibitors negatively regulate cell proliferation and can promote differentiation. However, which members of these gene families, which cell type they interact in, and what they do to promote differentiation in that cell type during mouse development are largely unknown. To identify the cell types in which p107 and p27 interact, we generated compound mutant mice.
View Article and Find Full Text PDFCyclin-dependent kinase inhibitor p27, a critical determinant for cell cycle progression, is an important regulation target of mitogenic signals during arterial injury. In this study, we show in rat aortic smooth muscle cells that PDGF-BB down-regulated p27 protein and mRNA in an ERK-dependent mechanism. Inhibition of ERK, but not other subtypes of the mitogen-activated protein kinase family, prevented the reduction of p27 protein and mRNA.
View Article and Find Full Text PDFThe amount of p27(Kip1) establishes a threshold to which G(1) cyclin-cyclin-dependent kinase complexes must surpass prior to cells progressing into S-phase. The amount of p27 is greatest in G(0) cells, intermediate in G(1) cells, and lowest in S-phase cells. However, there is little known regarding the pathways and mechanisms controlling p27 accumulation in G(0) cells.
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