Jared T Winston

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Stimulation of quiescent Balb/c 3T3 fibroblasts into S phase requires the synergistic action of platelet-derived growth factor (PDGF) and progression factors found in platelet-poor plasma (PPP). Traverse of the G1/S phase boundary and the initiation of DNA replication require functional cyclin E-cyclin-dependent kinase (Cdk) 2 and cyclin A-Cdk2 complexes;(More)
The ras proto-oncogene has been implicated during the formation of tumors in vivo as well as the transformation of cell lines in culture. Conditional expression of an activated ras mutant in Balb/c-3T3 fibroblasts failed to stimulate S phase entry in the absence of plasma-derived progression factors, but did shorten the G1 interval from 12 to 6 h and(More)
Overexpression of the cyclin D1/PRAD1 oncogene has been observed in a number of tumorigenic cell lines, suggesting that regulation of D1 expression may represent an important step in the control of cellular proliferation. We have examined the mRNA expression of cyclin D1, as well as two related D-type cyclins, D2 and D3, in response to defined growth(More)
Misfolded protein aggregation causes disease and aging; autophagy counteracts this by eliminating damaged components, enabling cells to survive starvation. The cytoplasm-to-vacuole targeting pathway in yeast encompasses the aggregation of the premature form of aminopeptidase 1 (prApe1) in cytosol and its sequestration by autophagic proteins into a vesicle(More)
Density-arrested BALB/c-3T3 cells stimulated to proliferate in an amino acid-deficient medium arrest in mid-G1 at a point termed the V point. Cells released from V point arrest require 6 hr to traverse late G1 and enter S phase. As data presented here show that mRNA synthesis is needed for 2-3 hr after release of cells from the V point, after which(More)
Addition of tumor promoting phorbol esters, such as phorbol 12-myristate 13-acetate (PMA), to many cell lines results in a decrease of 125I-epidermal growth factor (EGF) binding and increased serine/threonine phosphorylation of the EGF receptor in a process termed transmodulation. It is, however, unclear whether or not receptor phosphorylation is causally(More)
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