Julie C Roth

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The hdm2 gene is overexpressed in a variety of human tumors. Its gene product localizes predominantly to the nucleus, where it acts as an inhibitor of the p53 tumor suppressor gene product. It is shown here that the hdm2 oncoprotein constantly shuttles between the nucleus and the cytoplasm. Shuttling of hdm2 does not depend on its interaction with p53.(More)
BACKGROUND The cellular mdm2 gene has transforming activity when overexpressed and is amplified in a variety of human tumors. At least part of the transforming ability of the MDM2 protein is due to binding and inactivating the p53 tumor suppressor protein. Additionally, this protein forms a complex in vivo with the L5 ribosomal protein and its associated 5S(More)
OBJECTIVE As the pharmacological suppression of angiotensin has been associated with cardioprotective effects in cardiomyopathy, our primary aim was to determine whether the expression of Smad protein components of the cardiac TGF-beta signaling cascade is modulated by chronic AT(1) receptor blockade. Furthermore, we examined the relationship between(More)
We examined the role of the transforming growth factor (TGF)-beta(1) signaling inhibitor Smad 7 in cardiac fibrosis. TGF-beta(1) (10 ng/ml) was found to increase cytosolic Smad 7 expression in primary adult rat fibroblasts and induce rapid nuclear export of exogenous Smad 7 in COS-7 cells. Furthermore, overexpression of Smad 7 in primary adult fibroblasts(More)
The E1B 55-kDa and E4 34-kDa oncoproteins of adenovirus type 5 (abbreviated here as E1B-55kD and E4-34kD) promote the export of viral mRNA and inhibit the export of most cellular mRNA species. We show that the intracellular complex containing E1B-55kD and E4-34kD continuously shuttles between the nucleus and the cytoplasm, and may thus serve as a(More)
BACKGROUND The MDM2 oncoprotein binds to the tumor suppressor p53 and inhibits its anti-oncogenic functions. MATERIALS AND METHODS To determine the amino acids of MDM2 that are critical for binding to p53, a modified two-hybrid screen was performed in yeast. Site-directed mutagenesis was then performed to identify MDM2 residues important for p53(More)
The p53 tumor suppressor protein induces apoptosis through a mechanism that may involve the transcriptional activation of cellular genes, including the PIG3 gene. A p53 protein lacking the proline-rich region (p53delta62-91) induces many p53-responsive genes but not PIG3. In parallel, this mutant induces growth arrest but not apoptosis. We show here that(More)