Patricia O'Brien

Florida College

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Laurie G. Hudson

University of New Mexico

Ben M. Dunn

University of Florida

Stéphanie Rose

Centre National de la Recherche Scientifique

John W. Sleasman

Duke University

Maureen M. Goodenow

National Institutes of Health

Lisa J. McCawley

Vanderbilt University

Steven Pomeroy

University of Florida

Joshua C. Bunger

University of Florida

ÁO

Álvaro Osornio-Vargas

University of Alberta

Irma Rosas

Universidad Nacional Autónoma de México

Cooperative Institutions

University of Florida

Florida College

National Institute of Environmental Health Sciences

National Institutes of Health

Northwestern University

Instituto Nacional de Cancerología

Duke University

Research Triangle Park Foundation

North Carolina State University

Environmental Protection Agency

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Enhanced Modulation of Keratinocyte Motility by Transforming Growth Factor-α (TGF-α) Relative to Epidermal Growth Factor (EGF)

Journal of Investigative Dermatology (1996)

Donald Cha Patricia O'Brien Edel A. O’Toole David T. Woodley Laurie G. Hudson

10.1111/1523-1747.ep12345083

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Citations (155)

Drug-associated changes in amino acid residues in Gag p2, p7NC, and p6Gag/p6Pol in human immunodeficiency virus type 1 (HIV-1) display a dominant effect on replicative fitness and drug response

Virology (2008)

Sarah K Ho Roxana M. Coman Joshua C. Bunger Stéphanie Rose Patricia O'Brien

Regions of HIV-1 gag between p2 and p6(Gag)/p6(Pol), in addition to protease (PR), develop genetic diversity in HIV-1 infected individuals who fail to suppress virus replication by combination protease inhibitor (PI) therapy. To elucidate functional consequences for viral replication and PI susceptibility by changes in Gag that evolve in vivo during PI therapy, a panel of recombinant viruses was constructed. Residues in Gag p2/p7(NC) cleavage site and p7(NC), combined with residues in the flap of PR, defined novel fitness determinants that restored replicative capacity to the posttherapy virus. Multiple determinants in Gag have a dominant effect on PR phenotype and increase susceptibility to inhibitors of drug-resistant or drug-sensitive PR genes. Gag determinants of drug sensitivity and replication alter the fitness landscape of the virus, and viral replicative capacity can be independent of drug sensitivity. The functional linkage between Gag and PR provides targets for novel therapeutics to inhibit drug-resistant viruses.

Group-specific antigen

10.1016/j.virol.2008.05.029

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Citations (40)

Epidermal growth factor (EGF)- and scatter factor/hepatocyte growth factor (SF/HGF)-mediated keratinocyte migration is coincident with induction of matrix metalloproteinase (MMP)-9

Journal of Cellular Physiology (1998)

Lisa J. McCawley Patricia O'Brien Laurie G. Hudson

Receptor tyrosine kinases are key regulators of cellular function including cell growth, differentiation, migration, and morphogenesis. Disruptions of receptor tyrosine kinase signaling pathways are often associated with changes in cellular proliferative capacity and tumorigenesis. Both receptor-specific and cell type-specific factors may contribute to the ultimate cellular responses observed after receptor activation. In this regard, we find that both normal keratinocytes and their tumorigenic counterparts display differential responses to activation of receptor tyrosine kinases. Multiple ligands were mitogenic for keratinocytes, but only epidermal growth factor (EGF), transforming growth factor α (TGFα), and scatter factor/hepatocyte growth factor (SF/HGF) promoted cell motility as assessed by colony dispersion (scattering) and in vitro reepithelialization. Interestingly, growth factor specificity for motility coincided with ligand-mediated cell invasion through a reconstituted basement membrane and induction of the 92-kDa metalloproteinase (MMP-9) activity as determined by gelatin zymogram analysis. Inhibitors of MMP activity or addition of an MMP-9 neutralizing antibody resulted in the loss of growth factor-induced colony dispersion, suggesting a functional role for MMP-9 induction during this response. Coordinate regulation of MMP-9 induction and the migratory response are likely to contribute to the enhanced invasive potential observed in response to EGF and SF/HGF. Our findings suggest that alternate receptor-mediated signaling pathways leading to differences in gene expression may be involved in complex cellular responses such as colony dispersion or invasion. J. Cell. Physiol. 176:255–265, 1998. © 1998 Wiley-Liss, Inc.

10.1002/(sici)1097-4652(199808)176:2<255::aid-jcp4>3.0.co;2-n

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Citations (221)

Induction of the Lung Myofibroblast PDGF Receptor System by Urban Ambient Particles from Mexico City

American Journal of Respiratory Cell and Molecular Biology (1998)

James C. Bonner Annette B. Rice Pamela M. Lindroos Patricia O'Brien Kevin L. Dreher

Platelet-derived growth factor (PDGF) and its receptor system regulate mesenchymal cell proliferation. We recently reported that emission-source fly-ash particles and asbestos fibers induce the PDGF alpha-receptor through a macrophage-dependent pathway, and upregulation of this receptor greatly enhances the mitogenic response of lung myofibroblasts to PDGF (Lindroos and colleagues, Am. J. Respir. Cell Mol. Biol. 1997;16:283-292). In the present study we investigated the effect of particulate matter <= 10 micrometers in size (PM10) from the southern, central, and northern regions of Mexico City on PDGF receptor induction and compared these urban, ambient particles with Mt. St. Helen's volcanic ash particles as a negative control. All Mexico City PM10 samples, but not volcanic ash, stimulated rat alveolar macrophages to secrete a soluble, upregulatory factor(s) for the PDGF alpha-receptor on early passage rat lung myofibroblasts. The macrophage-derived upregulatory activity was blocked by the interleukin (IL)-1 receptor antagonist. The ability of PM10 to stimulate IL-1beta release was blocked in part by a recombinant endotoxin neutralizing protein (rENP). Lipopolysaccharide/endotoxin (LPS) and vanadium, both constituents that were present within these PM10 samples, also stimulated macrophages to secrete factor(s) that upregulated PDGF-Ralpha on lung myofibroblasts. Direct exposure of myofibroblasts to PM10 also elicited upregulation of the PDGF alpha-receptor, and this effect was blocked by rENP and mimicked by LPS, but not vanadium. These findings suggest that PM10 particles induce expression of the PDGF receptor system through macrophage-dependent and -independent mechanisms involving endotoxin and metals.

Platelet-derived growth factor

Myofibroblast

Alveolar macrophage

10.1165/ajrcmb.19.4.3176

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Citations (116)

Naturally Occurring Amino Acid Polymorphisms in Human Immunodeficiency Virus Type 1 (HIV-1) Gag p7NC and the C-Cleavage Site Impact Gag-Pol Processing by HIV-1 Protease

Virology (2002)

Maureen M. Goodenow Gregory Bloom Stéphanie Rose Steven Pomeroy Patricia O'Brien

Cleavage (geology)

NS2-3 protease

Group-specific antigen

10.1006/viro.2001.1184

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Citations (26)