Elia T. Ben‐Ari

Arlington Free Clinic

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Lori R. Bernstein

University of Maryland, Baltimore

Nancy H. Colburn

Center for Cancer Research

James C. Garrison

Memorial Hermann

Rebecca Chasan

Health Affairs

Stephanie L. Simek

Washington Department of Fish and Wildlife

Kevin R. Lynch

University of Virginia

Daniel Simberloff

University of Tennessee at Knoxville

Michael J. Birrer

Winthrop Rockefeller Foundation

Grady Editor-In-Chief

American Institute of Biological Sciences

Terry Griggs

American Institute of Biological Sciences

Cooperative Institutions

American Institute of Biological Sciences

National Institutes of Health

National Cancer Institute

Center for Cancer Research

University of California, Berkeley

Science Applications International Corporation (United States)

National Institute of Allergy and Infectious Diseases

University of Virginia

Frederick National Laboratory for Cancer Research

University of Tennessee at Knoxville

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Regulation of angiotensinogen mRNA accumulation in rat hepatocytes

AJP Endocrinology and Metabolism (1988)

Elia T. Ben‐Ari James C. Garrison

Experiments were undertaken using isolated rat liver cells to determine whether the stimulation of angiotensinogen synthesis by glucocorticoids, estrogens, and angiotensin II is due to a direct action on the liver and whether these effects involve an increase in angiotensinogen mRNA levels. Dexamethasone and other corticosteroids stimulated angiotensinogen mRNA accumulation in hepatocytes up to 3.5-fold after 2.5-3 h of incubation. The effect of dexamethasone was inhibited competitively by the glucocorticoid antagonist RU486. These results indicate that the stimulation of hepatic angiotensinogen production by glucocorticoids is a direct, receptor-mediated effect and occurs via an increase in angiotensinogen mRNA accumulation. The stimulatory diastereomer of adenosine 3',5'-cyclic phosphorothioate, an active adenosine 3',5'-cyclic monophosphate analogue, caused a 1.8-fold increase in angiotensinogen mRNA accumulation, and this effect was additive with that of dexamethasone, suggesting a distinct mechanism of action. Angiotensin II increased angiotensinogen mRNA levels by only 1.2-fold after 2.5 h, whereas ethinyl estradiol had no effect.

Mechanism of Action

Antiglucocorticoid

10.1152/ajpendo.1988.255.1.e70

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Citations (34)

Paternity Battles

BioScience (1999)

Elia T. Ben‐Ari

10.1525/bisi.1999.49.12.951

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Citations (0)

The silence of the genes

BioScience (1999)

Elia T. Ben‐Ari

Silence

10.2307/1313550

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Citations (4)

Gene regulation and genetic susceptibility to neoplastic transformation: AP-1 and p80 expression in JB6 cells.

Environmental Health Perspectives (1991)

Lori R. Bernstein Elia T. Ben‐Ari Stephanie L. Simek Nancy H. Colburn

The mouse epidermal JB6 cell system consists of clonal genetic variants that are sensitive (P+) or resistant (P-) to the promotion of neoplastic transformation by phorbol esters and other tumor-promoting agents. P+ cells display AP-1-dependent phorbol-ester-inducible transactivation of gene expression, whereas P- cells have a defect in transactivation. Transfection of promotion sensitivity gene pro-1 into P- cells reconstituted both P+ phenotype and AP-1-dependent phorbol-ester-inducible transactivation. P- and P+ cells exhibited induction of c-jun and c-fos messenger RNA levels by phorbol ester, but P- cells had significantly lower basal and induced levels of jun mRNA than P+ cells. Basal and induced levels of c-jun protein were significantly lower in P- cells as well. Differences in levels the 80-kDa pI 4.5 protein p80 were also observed in JB6 cells as a function of preneoplastic progression; high levels of p80 protein and mRNA were observed in P- cells, intermediate levels in P+ cells, and negligible levels were observed in transformed derivatives of JB6 cells. Phorbol ester treatment induced phosphorylation but not synthesis of p80. These data are consistent with the hypotheses that AP-1 is required in the signal transduction pathway for promotion of neoplastic transformation by tumor promoter, that pro genes may control AP-1 activity, that threshold levels of Jun mRNA and protein may play a role in transactivation and promotion sensitivity, and that the p80 protein in JB6 cells may behave in vivo as a suppressor of cellular transformation.

Tumor promotion

Neoplastic transformation

Phorbol

Malignant Transformation

10.1289/ehp.9193111

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Citations (22)

Understanding Bacterial Crowd Control

BioScience (2008)

Elia T. Ben‐Ari

10.1641/b580117

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Citations (2)

Special Book Article: Electronic Publishing: Past, Present, and Future

BioSCIENCE (1999)

Elia T. Ben‐Ari

Electronic publishing

10.2307/1313514

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Citations (1)

Gene Regulation and Genetic Susceptibility to Neoplastic Transformation: AP-1 and p80 Expression in JB6 Cells

Environmental Health Perspectives (1991)

Lori R. Bernstein Elia T. Ben‐Ari Stephanie L. Simek Nancy H. Colburn

Tumor promotion

Neoplastic transformation

Phorbol

Malignant Transformation

10.2307/3431178

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Citations (10)

Making Science News

BioSCIENCE (1998)

Elia T. Ben‐Ari

A t the end of a busy day, Jane Jones, a science writer in the public information office at State University, leans back in her desk chair and leafs through the latest issue of Science. Suddenly, she emits a strangled cry. She has just discovered that Dr. Betty Baker, a biologist at State U., has a rather interesting article in the journal. So why is Jones dismayed? Because if she had known about Baker's upcoming publication she could have written a news release that might have garnered some media coverage for Baker's research-as well as some positive publicity for the university.

Desk

10.2307/1313292

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Citations (4)

What Next for Biology?

BioScience (2000)

Elia T. Ben‐Ari

10.1641/0006-3568(2000)050[0848:wnfb]2.0.co;2

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Citations (2)

Defender of the Voiceless: Wallace Stegner's Conservation Legacy

BioSCIENCE (2000)

Elia T. Ben‐Ari

10.1641/0006-3568(2000)050[0253:dotvws]2.3.co;2

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Citations (5)