Ten years after: reclassification of steroid-responsive genes.

Dean, Diane M.; Sanders, Michel M.

doi:10.1210/mend.10.12.8961259

Cited by 30 publications

(29 citation statements)

References 2 publications

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“…Our results do not distinguish a pure secondary response from a recently proposed delayed primary response mechanism [19]. A classic secondary response consists of inducer 1 inducing an independent inducer 2 that is solely responsible for the induction of the measured gene product.…”

Section: Discussioncontrasting

confidence: 88%

“…It is well known that only a few minutes are required for activated GR to enter the nucleus and bind to a simple promoter regulating gene expression [12,19]. This implies that the regulation of cjun expression by Dex most likely is not by the mechanism of directly and solely binding of GR to the c-jun promoter.…”

Section: Discussionmentioning

confidence: 99%

“…Since concomitant protein synthesis is typically required for secondary response mechanisms [19], the protein synthesis inhibitor CHX was employed. CHX itself, however, was found to induce c-jun mRNA levels higher than did Dex alone in an equivalent time.…”

Section: Discussionmentioning

confidence: 99%

“…A classic test for secondary induction is to block protein synthesis while inducer is added; then to follow the relevant mRNA [19]. Hence, to try to determine whether de novo synthesis of protein was required for the Dex induction of c-jun, 10 µg/ml cycloheximide (CHX) was added to the cultures to inhibit protein synthesis.…”

Section: Levels Of C-jun Mrna Were Increased By Cycloheximidementioning

confidence: 99%

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The delayed induction of c-jun in apoptotic human leukemic lymphoblasts is primarily transcriptional

Zhou

Medh

Zhang

et al. 2000

The Journal of Steroid Biochemistry and Molecular Biology

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Because of their ability to induce lymphoid cell apoptosis, glucocorticoids have been used for decades to treat certain human leukemias and lymphomas. Studies presented in this paper complement our previous work demonstrating that sustained induction of the proto-oncogene c-jun plays a crucial role in the glucocorticoid-induced apoptotic pathway in CEM cells, human leukemic lymphoblasts.Results from measurements of c-jun mRNA half-life with RNase protection assays and of transcription by nuclear run-on assays indicate that, in the dexamethasone-sensitive cloned CEM-C7 cells, c-jun is induced at the transcriptional level. Consideration of time-course, however, suggested that this might be a secondary or possibly a delayed primary response. Use of cycloheximide to block protein synthesis strongly induced c-jun mRNA, suggesting that there had been relief from a labile protein repressor of transcription. Comparing the level of induction by cycloheximide with that of dexamethasone indicated that the two did not induce by an identical mechanism. The high induction by cycloheximide obscured simple interpretation of elevated c-jun mRNA levels after concomitant administration of cycloheximide and dexamethasone. This was resolved by nuclear run-on experiments, which showed that the dexamethasone induction of c-jun mRNA in this system does require protein synthesis.

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Section: Discussioncontrasting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Levels Of C-jun Mrna Were Increased By Cycloheximidementioning

confidence: 99%

See 2 more Smart Citations

The delayed induction of c-jun in apoptotic human leukemic lymphoblasts is primarily transcriptional

Zhou

Medh

Zhang

et al. 2000

The Journal of Steroid Biochemistry and Molecular Biology

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“…Cheng and Pollard (35) showed that uterine expression of c-rasH and ornithine decarboxylase increased 6-12 hr after estradiol treatment. Dean and Sanders (36) suggested that there are two classes of genes which respond to estrogenic stimuli in a delayed manner: the secondary response genes that are dependent on the products of the early primary response genes for their stimulation, and the delayed primary response genes that are dependent on a direct interaction of steroid receptor with the gene's promoter and concomitant enhancement by a product of the early primary response gene. It may be that the delayed response genes stimulated by E2 in both S-D and F344 rats are not induced by BPA in the S-D rat but are induced by BPA in the F344 rat; this possibility requires further investigation.…”

Section: Resultsmentioning

confidence: 99%

Strain differences in vaginal responses to the xenoestrogen bisphenol A.

Long

Steinmetz

Ben‐Jonathan

et al. 2000

Environ Health Perspect

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Bisphenol A (BPA) is the monomer component of polycarbonate plastics and epoxy resins; human exposure derives from leachate in foodstuffs packaged in certain plastics or from epoxybased dental appliances. BPA (6). Although it is almost entirely in its polymerized form, the BPA monomer finds its way into foodstuffs as a leachate of plastic packaging (7,8). Also, humans can be exposed to BPA from certain dental appliances (9,10). Because of its estrogenic activity, there is concern over human exposure to BPA.When assessing the biologic activity of a putative estrogenic compound in animal model systems, it is important to consider species and strain differences. We previously found that BPA increased blood prolactin levels in Fischer 344 (F344) but not SpragueDawley (S-D) rats (3). Such a finding is congruent with the earlier observation that estrogens stimulate growth of the pituitary through replication of the prolactin-secreting cells in F344 rats but not in outbred rat strains (11-13). We also found that the uterine epithelium of F344 rats but not that of S-D rats exhibited a hypertrophic response to BPA administered in low doses (2 (15)(16)(17)(18). The induction of these genes is believed to play a key role in cell proliferation (19,20). In the present study, we determined the potency of BPA to induce immediate early gene expression and DNA synthetic activity in the vaginal epithelium of F344 and S-D rats. Materials and MethodsAnimals. All procedures performed on animals followed the NIH Guide for the Care and Use ofLaboratory Animals (21) and were approved by the Indiana University Animal Care and Use Committee. F344 and S-D rats were supplied at 6-8 weeks of age by Harlan Sprague-Dawley (Indianapolis, IN). One week after arrival, animals were ovariectomized under ketamine anesthesia; they were subjected to experimental manipulation 3 weeks later. BPA (Aldrich Chemical Co., Milwaukee, WI) and 17,B-estradiol (E2; Sigma Chemical Company, St. Louis, MO) were dissolved in ethanol and diluted in sesame oil. Compounds were injected intraperitoneally (ip) in 50 pL of solution. We injected BPA at 0.2-150 mg/kg body weight (bw) and E2 at 0.02-2.0 pg/kg bw.Bromodeoxyuridine immunostaining. Animals were injected with bromodeoxyuridine (BrdU; 100 mg/kg bw in 500 pL saline, ip) and killed 1 hr later. Tissue taken from treated animals was fixed in ethanol-chloroform-acetic acid (60:30:10, vol/vol/vol)

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Androgen Receptor Regulation of G1 Cyclin and Cyclin‐Dependent Kinase Function in the CWR22 Human Prostate Cancer Xenograft

GREGORY,

JR,

PRESNELL

et al. 2001

Journal of Andrology

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Human prostate cancer is initially dependent on androgens for growth, and androgen‐dependent cells undergo apoptosis after castration. However, a subset of androgen‐responsive cells survives and eventually proliferates in the absence of testicular androgen. The high levels of androgen receptor in both androgen‐de‐pendent and recurrent tumors led us to investigate androgen regulation of cell cycle proteins in human prostate cancer using the CWR22 xenograft. Cellular proliferation decreased dramatically in CWR22 tumors after castration. Testosterone propionate (TP) treatment of castrated mice restored cellular proliferation after 24–48 hours. Growth of CWR22 tumors in the absence of testicular androgen recurred several months after castration. CDK1 and CDK2, and cyclin A and cyclin B1 messenger RNAs were decreased 6 days after castration, increased 6–12 hours after TP treatment, and were expressed at high levels in recurrent CWR22 tumors. Coimmunoprecipitated cyclin B1/CDK1 and cyclin D1/CDK4 protein complexes decreased after castration and increased after TP treatment of castrated mice. In addition, CDK1 and CDK2 kinase activities were up‐regulated by androgen in parallel with hyperphosphorylation of retinoblastoma (Rb) protein. Despite the absence of testicular androgen in recurrent CWR22, the levels of these androgen‐regulated cyclin/CDK protein complexes and hyperphosphorylation of Rb were equal to or greater than in tumors from intact mice. The results indicate that androgen receptor regulates cellular proliferation by control of CDK and cyclins at the transcriptional level and by post‐translational modifications that influence cell cycle protein activity.

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Ten years after: reclassification of steroid-responsive genes.

Cited by 30 publications

References 2 publications

The delayed induction of c-jun in apoptotic human leukemic lymphoblasts is primarily transcriptional

The delayed induction of c-jun in apoptotic human leukemic lymphoblasts is primarily transcriptional

Strain differences in vaginal responses to the xenoestrogen bisphenol A.

Androgen Receptor Regulation of G1 Cyclin and Cyclin‐Dependent Kinase Function in the CWR22 Human Prostate Cancer Xenograft

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