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  • 1
    Electronic Resource
    Electronic Resource
    Coumestrol, NBD-norhexestrol, and dansyl-norhexestrol, fluorescent probes of estrogen-binding proteins (1977)
    s.l. : American Chemical Society
    Biochemistry 16 (1977), S. 2896-2901 
    Details
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/bi00632a015
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  • 2
    Electronic Resource
    Electronic Resource
    Photoaddition and photoreduction of azastilbenes. Solvent effects on the photoreactivity of aza aromatics (1972)
    s.l. : American Chemical Society
    Journal of the American Chemical Society 94 (1972), S. 9142-9148 
    Details
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ja00781a026
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  • 3
    Electronic Resource
    Electronic Resource
    Importance of 1n,.pi.* states in N-heterocycles. Internal conversion, intersystem crossing, and isomerization in azastilbenes (1971)
    s.l. : American Chemical Society
    Journal of the American Chemical Society 93 (1971), S. 6330-6332 
    Details
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ja00752a090
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  • 4
    Electronic Resource
    Electronic Resource
    Energy transfer in fluorescent derivatives of uracil and thymine (1977)
    s.l. : American Chemical Society
    Journal of the American Chemical Society 99 (1977), S. 7679-7685 
    Details
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ja00465a044
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  • 5
    Electronic Resource
    Electronic Resource
    Regulation of HSP70 and HSP28 gene expression: absence of compensatory interactions (1994)
    Springer
    Molecular and cellular biochemistry 137 (1994), S. 155-167 
    Details
    ISSN: 1573-4919
    Keywords: HSP70 ; HSP28 ; transfection ; compensatory interactions ; northern blots ; two-dimensional polyacrylamide gel electrophoresis ; gel mobility shift assay
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract We have previously reported the lack of HSP28 gene expression during acute and chronic thermotolerance development in L929 cells (J Cell Physiol 152: 118–125, 1992; Cancer Res 52: 5787, 1992). In contrast to HSP28, an extremely high level of inducible HSP70 synthesis was observed. These results led us to investigate the possibility of compensatory interactions between HSP70 and HSP28. To test the hypothesis, L929 cells were transfected with the human HSP28 gene contained in plasmid pCMV27. Data from Western blot and two-dimensional gel electrophoresis of [3H] leucine and [32P] orthophosphate-labeled proteins showed the synthesis and phosphorylation of HSP28 in transfected cells after heating at 45°C for 10 min. However, the expression of constitutive and inducible HSP70 genes, along with the synthesis of their proteins, was not decreased after heat shock. These results suggest an independent regulation of HSP28 and HSP70 gene expression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00944077
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  • 6
    Electronic Resource
    Electronic Resource
    Potential involvement of a constitutive heat shock element binding factor in the regulation of chemical stress-inducedhsp70 gene expression (1995)
    Springer
    Molecular and cellular biochemistry 144 (1995), S. 27-34 
    Details
    ISSN: 1573-4919
    Keywords: chemical stress ; HSP70 synthesis ; gene regulation ; heat shock factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract It was reported that chemical stresses such as arsenite, cadmium or salicylate fail to induce synthesis of the inducible form of HSP70 (HSP70i). We report here that exposure of cells to higher doses of these chemical treatments induced significant synthesis of HSP70i in CHO cells as well as other cell lines. The synthesis of HSP70i is primarily regulated at the transcriptional level. Although all tested chemical treatments induced heat shock factor (HSF) binding to the heat shock element (HSE), HSP70i synthesis appears to be regulated by an alternative factor (CHBF) which constitutively binds to the HSE at 37°C. The treatments, which dissociate the HSE-CHBF complex, induced significant HSP70i synthesis. The treatments, which failed to induce HSP70i synthesis, still activated HSF binding to HSE but the HSE-CHBF complex remained as that of untreated control cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00926737
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  • 7
    Electronic Resource
    Electronic Resource
    Hypoglycemia-induced AP-1 transcription factor and basic fibroblast growth factor gene expression in multidrug resistant human breast carcinoma MCF-7/ADR cells (1996)
    Springer
    Molecular and cellular biochemistry 155 (1996), S. 163-171 
    Details
    ISSN: 1573-4919
    Keywords: AP-1 binding activity ; basic fibroblast growth factor ; c-Jun mutant protein ; H-7
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract We investigated the effect of hypoglycemic treatment on the activation of the AP-1 transcription factors and the regulation of basic fibroblast growth factor (bFGF) gene expression in multidrug resistant human breast carcinoma MCF-7/ADR cells. Northern blot and gel mobility shift assays showed that hypoglycemic treatment induced c-jun and c-fos gene expression, AP-1 binding activity, as well as bFGF gene expression. Moreover, transfected cells expressing high levels of abnormal c-Jun protein exhibited a reduction in the bFGF protein levels compared to parental cells. A potent protein kinase C (PKC) inhibitor, H-7 (60 μg/ml) suppressed the stress-induced bFGF gene expression. Our study also demonstrated that H-7 did not facilitate the decay of bFGF mRNA. Thus, the suppression of bFGF gene expression by treatment with H-7 was due to the effect of the drug on the synthesis of bFGF mRNA rather than the stability of bFGF mRNA. Our data suggest that hypoglycemia-induced bFGF gene expression is mediated through the activation of PKC and the AP-1 transcription factors. (Mol Cell Biochem 155: 163–171, 1996)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00229313
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  • 8
    Electronic Resource
    Electronic Resource
    Examination of the molecular basis for the lack of αB-crystallin expression in L929 cells (1997)
    Springer
    Molecular and cellular biochemistry 170 (1997), S. 31-42 
    Details
    ISSN: 1573-4919
    Keywords: aB-Crystallin ; L929 cells ; methylation ; genomic footprinting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract We have previously shown that murine L929 cells do not express the small heat shock protein αB-crystallin upon exposure to thermal stress (Mol Cell Biochem 155: 51–60, 1996). In these studies, we demonstrate that L929 cells also fail to express αB-crystallin upon exposure dexamethasone, whereas NIH 3T3 and Swiss 3T3 murine cells exhibit αB-crystallin expression under identical conditions. Mobility shift assays demonstrated heat-inducible binding, presumably by heat shock factor(s), to an αB-crystallin heat shock element (HSE) oligomeric sequence in total cellular extracts from L929 cells. Transient transfection of a plasmid containing the αB-crystallin promoter linked to a CAT reporter gene exhibited heat-inducible expression in L929 cells. In addition, L929 cells stably transfected with a plasmid containing the complete αB-crystallin gene showed expression of this gene following heat shock. The presence of the endogenous αB-crystallin gene was detected by Southern blot hybridization of genomic L929 DNA, and sequence analysis revealed identical nucleotide structure to published murine sequences throughout the entire promoter. Treatment of L929 cells with 5-azacytidine enabled heat-inducible expression of αB-crystallin from the endogenous gene, however, methylation of the putative heat shock element (HSE) and flanking promoter sequences of L929 cell genomic DNA was not detected. In vivo genomic footprinting demonstrated constitutive binding to the endogenous HSE of the αB-crystallin promoter in L929, L929/αB-crystallin transfectant cells, and Swiss 3T3 cells during unstressed and heat stressed conditions. Therefore, the genomic αB-crystallin HSE region in L929 cells appears to be available for binding of putative transcription factors, but methylation in other regions of the gene or genome repress the expression of αB-crystallin in L929 cells. In vitro culture of L929 cells appears to have rendered the αB-crystallin gene loci inactive through methylation, thus providing a unique system by which to study the function of transfected small heat shock proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006810005545
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  • 9
    Electronic Resource
    Electronic Resource
    Hypoxia-induced bFGF gene expression is mediated through the JNK signal transduction pathway (1999)
    Springer
    Molecular and cellular biochemistry 202 (1999), S. 1-8 
    Details
    ISSN: 1573-4919
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Although the synthesis of angiogenic factors in hypoxic regions of solid tumors is recognized as one of the critical steps in tumor growth and metastasis, the signal transduction pathway involved in hypoxic induction of basic fibroblast growth factor (bFGF) gene expression is still obscure. In the study described here, we investigated the intracellular responses to hypoxia and the mechanisms triggering the initiation of angiogenic activity in drug-resistant human breast carcinoma MCF-7/ADR cells. Northern blots showed an increase in the level of c-jun, c-fos, and bFGF mRNA during hypoxia. Gel mobility-shift analysis of nuclear extracts from hypoxia-exposed cells showed an increase in AP-1 binding activity. In addition, hypoxic treatment strongly activated c-Jun N-terminal kinase 1 (JNK1), leading to phosphorylation and activation of c-Jun. Expression of a dominant negative mutant of JNK1 suppressed hypoxia-induced JNK1 activation as well as bFGF gene expression. Taken together, hypoxia-induced bFGF gene expression is mediated through the stress-activated protein kinase (SAPK) signal transduction pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007059806016
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  • 10
    Electronic Resource
    Electronic Resource
    Mechanism of Quercetin-induced suppression and delay of heat shock gene expression and thermotolerance development in HT-29 cells (1994)
    Springer
    Molecular and cellular biochemistry 137 (1994), S. 141-154 
    Details
    ISSN: 1573-4919
    Keywords: Quercetin ; heat shock transcription factor ; heat shock element ; nuclear run-on assay ; thermotolerance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Previous studies have shown that a combination of low pH and quercetin (QCT) treatment following heat shock markedly suppresses and delays the expression of heat shock protein genes, particularly the HSP70 gene (Lee et al., Biochem. Biophys. Res. Commun., 186:1121–1128, 1992). The possible mechanism for alteration of gene expression by treatment with QCT at low pH was investigated in human colon carcinoma cells. Cells were heated at 45°C for 15 min and then incubated at 37°C for various times (0–12 h) with QCT (0.05–0.2 mM) at pH 7.4 or 6.5. Gel mobility-shift analysis of whole cell extracts from heated cells showed the formation of the heat shock transcription factor (HSF)-heat shock element (HSE) complex. Dissociation of HSF from the HSE of the human HSP70 promotor occurred within 4 h under both pH conditions. The kinetics of recovery were not affected by treatment with 0.1% dimethyl sulfoxide (DMSO). However, the dissociation of HSF-HSE complex was markedly delayed during treatment with a combination of low pH and QCT. In addition,in vitro transcription assays showed a suppression of initiation and elongation of HSP70 mRNA. These results may explain why the combination of low pH and QCT treatment suppresses and delays the HSP70 gene expression as well as thermotolerance development.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00944076
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