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Immunologie, Immunopathologie et Chimie Thérapeutique
Publications
2004
Popiela A., Keith G., Borzecki A., Popiela G., Manowiec M., Gabrys M.
The meaning of the methylation of genomic DNA in the regulation of gene expression levels Article de journal
Dans: Eur J Gynaecol Oncol, vol. 25, non 2, p. 145-9, 2004, (0392-2936 Journal Article Review Review, Tutorial).
Résumé | BibTeX | Étiquettes: *DNA, *Gene, Expression, Human, KEITH, Methylation, Neoplasms/*genetics, Neoplastic, Regulation
@article{,
title = {The meaning of the methylation of genomic DNA in the regulation of gene expression levels},
author = { A. Popiela and G. Keith and A. Borzecki and G. Popiela and M. Manowiec and M. Gabrys},
year = {2004},
date = {2004-01-01},
journal = {Eur J Gynaecol Oncol},
volume = {25},
number = {2},
pages = {145-9},
abstract = {INTRODUCTION: Methylation of genomic DNA is one of the major mechanisms that deactivates genes and regulates their tissue-specific transcription levels. Its patterns are based on clonal inheritance that occurs in the early stages of embryogenesis. All changes in the DNA methylation levels occurring especially in the promoter region of the genes, which involve hypo- as well as hyper-methylation, lead to cell differentiation and growth disorders. Therefore it can become an impulse that initiates different pathological processes including carcinogenesis. MATERIAL AND METHODS: The purpose of this review was to present the recent knowledge concerning methylation of genomic DNA based on recent references and authors' experience. RESULTS AND CONCLUSION: Genome stability disorders could be caused either by mutations, which damage the structure of the genes and have not been formerly removed, or as the consequence of an epigenetic mechanism. Methylation plays a decisive role in the activity of many genes and could be a natural weapon of an organism against the expression of foreign genetic material that degrades the original genome structure.},
note = {0392-2936
Journal Article
Review
Review, Tutorial},
keywords = {*DNA, *Gene, Expression, Human, KEITH, Methylation, Neoplasms/*genetics, Neoplastic, Regulation},
pubstate = {published},
tppubtype = {article}
}
INTRODUCTION: Methylation of genomic DNA is one of the major mechanisms that deactivates genes and regulates their tissue-specific transcription levels. Its patterns are based on clonal inheritance that occurs in the early stages of embryogenesis. All changes in the DNA methylation levels occurring especially in the promoter region of the genes, which involve hypo- as well as hyper-methylation, lead to cell differentiation and growth disorders. Therefore it can become an impulse that initiates different pathological processes including carcinogenesis. MATERIAL AND METHODS: The purpose of this review was to present the recent knowledge concerning methylation of genomic DNA based on recent references and authors' experience. RESULTS AND CONCLUSION: Genome stability disorders could be caused either by mutations, which damage the structure of the genes and have not been formerly removed, or as the consequence of an epigenetic mechanism. Methylation plays a decisive role in the activity of many genes and could be a natural weapon of an organism against the expression of foreign genetic material that degrades the original genome structure.
Zukiel R., Nowak S., Barciszewska A. M., Gawronska I., Keith G., Barciszewska M. Z.
A simple epigenetic method for the diagnosis and classification of brain tumors Article de journal
Dans: Mol Cancer Res, vol. 2, non 3, p. 196-202, 2004, (1541-7786 Journal Article).
Résumé | BibTeX | Étiquettes: *DNA, *Epigenesis, 5-Methylcytosine/*analysis, Adult, Aged, and, Brain, Chromatography, DNA, Female, Genetic, Gov't, Human, KEITH, Layer, Male, Methylation, Middle, Neoplasm/*chemistry/*metabolism, Neoplasms/*classification/*diagnosis/genetics/pathology, Non-U.S., Oxidative, oxygen, Reactive, Sensitivity, Species/metabolism, Specificity, Stress, Support, Thin
@article{,
title = {A simple epigenetic method for the diagnosis and classification of brain tumors},
author = { R. Zukiel and S. Nowak and A. M. Barciszewska and I. Gawronska and G. Keith and M. Z. Barciszewska},
year = {2004},
date = {2004-01-01},
journal = {Mol Cancer Res},
volume = {2},
number = {3},
pages = {196-202},
abstract = {The new, simple, and reliable method for the diagnosis of brain tumors is described. It is based on a TLC quantitative determination of 5-methylcytosine (m(5)C) in relation to its damage products of DNA from tumor tissue. Currently, there is evidence that oxidative stress through reactive oxygen species (ROS) plays an important role in the etiology and progression of several human diseases. Oxidative damage of DNA, lipids, and proteins is deleterious for the cell. m(5)C, along with other basic components of DNA, is the target for ROS, which results in the appearance of new modified nucleic acid bases. If so, m(5)C residue constitutes a mutational hotspot position, whether it occurs within a nucleotide sequence of a structural gene or a regulatory region. Here, we show the results of the analysis of 82 DNA samples taken from brain tumor tissues. DNA was isolated and hydrolyzed into nucleotides, which, after labeling with [gamma-(32)P]ATP, were separated on TLC. Chromatograms were evaluated using PhosphorImager and the amounts of 5-methyldeoxycytosine (m(5)dC) were calculated as a ratio (R) of m(5)dC to m(5)dC + deoxycytosine + deoxythymidine spot intensities. The R value could not only be a good diagnostic marker for brain tumors but also a factor differentiating low-grade and high-grade gliomas. Therefore, DNA methylation pattern might be a useful tool to give a primary diagnosis of a brain tumor or as a marker for the early detection of the relapse of the disease. This method has several advantages over those existing nowadays.},
note = {1541-7786
Journal Article},
keywords = {*DNA, *Epigenesis, 5-Methylcytosine/*analysis, Adult, Aged, and, Brain, Chromatography, DNA, Female, Genetic, Gov't, Human, KEITH, Layer, Male, Methylation, Middle, Neoplasm/*chemistry/*metabolism, Neoplasms/*classification/*diagnosis/genetics/pathology, Non-U.S., Oxidative, oxygen, Reactive, Sensitivity, Species/metabolism, Specificity, Stress, Support, Thin},
pubstate = {published},
tppubtype = {article}
}
The new, simple, and reliable method for the diagnosis of brain tumors is described. It is based on a TLC quantitative determination of 5-methylcytosine (m(5)C) in relation to its damage products of DNA from tumor tissue. Currently, there is evidence that oxidative stress through reactive oxygen species (ROS) plays an important role in the etiology and progression of several human diseases. Oxidative damage of DNA, lipids, and proteins is deleterious for the cell. m(5)C, along with other basic components of DNA, is the target for ROS, which results in the appearance of new modified nucleic acid bases. If so, m(5)C residue constitutes a mutational hotspot position, whether it occurs within a nucleotide sequence of a structural gene or a regulatory region. Here, we show the results of the analysis of 82 DNA samples taken from brain tumor tissues. DNA was isolated and hydrolyzed into nucleotides, which, after labeling with [gamma-(32)P]ATP, were separated on TLC. Chromatograms were evaluated using PhosphorImager and the amounts of 5-methyldeoxycytosine (m(5)dC) were calculated as a ratio (R) of m(5)dC to m(5)dC + deoxycytosine + deoxythymidine spot intensities. The R value could not only be a good diagnostic marker for brain tumors but also a factor differentiating low-grade and high-grade gliomas. Therefore, DNA methylation pattern might be a useful tool to give a primary diagnosis of a brain tumor or as a marker for the early detection of the relapse of the disease. This method has several advantages over those existing nowadays.
2003
Miturski R., Postawski K., Semczuk A., Bogusiewicz M., Baranowski W., Jakowicki J. A., Keith G.
Global DNA methylation in relation to hMLH1 and hMSH2 protein immunoreactivity in sporadic human endometrial carcinomas Article de journal
Dans: Int J Mol Med, vol. 11, non 5, p. 569-74, 2003, (1107-3756 Journal Article).
Résumé | BibTeX | Étiquettes: *DNA, Base, Carcinoma/genetics/*metabolism/pathology, DNA, Endometrial, Female, Gov't, Human, Immunohistochemistry, Methylation, Mismatch, Neoplasm, Neoplasms/genetics/*metabolism/pathology, Non-U.S., Pair, Proteins/*metabolism, Proto-Oncogene, Repair, Support
@article{,
title = {Global DNA methylation in relation to hMLH1 and hMSH2 protein immunoreactivity in sporadic human endometrial carcinomas},
author = { R. Miturski and K. Postawski and A. Semczuk and M. Bogusiewicz and W. Baranowski and J. A. Jakowicki and G. Keith},
year = {2003},
date = {2003-01-01},
journal = {Int J Mol Med},
volume = {11},
number = {5},
pages = {569-74},
abstract = {Overall DNA methylation status was studied in a group of 28 sporadic human endometrial carcinomas (ECs) using the [32P]-postlabeling technique. Moreover, expression of the DNA mismatch repair proteins (hMLH1 and hMSH2) was investigated in ECs using immunohistochemistry. Mean 5-methyldeoxycytosine (m5dC) content in the studied group was 3.48+/-0.37% (range, 2.89-4.12%). The mean m5dC scores were significantly different between early (3.35+/-0.33%) and advanced (3.66+/-0.36%) endometrial neoplasms (chi2-test; p=0.03). There was a markedly increased overall DNA methylation with the degree of histological differentiation and with the infiltration of the myometrium (p<0.05). Loss of hMLH1 and hMSH2 expression was reported in 7 (25%) and 5 (18%) tumors, respectively, but the immunoreactivity did not correlate with the known clinicopathological variables of cancer. In addition, no obvious correlation was found between global m5dC content and the lack of hMLH1 and hMSH2 protein expression in human uterine tumors (p=0.97 and p=0.19 for hMLH1 and hMSH2, respectively; Spearman's rank correlation test). Our results clearly show that alterations in global DNA methylation may influence tumor progression, but they are not directly associated with the inactivation of the mismatch-repair machinery in sporadic human ECs.},
note = {1107-3756
Journal Article},
keywords = {*DNA, Base, Carcinoma/genetics/*metabolism/pathology, DNA, Endometrial, Female, Gov't, Human, Immunohistochemistry, Methylation, Mismatch, Neoplasm, Neoplasms/genetics/*metabolism/pathology, Non-U.S., Pair, Proteins/*metabolism, Proto-Oncogene, Repair, Support},
pubstate = {published},
tppubtype = {article}
}
Overall DNA methylation status was studied in a group of 28 sporadic human endometrial carcinomas (ECs) using the [32P]-postlabeling technique. Moreover, expression of the DNA mismatch repair proteins (hMLH1 and hMSH2) was investigated in ECs using immunohistochemistry. Mean 5-methyldeoxycytosine (m5dC) content in the studied group was 3.48+/-0.37% (range, 2.89-4.12%). The mean m5dC scores were significantly different between early (3.35+/-0.33%) and advanced (3.66+/-0.36%) endometrial neoplasms (chi2-test; p=0.03). There was a markedly increased overall DNA methylation with the degree of histological differentiation and with the infiltration of the myometrium (p<0.05). Loss of hMLH1 and hMSH2 expression was reported in 7 (25%) and 5 (18%) tumors, respectively, but the immunoreactivity did not correlate with the known clinicopathological variables of cancer. In addition, no obvious correlation was found between global m5dC content and the lack of hMLH1 and hMSH2 protein expression in human uterine tumors (p=0.97 and p=0.19 for hMLH1 and hMSH2, respectively; Spearman's rank correlation test). Our results clearly show that alterations in global DNA methylation may influence tumor progression, but they are not directly associated with the inactivation of the mismatch-repair machinery in sporadic human ECs.
2002
Kowal M., Roslinski J., Dmoszynska A., Borzecki A., Borzecka H., Keith G.
Genomic hypomethylation in patients with B-cell chronic lymphocytic leukemia Article de journal
Dans: Acta Haematol Pol, vol. 33, non 3, p. 323-330, 2002.
Résumé | BibTeX | Étiquettes: Chronic, DNA, GIEGE, leukemia, lymphocytic, Methylation
@article{,
title = {Genomic hypomethylation in patients with B-cell chronic lymphocytic leukemia},
author = { M. Kowal and J. Roslinski and A. Dmoszynska and A. Borzecki and H. Borzecka and G. Keith},
year = {2002},
date = {2002-01-01},
journal = {Acta Haematol Pol},
volume = {33},
number = {3},
pages = {323-330},
abstract = {During the last few years, increasing attention has been paid to the relationship between DNA methylation and cancer. Hypo- or hypermethylation of DNA may result in up or down regulation of genes involved in the pathogenesis of leukemias. In this study we have analyzed DNA methylation in peripheral blood and bone marrow B (CD19+) and T (CD3+) lymphocytes from untreated patients with B-cell chronic lymphocytic leukemia.},
keywords = {Chronic, DNA, GIEGE, leukemia, lymphocytic, Methylation},
pubstate = {published},
tppubtype = {article}
}
During the last few years, increasing attention has been paid to the relationship between DNA methylation and cancer. Hypo- or hypermethylation of DNA may result in up or down regulation of genes involved in the pathogenesis of leukemias. In this study we have analyzed DNA methylation in peripheral blood and bone marrow B (CD19+) and T (CD3+) lymphocytes from untreated patients with B-cell chronic lymphocytic leukemia.
Popiela A., Gabrys M. S., Rabczynski J., Panszczyk M., Keith G., Baranowski W.
[Estimation of DNA methylation level in endometrial cancer tissues] Article de journal
Dans: Ginekol Pol, vol. 73, non 11, p. 966-9, 2002, (0017-0011 Journal Article).
Résumé | BibTeX | Étiquettes: *DNA, 80, Abstract, Adenocarcinoma/chemistry/*genetics, Aged, and, Case-Control, Endometrial, English, Expression, Female, Gene, Human, Hyperplasia/genetics, Methylation, Middle, Neoplasms/chemistry/*genetics, Neoplastic, over, Regulation, Studies
@article{,
title = {[Estimation of DNA methylation level in endometrial cancer tissues]},
author = { A. Popiela and M. S. Gabrys and J. Rabczynski and M. Panszczyk and G. Keith and W. Baranowski},
year = {2002},
date = {2002-01-01},
journal = {Ginekol Pol},
volume = {73},
number = {11},
pages = {966-9},
abstract = {OBJECTIVES: A level of DNA methylation plays an important role in regulation of cellular gene's expression. Estimation of DNA methylation level in endometrial neoplastic tissues compared to normal endometrial samples was the aim of this study. DESIGN: It was to be shown, that changes in methylation rate in promotory regions could lead to carcinogenesis in particular cell. Authors describe an analysis of DNA methylation level in endometrial cancer tissues compared to DNA methylation level in normal or hyperplastic endometrium. MATERIAL AND METHODS: Endometrial samples from 88 women were collected. 56 of them were classified as adenocarcinoma, 20 as hyperplastic changes, 12 as normal endometrium-control group. DNA was isolated from tissues and than prepared to pm5dC and pdC. Than we performed a statistical analysis of results. RESULTS: The median DNA methylation level was significantly higher in neoplastic tissues than in normal endometrium. There was no difference between DNA methylation level between normal endometrium and hyperplastic changes. CONCLUSIONS: Authors conclude that neoplastic endometrial tissues show high DNA methylation rate compared to normal or hyperplastic endometrium.},
note = {0017-0011
Journal Article},
keywords = {*DNA, 80, Abstract, Adenocarcinoma/chemistry/*genetics, Aged, and, Case-Control, Endometrial, English, Expression, Female, Gene, Human, Hyperplasia/genetics, Methylation, Middle, Neoplasms/chemistry/*genetics, Neoplastic, over, Regulation, Studies},
pubstate = {published},
tppubtype = {article}
}
OBJECTIVES: A level of DNA methylation plays an important role in regulation of cellular gene's expression. Estimation of DNA methylation level in endometrial neoplastic tissues compared to normal endometrial samples was the aim of this study. DESIGN: It was to be shown, that changes in methylation rate in promotory regions could lead to carcinogenesis in particular cell. Authors describe an analysis of DNA methylation level in endometrial cancer tissues compared to DNA methylation level in normal or hyperplastic endometrium. MATERIAL AND METHODS: Endometrial samples from 88 women were collected. 56 of them were classified as adenocarcinoma, 20 as hyperplastic changes, 12 as normal endometrium-control group. DNA was isolated from tissues and than prepared to pm5dC and pdC. Than we performed a statistical analysis of results. RESULTS: The median DNA methylation level was significantly higher in neoplastic tissues than in normal endometrium. There was no difference between DNA methylation level between normal endometrium and hyperplastic changes. CONCLUSIONS: Authors conclude that neoplastic endometrial tissues show high DNA methylation rate compared to normal or hyperplastic endometrium.
Popiela A., Gabrys M. S., Rabczynski J., Panszczyk M., Keith G., Baranowski W.
[Estimation of DNA methylation level in nonendometrial uterus malignancies] Article de journal
Dans: Ginekol Pol, vol. 73, non 11, p. 962-5, 2002, (0017-0011 Journal Article).
Résumé | BibTeX | Étiquettes: *DNA, 80, Abstract, Age, Aged, and, Case-Control, English, Expression, Factors, Female, Gene, Human, Mesodermal/genetics/*metabolism, Methylation, Middle, Mixed, Neoplasms/genetics/*metabolism, Neoplastic, over, Regulation, silencing, Studies, tumor, Uterine
@article{,
title = {[Estimation of DNA methylation level in nonendometrial uterus malignancies]},
author = { A. Popiela and M. S. Gabrys and J. Rabczynski and M. Panszczyk and G. Keith and W. Baranowski},
year = {2002},
date = {2002-01-01},
journal = {Ginekol Pol},
volume = {73},
number = {11},
pages = {962-5},
abstract = {OBJECTIVES: Rebuilding of genome structure leads to many pathological states including neoplastic malignancies. Rebuilding often occurs as a process caused by disturbances in gene silencing mechanism. DNA methylation pattern is one of the most important mechanisms connected to gene's silencing. Estimation of DNA methylation level in nonendometrial uterine neoplastic tissues compared to normal endometrial samples was the aim of this study. DESIGN: It was to be shown, that changes in methylation rate in promotory regions could lead to carcinogenesis in particular cell. Authors describe an analysis of DNA methylation level in nonendometrial neoplastic uterine tissues compared to DNA methylation level in normal endometrium. MATERIALS AND METHODS: Tissue samples from 9 women with tumor mixtus mesodermalis were collected. 12 samples were normal endometrium-control group. DNA was isolated from tissues and than we performed an estimation of DNA methylation levels. Than we performed a statistical analysis of results. RESULTS: The median DNA methylation level was significantly higher in neoplastic tissues than in normal endometrium. CONCLUSIONS: Authors conclude, that DNA methylation level is higher in neoplastic tissues, but does not correlate with clinical stage of the disease.},
note = {0017-0011
Journal Article},
keywords = {*DNA, 80, Abstract, Age, Aged, and, Case-Control, English, Expression, Factors, Female, Gene, Human, Mesodermal/genetics/*metabolism, Methylation, Middle, Mixed, Neoplasms/genetics/*metabolism, Neoplastic, over, Regulation, silencing, Studies, tumor, Uterine},
pubstate = {published},
tppubtype = {article}
}
OBJECTIVES: Rebuilding of genome structure leads to many pathological states including neoplastic malignancies. Rebuilding often occurs as a process caused by disturbances in gene silencing mechanism. DNA methylation pattern is one of the most important mechanisms connected to gene's silencing. Estimation of DNA methylation level in nonendometrial uterine neoplastic tissues compared to normal endometrial samples was the aim of this study. DESIGN: It was to be shown, that changes in methylation rate in promotory regions could lead to carcinogenesis in particular cell. Authors describe an analysis of DNA methylation level in nonendometrial neoplastic uterine tissues compared to DNA methylation level in normal endometrium. MATERIALS AND METHODS: Tissue samples from 9 women with tumor mixtus mesodermalis were collected. 12 samples were normal endometrium-control group. DNA was isolated from tissues and than we performed an estimation of DNA methylation levels. Than we performed a statistical analysis of results. RESULTS: The median DNA methylation level was significantly higher in neoplastic tissues than in normal endometrium. CONCLUSIONS: Authors conclude, that DNA methylation level is higher in neoplastic tissues, but does not correlate with clinical stage of the disease.
2000
Postawski K., Olech-Fudali E., Jakowicki J. A., Korobowicz E., Keith G., Baranowski W.
[Overall genomic DNA methylation in relation to estrogen] Article de journal
Dans: Ginekol Pol, vol. 71, non 9, p. 1206-11, 2000, (0017-0011 Journal Article).
Résumé | BibTeX | Étiquettes: 80, Abstract, Aged, and, Biopsy, DNA, English, Estrogen/*metabolism, Female, Gov't, Human, Methylases/metabolism, Methylation, Middle, modification, Neoplasms/*metabolism/*pathology, Non-U.S., over, Progesterone/*metabolism, Receptors, Support, Uterine, Uterus/*metabolism/pathology
@article{,
title = {[Overall genomic DNA methylation in relation to estrogen]},
author = { K. Postawski and E. Olech-Fudali and J. A. Jakowicki and E. Korobowicz and G. Keith and W. Baranowski},
year = {2000},
date = {2000-01-01},
journal = {Ginekol Pol},
volume = {71},
number = {9},
pages = {1206-11},
abstract = {Overall genomic DNA methylation was analyzed using enzymatic digestion into nucleotides, 32P postlabeling, two-dimensional thin-layer chromatography on cellulose plates and phosphobioimaging quantitation, in relation to immunohistochemically measured estrogen (ER) and progesterone receptor (PR) status of 15 uterine cancers. Mean 5-methyldeoxycytosine (m5dC) content did not differ between ER-positive and ER-negative neoplasms. Highest values of m5dC were noted both in ER-negative and ER-positive tumors. Additionally, there was no low DNA methylation in ER negative uterine cancer tissues. Decrease of the overall genomic DNA methylation could be related to the increase of ER/PR ratio, however it was not significant in our investigation. The potential role of steroid receptors status in uterine cancer tissue is discussed.},
note = {0017-0011
Journal Article},
keywords = {80, Abstract, Aged, and, Biopsy, DNA, English, Estrogen/*metabolism, Female, Gov't, Human, Methylases/metabolism, Methylation, Middle, modification, Neoplasms/*metabolism/*pathology, Non-U.S., over, Progesterone/*metabolism, Receptors, Support, Uterine, Uterus/*metabolism/pathology},
pubstate = {published},
tppubtype = {article}
}
Overall genomic DNA methylation was analyzed using enzymatic digestion into nucleotides, 32P postlabeling, two-dimensional thin-layer chromatography on cellulose plates and phosphobioimaging quantitation, in relation to immunohistochemically measured estrogen (ER) and progesterone receptor (PR) status of 15 uterine cancers. Mean 5-methyldeoxycytosine (m5dC) content did not differ between ER-positive and ER-negative neoplasms. Highest values of m5dC were noted both in ER-negative and ER-positive tumors. Additionally, there was no low DNA methylation in ER negative uterine cancer tissues. Decrease of the overall genomic DNA methylation could be related to the increase of ER/PR ratio, however it was not significant in our investigation. The potential role of steroid receptors status in uterine cancer tissue is discussed.
1999
Perreau V. M., Keith G., Holmes W. M., Przykorska A., Santos M. A., Tuite M. F.
The Candida albicans CUG-decoding ser-tRNA has an atypical anticodon stem-loop structure Article de journal
Dans: J Mol Biol, vol. 293, non 5, p. 1039-53, 1999, (0022-2836 Journal Article).
Résumé | BibTeX | Étiquettes: *Nucleic, Acid, albicans/*genetics, Anticodon/*chemistry/*genetics/metabolism, Base, Candida, cerevisiae/genetics, Code/genetics, Conformation, Evolution, Fungal/chemistry/genetics/metabolism, Genetic, Gov't, Imidazoles/metabolism, Lead/metabolism, Methylation, Methyltransferases/metabolism, Molecular, Mutation/genetics, Non-P.H.S., Non-U.S., Nucleosides/genetics/metabolism, P.H.S., Ribonucleases/metabolism, RNA, Saccharomyces, Sequence, Ser/*chemistry/*genetics/metabolism, Solutions, Support, Transfer, tRNA, U.S.
@article{,
title = {The Candida albicans CUG-decoding ser-tRNA has an atypical anticodon stem-loop structure},
author = { V. M. Perreau and G. Keith and W. M. Holmes and A. Przykorska and M. A. Santos and M. F. Tuite},
year = {1999},
date = {1999-01-01},
journal = {J Mol Biol},
volume = {293},
number = {5},
pages = {1039-53},
abstract = {In many Candida species, the leucine CUG codon is decoded by a tRNA with two unusual properties: it is a ser-tRNA and, uniquely, has guanosine at position 33 (G33). Using a combination of enzymatic (V1 RNase, RnI nuclease) and chemical (Pb(2+), imidazole) probing of the native Candida albicans ser-tRNACAG, we demonstrate that the overall tertiary structure of this tRNA resembles that of a ser-tRNA rather than a leu-tRNA, except within the anticodon arm where there is considerable disruption of the anticodon stem. Using non-modified in vitro transcripts of the C. albicans ser-tRNACAG carrying G, C, U or A at position 33, we demonstrate that it is specifically a G residue at this position that induces the atypical anticodon stem structure. Further quantitative evidence for an unusual structure in the anticodon arm of the G33-tRNA is provided by the observed change in kinetics of methylation of the G at position 37, by purified Escherichia coli m(1)G37 methyltransferase. We conclude that the anticodon arm distortion, induced by a guanosine base at position 33 in the anticodon loop of this novel tRNA, results in reduced decoding ability which has facilitated the evolution of this tRNA without extinction of the species encoding it.},
note = {0022-2836
Journal Article},
keywords = {*Nucleic, Acid, albicans/*genetics, Anticodon/*chemistry/*genetics/metabolism, Base, Candida, cerevisiae/genetics, Code/genetics, Conformation, Evolution, Fungal/chemistry/genetics/metabolism, Genetic, Gov't, Imidazoles/metabolism, Lead/metabolism, Methylation, Methyltransferases/metabolism, Molecular, Mutation/genetics, Non-P.H.S., Non-U.S., Nucleosides/genetics/metabolism, P.H.S., Ribonucleases/metabolism, RNA, Saccharomyces, Sequence, Ser/*chemistry/*genetics/metabolism, Solutions, Support, Transfer, tRNA, U.S.},
pubstate = {published},
tppubtype = {article}
}
In many Candida species, the leucine CUG codon is decoded by a tRNA with two unusual properties: it is a ser-tRNA and, uniquely, has guanosine at position 33 (G33). Using a combination of enzymatic (V1 RNase, RnI nuclease) and chemical (Pb(2+), imidazole) probing of the native Candida albicans ser-tRNACAG, we demonstrate that the overall tertiary structure of this tRNA resembles that of a ser-tRNA rather than a leu-tRNA, except within the anticodon arm where there is considerable disruption of the anticodon stem. Using non-modified in vitro transcripts of the C. albicans ser-tRNACAG carrying G, C, U or A at position 33, we demonstrate that it is specifically a G residue at this position that induces the atypical anticodon stem structure. Further quantitative evidence for an unusual structure in the anticodon arm of the G33-tRNA is provided by the observed change in kinetics of methylation of the G at position 37, by purified Escherichia coli m(1)G37 methyltransferase. We conclude that the anticodon arm distortion, induced by a guanosine base at position 33 in the anticodon loop of this novel tRNA, results in reduced decoding ability which has facilitated the evolution of this tRNA without extinction of the species encoding it.
1998
Duranton B., Keith G., Goss, Bergmann C., Schleiffer R., Raul F.
Concomitant changes in polyamine pools and DNA methylation during growth inhibition of human colonic cancer cells Article de journal
Dans: Exp Cell Res, vol. 243, non 2, p. 319-25, 1998, (0014-4827 Journal Article).
Résumé | BibTeX | Étiquettes: *Cell, *DNA, &, Adenosylmethionine, Amidines/pharmacology, Caco-2, Cells, Decarboxylase/antagonists, Differentiation/drug, Division/drug, effects, Eflornithine/pharmacology, enzyme, Gov't, Human, Indans/pharmacology, inhibitors/metabolism, Inhibitors/pharmacology, Methylation, Non-U.S., Ornithine, Polyamines/*metabolism, Support
@article{,
title = {Concomitant changes in polyamine pools and DNA methylation during growth inhibition of human colonic cancer cells},
author = { B. Duranton and G. Keith and Goss and C. Bergmann and R. Schleiffer and F. Raul},
year = {1998},
date = {1998-01-01},
journal = {Exp Cell Res},
volume = {243},
number = {2},
pages = {319-25},
abstract = {The effects of CGP 48664 and DFMO, selective inhibitors of the key enzymes of polyamine biosynthesis, namely, of S-adenosylmethionine decarboxylase (AdoMetDC) and ornithine decarboxylase (ODC), were investigated on growth, polyamine metabolism, and DNA methylation in the Caco-2 cell line. Both inhibitors caused growth inhibition and affected similarly the initial expression of the differentiation marker sucrase. In the presence of the AdoMetDC inhibitor, ODC activity and the intracellular pool of putrescine were enhanced, whereas the spermidine and spermine pools were decreased. In the presence of the ODC inhibitor, the AdoMetDC activity was enhanced and the intracellular pools of putrescine and spermidine were decreased. With both compounds, the degree of global DNA methylation was increased. Spermine and spermidine (but not putrescine) selectively inhibited cytosine-DNA methyltransferase activity. Our observations suggest that spermidine (and to a lesser extent spermine) controls DNA methylation and may represent a crucial step in the regulation of Caco-2 cell growth and differentiation.},
note = {0014-4827
Journal Article},
keywords = {*Cell, *DNA, &, Adenosylmethionine, Amidines/pharmacology, Caco-2, Cells, Decarboxylase/antagonists, Differentiation/drug, Division/drug, effects, Eflornithine/pharmacology, enzyme, Gov't, Human, Indans/pharmacology, inhibitors/metabolism, Inhibitors/pharmacology, Methylation, Non-U.S., Ornithine, Polyamines/*metabolism, Support},
pubstate = {published},
tppubtype = {article}
}
The effects of CGP 48664 and DFMO, selective inhibitors of the key enzymes of polyamine biosynthesis, namely, of S-adenosylmethionine decarboxylase (AdoMetDC) and ornithine decarboxylase (ODC), were investigated on growth, polyamine metabolism, and DNA methylation in the Caco-2 cell line. Both inhibitors caused growth inhibition and affected similarly the initial expression of the differentiation marker sucrase. In the presence of the AdoMetDC inhibitor, ODC activity and the intracellular pool of putrescine were enhanced, whereas the spermidine and spermine pools were decreased. In the presence of the ODC inhibitor, the AdoMetDC activity was enhanced and the intracellular pools of putrescine and spermidine were decreased. With both compounds, the degree of global DNA methylation was increased. Spermine and spermidine (but not putrescine) selectively inhibited cytosine-DNA methyltransferase activity. Our observations suggest that spermidine (and to a lesser extent spermine) controls DNA methylation and may represent a crucial step in the regulation of Caco-2 cell growth and differentiation.
1993
Baranowski W., Tomaszewski J., Keith G.
[Methylation of DNA in tissue of ovarian malignant tumors in women] Article de journal
Dans: Ginekol Pol, vol. 64, non 4, p. 169-73, 1993, (0017-0011 Journal Article).
Résumé | BibTeX | Étiquettes: Abstract, Adult, Aged, Carcinoma/genetics, Cell, DNA, English, Female, Human, Methylation, Middle, Neoplasm/*metabolism, Neoplasms/*genetics, Ovarian, Sertoli, Tumor/genetics
@article{,
title = {[Methylation of DNA in tissue of ovarian malignant tumors in women]},
author = { W. Baranowski and J. Tomaszewski and G. Keith},
year = {1993},
date = {1993-01-01},
journal = {Ginekol Pol},
volume = {64},
number = {4},
pages = {169-73},
abstract = {DNA methylation level from woman ovarian malignant tissues was investigated by 32P postlabeling of the single nucleotides, separation on TLC with followed autoradiography and Cerenkov counting. Slight differences in DNA methylation extent were found in malignant ovarian tumors as compared to normal myometrium and benign uterine tumor [myomas]. Lowest level of m5dC in relation to C and also in relation to total DNA was found in carcinoma embryonal tissue whereas maximal DNA methylation level was obtained in folliculoma tissue. This preliminary report needs further investigation of particularly genes methylation.},
note = {0017-0011
Journal Article},
keywords = {Abstract, Adult, Aged, Carcinoma/genetics, Cell, DNA, English, Female, Human, Methylation, Middle, Neoplasm/*metabolism, Neoplasms/*genetics, Ovarian, Sertoli, Tumor/genetics},
pubstate = {published},
tppubtype = {article}
}
DNA methylation level from woman ovarian malignant tissues was investigated by 32P postlabeling of the single nucleotides, separation on TLC with followed autoradiography and Cerenkov counting. Slight differences in DNA methylation extent were found in malignant ovarian tumors as compared to normal myometrium and benign uterine tumor [myomas]. Lowest level of m5dC in relation to C and also in relation to total DNA was found in carcinoma embryonal tissue whereas maximal DNA methylation level was obtained in folliculoma tissue. This preliminary report needs further investigation of particularly genes methylation.