2024-03-29T11:02:20Zhttp://repository.helmholtz-hzi.de/oai/requestoai:repository.helmholtz-hzi.de:10033/1254482019-08-30T11:27:09Zcom_10033_107102com_10033_6799col_10033_107103
Klawonn, Frank
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http://orcid.org/0000-0001-9613-182X
Wüstefeld, T.
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500
Zender, Lars
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Helmholtz Center for Infection Research, Inhoffenstr. 7, D-38124 Braunschweig, Germany
2011-03-23T15:24:15Z
2011-03-23T15:24:15Z
2011-03-23T15:24:15Z
03029743
http://hdl.handle.net/10033/125448
Lecture Notes in Computer Science (including subseries Lecture Notes in Artificial Intelligence and Lecture Notes in Bioinformatics)
null
Springer
Statistical modelling for data from experiments with short hairpin RNAs
Article
2018-06-13T15:30:41Z
ORIGINAL
Klawonn et al_final.pdf
Klawonn et al_final.pdf
conference proceedings
application/pdf
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MD5
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CC-LICENSE
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LICENSE
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TEXT
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10033/125448
oai:hzi.openrepository.com:10033/125448
2019-08-30 11:27:09.424
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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oai:repository.helmholtz-hzi.de:10033/2106692019-08-30T11:29:17Zcom_10033_107102com_10033_6799col_10033_107103
Sirma, Hüseyin
27afbd8de50a5fbb7d4e496d5b0c193d
500
Kumar, Mukesh
16762e4c4e8458173a46384fa9cfbd01
500
Meena, Jitendra K
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500
Witt, Britta
8c99bda09834dbdcda38c1cb8278d4ab
500
Weise, Julia M
fa79716bdf42bbc0e43d0698ff2a2935
500
Lechel, Andre
a3ca030ccc7e556f148b2ac05e368138
500
Ande, Satyanarayana
4883c4aacf437369bf8ea8a96d5e5745
500
Sakk, Vadim
2fefe2bea664841e82982b77c43a67d5
500
Guguen-Guillouzo, Christiane
ba693574538856355625d1a3dcdd19de
500
Zender, Lars
1aad3f1afe5c2ede767347e7af1dc65c
500
Rudolph, Karl-Lenhard
551b398d5fb47f111a96731d37eb7671
500
Günes, Cagatay
db86d049bcf310390958ca9a45186813
500
Heinrich-Pette-Institute, Hamburg, Germany.
2012-02-14T10:14:50Z
2012-02-14T10:14:50Z
2011-07
The promoter of human telomerase reverse transcriptase is activated during liver regeneration and hepatocyte proliferation. 2011, 141 (1):326-37, 337.e1-3 Gastroenterology
1528-0012
21447332
10.1053/j.gastro.2011.03.047
http://hdl.handle.net/10033/210669
Gastroenterology
Telomerase activity has not been detected in healthy human liver biopsy samples, but it is up-regulated in most human liver tumors. It is not clear whether telomerase is activated in response to acute or chronic liver injury. Telomerase activity is closely associated with expression of its catalytic subunit, telomerase reverse transcriptase (TERT). We analyzed the activity of the human TERT (hTERT) promoter during liver regeneration in vivo and hepatocyte proliferation in vitro.
en
Animals
Binding Sites
Cell Differentiation
Cell Proliferation
Cells, Cultured
Chromatin Immunoprecipitation
E2F2 Transcription Factor
E2F7 Transcription Factor
Gene Expression Regulation, Enzymologic
Genes, Reporter
Hepatectomy
Hepatocytes
Humans
Lac Operon
Liver
Liver Regeneration
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Promoter Regions, Genetic
RNA Interference
Regulatory Elements, Transcriptional
Retinoblastoma Protein
Telomerase
Time Factors
Transcriptional Activation
The promoter of human telomerase reverse transcriptase is activated during liver regeneration and hepatocyte proliferation.
Article
2018-06-12T16:47:44Z
Telomerase activity has not been detected in healthy human liver biopsy samples, but it is up-regulated in most human liver tumors. It is not clear whether telomerase is activated in response to acute or chronic liver injury. Telomerase activity is closely associated with expression of its catalytic subunit, telomerase reverse transcriptase (TERT). We analyzed the activity of the human TERT (hTERT) promoter during liver regeneration in vivo and hepatocyte proliferation in vitro.
ORIGINAL
Sirma et al_final.pdf
Sirma et al_final.pdf
original manuscript
application/pdf
3201530
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MD5
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true
CC-LICENSE
license_url
license_url
text/plain
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https://hzi.openrepository.com/bitstream/10033/210669/2/license_url
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MD5
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license_text
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license_rdf
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LICENSE
license.txt
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THUMBNAIL
Sirma et al_final.pdf.jpg
Sirma et al_final.pdf.jpg
Generated Thumbnail
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TEXT
Sirma et al_final.pdf.txt
Sirma et al_final.pdf.txt
Extracted Text
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https://hzi.openrepository.com/bitstream/10033/210669/7/Sirma%20et%20al_final.pdf.txt
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MD5
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10033/210669
oai:hzi.openrepository.com:10033/210669
2019-08-30 11:29:17.597
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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oai:repository.helmholtz-hzi.de:10033/2422972019-08-30T11:27:46Zcom_10033_107102com_10033_6799col_10033_107103
Hoenicke, Lisa
e23b7c36d845c84ec0129b2abc43dfc2
500
Zender, Lars
1aad3f1afe5c2ede767347e7af1dc65c
500
Helmholtz Centre for Infection Research, Braunschweig, Germany.
2012-09-10T13:45:39Z
2012-09-10T13:45:39Z
2012-06
Immune surveillance of senescent cells--biological significance in cancer- and non-cancer pathologies. 2012, 33 (6):1123-6 Carcinogenesis
1460-2180
22470164
10.1093/carcin/bgs124
http://hdl.handle.net/10033/242297
Carcinogenesis
Cellular senescence, a state of stable growth arrest, can occur in response to various stress stimuli such as telomere shortening, treatment with chemotherapeutic drugs or the aberrant activation of oncogenes. Senescent cells communicate with their environment by secreting various cytokines and growth factors, and it has become clear that this 'secretory phenotype' can have pro- as well as anti-tumorigenic effects. Recent work from our laboratory showed that premalignant, senescent hepatocytes are recognized and cleared through an antigen-specific immune response and that this immune response, designated as 'senescence surveillance' is crucial for tumor suppression in the liver [(Kang,T.W. et al. (2011) Senescence surveillance of pre-malignant hepatocytes limits liver cancer development. Nature, 479, 547-551]. It is an emerging concept that immune responses against senescent cells have a broader biological significance in cancer- as well as non-cancer pathologies and current data suggest that distinct immune responses are engaged to clear senescent cells in different disease settings. In this review article, we will discuss different examples how immune responses against senescent cells are involved to restrict disease progression in cancer- and non-cancer pathologies.
en
Archived with thanks to Carcinogenesis
Immune surveillance of senescent cells--biological significance in cancer- and non-cancer pathologies.
Article
2013-12-15T00:00:00Z
Cellular senescence, a state of stable growth arrest, can occur in response to various stress stimuli such as telomere shortening, treatment with chemotherapeutic drugs or the aberrant activation of oncogenes. Senescent cells communicate with their environment by secreting various cytokines and growth factors, and it has become clear that this 'secretory phenotype' can have pro- as well as anti-tumorigenic effects. Recent work from our laboratory showed that premalignant, senescent hepatocytes are recognized and cleared through an antigen-specific immune response and that this immune response, designated as 'senescence surveillance' is crucial for tumor suppression in the liver [(Kang,T.W. et al. (2011) Senescence surveillance of pre-malignant hepatocytes limits liver cancer development. Nature, 479, 547-551]. It is an emerging concept that immune responses against senescent cells have a broader biological significance in cancer- as well as non-cancer pathologies and current data suggest that distinct immune responses are engaged to clear senescent cells in different disease settings. In this review article, we will discuss different examples how immune responses against senescent cells are involved to restrict disease progression in cancer- and non-cancer pathologies.
ORIGINAL
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original manuscript
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Table 1_Hoenicke_and_Zender_Carcinogenesis.pdf
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MD5
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Figure 1.pdf
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CC-LICENSE
license_url
license_url
text/plain
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https://hzi.openrepository.com/bitstream/10033/242297/4/license_url
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MD5
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license_text
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https://hzi.openrepository.com/bitstream/10033/242297/5/license_text
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LICENSE
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MD5
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TEXT
Hoenicke_Zender_final.pdf.txt
Hoenicke_Zender_final.pdf.txt
Extracted Text
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MD5
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Figure 1.pdf.txt
Figure 1.pdf.txt
Extracted Text
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https://hzi.openrepository.com/bitstream/10033/242297/15/Figure%201.pdf.txt
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MD5
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Table 1_Hoenicke_and_Zender_Carcinogenesis.pdf.txt
Table 1_Hoenicke_and_Zender_Carcinogenesis.pdf.txt
Extracted Text
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https://hzi.openrepository.com/bitstream/10033/242297/16/Table%201_Hoenicke_and_Zender_Carcinogenesis.pdf.txt
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MD5
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THUMBNAIL
Hoenicke_Zender_final.pdf.jpg
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Generated Thumbnail
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MD5
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Table 1_Hoenicke_and_Zender_Carcinogenesis.pdf.jpg
Table 1_Hoenicke_and_Zender_Carcinogenesis.pdf.jpg
Generated Thumbnail
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Figure 1.pdf.jpg
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Generated Thumbnail
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oai:repository.helmholtz-hzi.de:10033/2712922019-08-30T11:26:13Zcom_10033_107102com_10033_6799col_10033_107103
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Kitzing, Thomas
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Roessler, Stephanie
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Zuber, Johannes
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Krasnitz, Alexander
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Schultz, Nikolaus
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Revill, Kate
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Weissmueller, Susann
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Rappaport, Amy R
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Simon, Janelle
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Zhang, Jack
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Luo, Weijun
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Hicks, James
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Zender, Lars
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Wang, Xin Wei
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Powers, Scott
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Wigler, Michael
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Lowe, Scott W
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Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
2013-03-06T09:03:42Z
2013-03-06T09:03:42Z
2012-05-22
A cluster of cooperating tumor-suppressor gene candidates in chromosomal deletions. 2012, 109 (21):8212-7 Proc. Natl. Acad. Sci. U.S.A.
1091-6490
22566646
10.1073/pnas.1206062109
http://hdl.handle.net/10033/271292
Proceedings of the National Academy of Sciences of the United States of America
The large chromosomal deletions frequently observed in cancer genomes are often thought to arise as a "two-hit" mechanism in the process of tumor-suppressor gene (TSG) inactivation. Using a murine model system of hepatocellular carcinoma (HCC) and in vivo RNAi, we test an alternative hypothesis, that such deletions can arise from selective pressure to attenuate the activity of multiple genes. By targeting the mouse orthologs of genes frequently deleted on human 8p22 and adjacent regions, which are lost in approximately half of several other major epithelial cancers, we provide evidence suggesting that multiple genes on chromosome 8p can cooperatively inhibit tumorigenesis in mice, and that their cosuppression can synergistically promote tumor growth. In addition, in human HCC patients, the combined down-regulation of functionally validated 8p TSGs is associated with poor survival, in contrast to the down-regulation of any individual gene. Our data imply that large cancer-associated deletions can produce phenotypes distinct from those arising through loss of a single TSG, and as such should be considered and studied as distinct mutational events.
en
Archived with thanks to Proceedings of the National Academy of Sciences of the United States of America
Animals
Carcinoma, Hepatocellular
Cell Line, Transformed
Cell Line, Tumor
Chromosomes, Human, Pair 8
Female
Gene Deletion
Gene Expression Regulation, Neoplastic
Genes, Tumor Suppressor
Genomics
Haploinsufficiency
Humans
Liver
Liver Neoplasms, Experimental
Mice
Mice, Inbred C57BL
Mice, Nude
Monosomy
RNA Interference
Stem Cells
A cluster of cooperating tumor-suppressor gene candidates in chromosomal deletions.
Article
2018-06-13T15:18:07Z
The large chromosomal deletions frequently observed in cancer genomes are often thought to arise as a "two-hit" mechanism in the process of tumor-suppressor gene (TSG) inactivation. Using a murine model system of hepatocellular carcinoma (HCC) and in vivo RNAi, we test an alternative hypothesis, that such deletions can arise from selective pressure to attenuate the activity of multiple genes. By targeting the mouse orthologs of genes frequently deleted on human 8p22 and adjacent regions, which are lost in approximately half of several other major epithelial cancers, we provide evidence suggesting that multiple genes on chromosome 8p can cooperatively inhibit tumorigenesis in mice, and that their cosuppression can synergistically promote tumor growth. In addition, in human HCC patients, the combined down-regulation of functionally validated 8p TSGs is associated with poor survival, in contrast to the down-regulation of any individual gene. Our data imply that large cancer-associated deletions can produce phenotypes distinct from those arising through loss of a single TSG, and as such should be considered and studied as distinct mutational events.
ORIGINAL
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Müller-Tidow, Carsten
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Helmholtz Centre for infection research, Inhoffenstr. 7, D-38124 Braunschweig, Germany.
2016-02-02T15:52:19Z
2016-02-02T15:52:19Z
2012
Integrative analyses for omics data: a Bayesian mixture model to assess the concordance of ChIP-chip and ChIP-seq measurements. 2012, 75 (8-10):461-70 J. Toxicol. Environ. Health Part A
1528-7394
22686305
10.1080/15287394.2012.674914
http://hdl.handle.net/10033/595412
Journal of toxicology and environmental health. Part A
The analysis of different variations in genomics, transcriptomics, epigenomics, and proteomics has increased considerably in recent years. This is especially due to the success of microarray and, more recently, sequencing technology. Apart from understanding mechanisms of disease pathogenesis on a molecular basis, for example in cancer research, the challenge of analyzing such different data types in an integrated way has become increasingly important also for the validation of new sequencing technologies with maximum resolution. For this purpose, a methodological framework for their comparison with microarray techniques in the context of smallest sample sizes, which result from the high costs of experiments, is proposed in this contribution. Based on an adaptation of the externally centered correlation coefficient ( Schäfer et al. 2009 ), it is demonstrated how a Bayesian mixture model can be applied to compare and classify measurements of histone acetylation that stem from chromatin immunoprecipitation combined with either microarray (ChIP-chip) or sequencing techniques (ChIP-seq) for the identification of DNA fragments. Here, the murine hematopoietic cell line 32D, which was transduced with the oncogene BCR-ABL, the hallmark of chronic myeloid leukemia, was characterized. Cells were compared to mock-transduced cells as control. Activation or inhibition of other genes by histone modifications induced by the oncogene is considered critical in such a context for the understanding of the disease.
en
Algorithms
Animals
Bayes Theorem
Capillary Electrochromatography
Chromatin Immunoprecipitation
DNA
Data Interpretation, Statistical
Epigenomics
Fusion Proteins, bcr-abl
Genomics
Hematopoietic Stem Cells
Histones
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Markov Chains
Mice
Microarray Analysis
Models, Statistical
Monte Carlo Method
Oncogenes
Proteomics
Sample Size
Sequence Analysis, DNA
Transduction, Genetic
Integrative analyses for omics data: a Bayesian mixture model to assess the concordance of ChIP-chip and ChIP-seq measurements.
Article
2018-06-13T17:03:49Z
The analysis of different variations in genomics, transcriptomics, epigenomics, and proteomics has increased considerably in recent years. This is especially due to the success of microarray and, more recently, sequencing technology. Apart from understanding mechanisms of disease pathogenesis on a molecular basis, for example in cancer research, the challenge of analyzing such different data types in an integrated way has become increasingly important also for the validation of new sequencing technologies with maximum resolution. For this purpose, a methodological framework for their comparison with microarray techniques in the context of smallest sample sizes, which result from the high costs of experiments, is proposed in this contribution. Based on an adaptation of the externally centered correlation coefficient ( Schäfer et al. 2009 ), it is demonstrated how a Bayesian mixture model can be applied to compare and classify measurements of histone acetylation that stem from chromatin immunoprecipitation combined with either microarray (ChIP-chip) or sequencing techniques (ChIP-seq) for the identification of DNA fragments. Here, the murine hematopoietic cell line 32D, which was transduced with the oncogene BCR-ABL, the hallmark of chronic myeloid leukemia, was characterized. Cells were compared to mock-transduced cells as control. Activation or inhibition of other genes by histone modifications induced by the oncogene is considered critical in such a context for the understanding of the disease.
ORIGINAL
Schaefer_et_al_2012_Preprint.pdf
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Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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