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Article ; Online: Conference Scene: chromatin, replication and chromosomal stability.

Helmrich, Anne

Epigenomics

2011 Volume 3, Issue 5, Page(s) 543–546

Abstract: The Chromatin, Replication and Chromosomal Stability Conference took place on June 20-21 in Stockholm, Sweden. In this article, I outline the broad scientific program of the meeting which reflected the wide diversity in epigenetics research. Distinct ... ...

Abstract	The Chromatin, Replication and Chromosomal Stability Conference took place on June 20-21 in Stockholm, Sweden. In this article, I outline the broad scientific program of the meeting which reflected the wide diversity in epigenetics research. Distinct histone modifications are linked with specific chromatin structures and intranuclear positioning, thereby impacting replication timing and replication initiation, which in turn are related to gene expression and cell differentiation. Interference in any of these interconnected mechanisms can result in DNA breakage and lead to the activation of repair pathways. The DNA repair mechanisms again are influenced by the chromatin structure. In summary, the conference highlighted the functional implication of epigenetics in chromatin compaction, transcription regulation, replication control and DNA repair. The tight control of all these mechanisms defines the final cellular character.
MeSH term(s)	Chromatin/physiology ; Chromosomal Instability ; Congresses as Topic ; DNA Repair/physiology ; DNA Replication/physiology ; DNA Replication Timing/physiology ; Epigenomics/methods ; Epigenomics/trends
Chemical Substances	Chromatin
Language	English
Publishing date	2011-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1750-192X
ISSN (online)	1750-192X
DOI	10.2217/epi.11.77
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book ; Online ; Thesis: Genomweite molekular-zytogenetische Charakterisierung INK4A/ARF-defizienter Mauslymphome und Untersuchungen zur evolutionären Konservierung von Common fragile sites

Helmrich, Anne

2005

Abstract: Im ersten Teil dieser Arbeit wurden mittels molekular-zytogenetischer Methoden die chromosomalen Aberrationen in c-myc aktivierten ARFnull- und INK4a/ARFnull-Mauslymphomen untersucht. Die zytogenetischen Ergebnisse wurden mit dem Therapieverlauf der ... ...

Author's details	von Anne Helmrich
Abstract	Im ersten Teil dieser Arbeit wurden mittels molekular-zytogenetischer Methoden die chromosomalen Aberrationen in c-myc aktivierten ARFnull- und INK4a/ARFnull-Mauslymphomen untersucht. Die zytogenetischen Ergebnisse wurden mit dem Therapieverlauf der Mäuse nach Cyclophosphamid-Behandlung verglichen. In den ARFnull-Lymphomen erkannten wir den Gewinn des Chromosoms 14 als einen Marker für gute und den Gewinn des Chromosoms 6 als Marker für schlechte Behandlungserfolge. Auf den Chromosomen 6 und 14 der Maus liegen demnach bisher unbekannte Gene, welche für die Wahl der Behandlungsmethode ARF-defizienter Tumore von entscheidender Bedeutung sind...
Language	German
Size	Online-Ressource
Publisher	Niedersächsische Staats- und Universitätsbibliothek
Publishing place	Göttingen
Document type	Book ; Online ; Thesis
Thesis / German Habilitation thesis	Techn. Univ., Diss--Dresden, 2005
Database	Former special subject collection: coastal and deep sea fishing

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Book ; Thesis: Genomweite molekular-zytogenetische Charakterisierung INK4A-ARF-defizierter Mauslymphome und Untersuchungen zur evolutionären Konservierung von common fragile sites

Helmrich, Anne

2005

Author's details	von Anne Helmrich
Language	German
Size	113 S, Ill., graph. Darst, 30 cm
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Techn. Univ., Diss (Nicht für den Austausch)--Dresden, 2005
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article ; Online: Transcription-replication encounters, consequences and genomic instability.

Helmrich, Anne / Ballarino, Monica / Nudler, Evgeny / Tora, Laszlo

Nature structural & molecular biology

2013 Volume 20, Issue 4, Page(s) 412–418

Abstract: To ensure accurate duplication of genetic material, the replication fork must overcome numerous natural obstacles on its way, including transcription complexes engaged along the same template. Here we review the various levels of interdependence between ... ...

Abstract	To ensure accurate duplication of genetic material, the replication fork must overcome numerous natural obstacles on its way, including transcription complexes engaged along the same template. Here we review the various levels of interdependence between transcription and replication processes and how different types of encounters between RNA- and DNA-polymerase complexes may result in clashes of those machineries on the DNA template and thus increase genomic instability. In addition, we summarize strategies evolved in bacteria and eukaryotes to minimize the consequences of collisions, including R-loop formation and topological stresses.
MeSH term(s)	DNA Replication ; Genomic Instability ; Transcription, Genetic
Language	English
Publishing date	2013-04-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2126708-X
ISSN	1545-9985 ; 1545-9993
ISSN (online)	1545-9985
ISSN	1545-9993
DOI	10.1038/nsmb.2543
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Book ; Online ; Thesis: Genomweite molekular-zytogenetische Charakterisierung INK4A/ARF-defizienter Mauslymphome und Untersuchungen zur evolutionären Konservierung von Common fragile sites

Helmrich, Anne [Verfasser]

2005

Author's details	von Anne Helmrich
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Collisions between replication and transcription complexes cause common fragile site instability at the longest human genes.

Helmrich, Anne / Ballarino, Monica / Tora, Laszlo

Molecular cell

2011 Volume 44, Issue 6, Page(s) 966–977

Abstract: We show that the time required to transcribe human genes larger than 800 kb spans more than one complete cell cycle, while their transcription speed equals that of smaller genes. Independently of their expression status, we find the long genes to ... ...

Abstract	We show that the time required to transcribe human genes larger than 800 kb spans more than one complete cell cycle, while their transcription speed equals that of smaller genes. Independently of their expression status, we find the long genes to replicate late. Regions of concomitant transcription and replication in late S phase exhibit DNA break hot spots known as common fragile sites (CFSs). This CFS instability depends on the expression of the underlying long genes. We show that RNA:DNA hybrids (R-loops) form at sites of transcription/replication collisions and that RNase H1 functions to suppress CFS instability. In summary, our results show that, on the longest human genes, collisions of the transcription machinery with a replication fork are inevitable, creating R-loops and consequent CFS formation. Functional replication machinery needs to be involved in the resolution of conflicts between transcription and replication machineries to ensure genomic stability.
MeSH term(s)	Cell Cycle/genetics ; Chromosome Fragile Sites/genetics ; DNA/genetics ; DNA/metabolism ; DNA Replication ; DNA Topoisomerases, Type I/metabolism ; Genes/genetics ; Genomic Instability/genetics ; Humans ; RNA/genetics ; RNA/metabolism ; RNA Polymerase II/metabolism ; Ribonuclease H/metabolism ; Time Factors ; Transcription, Genetic
Chemical Substances	RNA (63231-63-0) ; DNA (9007-49-2) ; RNA Polymerase II (EC 2.7.7.-) ; ribonuclease HII (EC 3.1.26.-) ; Ribonuclease H (EC 3.1.26.4) ; DNA Topoisomerases, Type I (EC 5.99.1.2)
Language	English
Publishing date	2011-12-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2011.10.013
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Article ; Online: Distribution of p53 binding protein 1 (53BP1) and phosphorylated H2A.X during mouse preimplantation development in the absence of DNA damage.

Ziegler-Birling, Céline / Helmrich, Anne / Tora, Làszlò / Torres-Padilla, Maria-Elena

The International journal of developmental biology

2009 Volume 53, Issue 7, Page(s) 1003–1011

Abstract: The cells in the preimplantation mammalian embryo undergo several rounds of fast cell division. Whether the known DNA repair pathways are active during these early stages of development where cell division is of primary importance, has not been fully ... ...

Abstract	The cells in the preimplantation mammalian embryo undergo several rounds of fast cell division. Whether the known DNA repair pathways are active during these early stages of development where cell division is of primary importance, has not been fully established. Because of the important role of phosphorylated H2A.X (gammaH2A.X) in the DNA damage response as well as its putative role in assembly of embryonic chromatin, we analysed its distribution in the preimplantation mouse embryo. We found that H2A.X is highly phosphorylated throughout preimplantation development in the absence of any induced DNA damage. Moreover, gammaH2A.X levels vary significantly throughout the cell cycle. Interestingly, after the 4-cell stage, we detected high levels of H2A.X phosphorylation in mitosis, where telomeres appeared focally enriched with gammaH2A.X. In contrast, 53BP1, which is known to be recruited to DNA damage sites, is undetectable at mitotic chromosomes at these stages and its localisation changes upon blastocyst formation from mainly nuclear to cytoplasmic. We also show that 53BP1 and gammaH2A.X rarely colocalise, suggesting that the high levels of phosphorylation of H2A.X in the embryo might not be directly linked to the DNA damage response in the embryo. Our data suggest that phosphorylation of H2A.X is an important event in the fast dividing cells of the early embryo in the absence of any induced DNA damage. We discuss the possible consequences of these findings on the genome-wide chromatin remodelling that ocurs in the preimplantation mammalian embryo.
MeSH term(s)	Animals ; Blastocyst/cytology ; Blastocyst/metabolism ; Blastomeres/cytology ; Blastomeres/metabolism ; Chromosomal Proteins, Non-Histone ; Cleavage Stage, Ovum/cytology ; Cleavage Stage, Ovum/metabolism ; DNA Damage ; DNA-Binding Proteins ; Embryonic Development/physiology ; Female ; Histones/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Male ; Mice ; Mitosis ; Morula/cytology ; Morula/metabolism ; Phosphorylation ; Pregnancy ; Tumor Suppressor p53-Binding Protein 1 ; Zygote/metabolism
Chemical Substances	Chromosomal Proteins, Non-Histone ; DNA-Binding Proteins ; Histones ; Intracellular Signaling Peptides and Proteins ; Trp53bp1 protein, mouse ; Tumor Suppressor p53-Binding Protein 1 ; gamma-H2AX protein, mouse
Language	English
Publishing date	2009
Publishing country	Spain
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1036070-0
ISSN	1696-3547 ; 0214-6282
ISSN (online)	1696-3547
ISSN	0214-6282
DOI	10.1387/ijdb.082707cz
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Article: Identification of the human/mouse syntenic common fragile site FRA7K/Fra12C1--relation of FRA7K and other human common fragile sites on chromosome 7 to evolutionary breakpoints.

Helmrich, Anne / Stout-Weider, Karen / Matthaei, Anja / Hermann, Klaus / Heiden, Thomas / Schrock, Evelin

International journal of cancer

2007 Volume 120, Issue 1, Page(s) 48–54

Abstract: Common fragile sites (CFSs) are expressed as chromosome gaps in cells of different species including human and mouse as a result of the inhibition of DNA replication. They may serve as hot spots for DNA breakage in processes such as tumorigenesis and ... ...

Abstract	Common fragile sites (CFSs) are expressed as chromosome gaps in cells of different species including human and mouse as a result of the inhibition of DNA replication. They may serve as hot spots for DNA breakage in processes such as tumorigenesis and chromosome evolution. Using multicolor fluorescence in situ hybridization mapping, the authors describe here human CFS FRA7K on chromosome band 7q31.1 and its murine homolog Fra12C1. Within the syntenic FRA7K/Fra12C1 region lies the IMMP2L/Immp2l gene with a size of 899/983 kb. The authors further mapped 2 amplification breakpoints of the breast cancer cell line SKBR3 to the CFSs FRA7G and FRA7H. The 5 molecularly defined CFSs on chromosome 7 do not preferentially colocalize with synteny breaks between the human and mouse genomes and with intragenomic duplications that have occurred during chromosome evolution. In addition, in contrast to all currently reported data, CFSs in chromosome band 7q31 do not show increased DNA helix flexibility in comparison with control regions without CFS expression.
MeSH term(s)	Animals ; Breast Neoplasms/genetics ; Chromosome Breakage ; Chromosome Fragile Sites/genetics ; Chromosome Fragility ; Chromosome Mapping ; Chromosomes, Artificial, Yeast ; Chromosomes, Human, Pair 7/genetics ; Databases, Genetic ; Evolution, Molecular ; Gene Amplification ; Genome ; Humans ; In Situ Hybridization, Fluorescence ; Karyotyping ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Spleen/metabolism ; Synteny
Language	English
Publishing date	2007-01-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.22049
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Article: Common fragile sites are conserved features of human and mouse chromosomes and relate to large active genes.

Helmrich, Anne / Stout-Weider, Karen / Hermann, Klaus / Schrock, Evelin / Heiden, Thomas

Genome research

2006 Volume 16, Issue 10, Page(s) 1222–1230

Abstract: Common fragile sites (CFSs) are seen as chromosomal gaps and breaks brought about by inhibition of replication, and it is thought that they cluster with tumor breakpoints. This study presents a comprehensive analysis using conventional and molecular ... ...

Abstract	Common fragile sites (CFSs) are seen as chromosomal gaps and breaks brought about by inhibition of replication, and it is thought that they cluster with tumor breakpoints. This study presents a comprehensive analysis using conventional and molecular cytogenetic mapping of CFSs and their expression frequencies in two mouse strains, BALB/c and C57BL/6, and in human probands. Here we show that induced mouse CFSs relate to sites of spontaneous gaps and breaks and that CFS expression levels in chromosome bands are conserved between the two mouse strains and between syntenic mouse and human DNA segments. Furthermore, four additional mouse CFSs were found to be homologous to human CFSs on the molecular cytogenetic level (Fra2D-FRA2G, Fra4C2-FRA9E, Fra6A3.1-FRA7G, and Fra6B1-FRA7H), increasing the number of such CFSs already described in the literature to eight. Contrary to previous reports, DNA helix flexibility is not increased in the 15 human and eight mouse CFSs molecularly defined so far, compared to large nonfragile control regions. Our findings suggest that the mechanisms that provoke instability at CFSs are evolutionarily conserved. The role that large transcriptionally active genes may play in CFS expression is discussed.
MeSH term(s)	Animals ; Chromosome Fragile Sites/genetics ; Chromosome Mapping ; Chromosomes, Artificial, Bacterial ; Computational Biology ; Conserved Sequence/genetics ; DNA/chemistry ; Gene Expression Profiling ; Humans ; In Situ Hybridization, Fluorescence ; Mice/genetics ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Species Specificity
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2006-10
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1284872-4
ISSN	1549-5469 ; 1088-9051 ; 1054-9803
ISSN (online)	1549-5469
ISSN	1088-9051 ; 1054-9803
DOI	10.1101/gr.5335506
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Article: Recurrent chromosomal aberrations in INK4a/ARF defective primary lymphomas predict drug responses in vivo.

Helmrich, Anne / Lee, Soyoung / O'Brien, Patricia / Dörken, Bernd / Lowe, Scott W / Schröck, Evelin / Schmitt, Clemens A

Oncogene

2005 Volume 24, Issue 26, Page(s) 4174–4182

Abstract: Predicting responsiveness to anticancer therapy based on molecular findings at diagnosis is important to optimize treatment decisions. Although clinical outcome correlates with distinct mutations in some cancer entities, treatment responses within these ... ...

Abstract	Predicting responsiveness to anticancer therapy based on molecular findings at diagnosis is important to optimize treatment decisions. Although clinical outcome correlates with distinct mutations in some cancer entities, treatment responses within these lesion-stratified subgroups still remain heterogeneous, underscoring the need for additional prognosticators. We previously demonstrated that defined genetic defects at the INK4a/ARF locus, which encodes the tumor suppressors p16INK4a and ARF, not only accelerated lymphomagenesis in the Emu-myc transgenic mouse but also interfered with treatment sensitivity. In this study, we take a nonbiased genome-wide approach to examine whether the responsiveness of these lymphomas can be further stratified based on cytogenetic information at diagnosis. Indeed, using spectral karyotyping, comparative genomic hybridization, and fluorescence in situ hybridization in 38 primary lymphomas, we find recurrent cytogenetic alterations that refine the predictive value of INK4a/ARF lesions on drug responses in vivo: gain of chromosome 14, which was never detected in INK4a/ARFnull lymphomas, defined an ARFnull subgroup with superior treatment outcome. Gain of chromosome 6 was identified as a recurrent chromosomal aberration that predisposed ARFnull tumors to their subsequent INK4a loss during therapy. These data illustrate how cytogenetic information from cancer specimens might complement established prognostic markers and may improve anticancer treatment strategies.
MeSH term(s)	Animals ; Chromosome Aberrations ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Decision Making ; Disease Models, Animal ; In Situ Hybridization, Fluorescence ; Karyotyping ; Lymphoma, B-Cell/drug therapy ; Lymphoma, B-Cell/genetics ; Mice ; Mice, Transgenic ; Predictive Value of Tests ; Treatment Outcome
Chemical Substances	Cyclin-Dependent Kinase Inhibitor p16
Language	English
Publishing date	2005-06-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/sj.onc.1208600
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