Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    German Medical Science GMS Publishing House; Düsseldorf
    In:  G-I-N Conference 2012; 20120822-20120825; Berlin; DOCP069 /20120710/
    Publication Date: 2012-07-11
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    facet.materialart.
    Unknown
    German Medical Science GMS Publishing House; Düsseldorf
    In:  G-I-N Conference 2012; 20120822-20120825; Berlin; DOCP054 /20120710/
    Publication Date: 2012-07-11
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2011-08-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parker, John N -- Vermeulen, Niki -- Penders, Bart -- England -- Nature. 2011 Aug 3;476(7358):33. doi: 10.1038/476033c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21814264" target="_blank"〉PubMed〈/a〉
    Keywords: Job Satisfaction ; Research/*organization & administration ; *Research Design ; Research Personnel/psychology/*standards
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 2013-03-01
    Description: The rapid cell turnover of the intestinal epithelium is achieved from small numbers of stem cells located in the base of glandular crypts. These stem cells have been variously described as rapidly cycling or quiescent. A functional arrangement of stem cells that reconciles both of these behaviours has so far been difficult to obtain. Alternative explanations for quiescent cells have been that they act as a parallel or reserve population that replace rapidly cycling stem cells periodically or after injury; their exact nature remains unknown. Here we show mouse intestinal quiescent cells to be precursors that are committed to mature into differentiated secretory cells of the Paneth and enteroendocrine lineage. However, crucially we find that after intestinal injury they are capable of extensive proliferation and can give rise to clones comprising the main epithelial cell types. Thus, quiescent cells can be recalled to the stem-cell state. These findings establish quiescent cells as an effective clonogenic reserve and provide a motivation for investigating their role in pathologies such as colorectal cancers and intestinal inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buczacki, Simon J A -- Zecchini, Heather Ireland -- Nicholson, Anna M -- Russell, Roslin -- Vermeulen, Louis -- Kemp, Richard -- Winton, Douglas J -- Cancer Research UK/United Kingdom -- England -- Nature. 2013 Mar 7;495(7439):65-9. doi: 10.1038/nature11965. Epub 2013 Feb 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23446353" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis/metabolism ; Cell Differentiation ; Cell Division ; *Cell Lineage ; Cell Separation ; Clone Cells/cytology/metabolism ; Intestinal Neoplasms/pathology ; Intestines/cytology/injuries/pathology ; Mice ; Multipotent Stem Cells/*cytology/metabolism/*secretion ; Paneth Cells/*cytology/*metabolism ; Receptors, G-Protein-Coupled/*metabolism ; Regeneration ; Staining and Labeling ; Stem Cell Niche
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Publication Date: 2013-05-10
    Description: There is strong circumstantial evidence that certain heavy, unstable atomic nuclei are 'octupole deformed', that is, distorted into a pear shape. This contrasts with the more prevalent rugby-ball shape of nuclei with reflection-symmetric, quadrupole deformations. The elusive octupole deformed nuclei are of importance for nuclear structure theory, and also in searches for physics beyond the standard model; any measurable electric-dipole moment (a signature of the latter) is expected to be amplified in such nuclei. Here we determine electric octupole transition strengths (a direct measure of octupole correlations) for short-lived isotopes of radon and radium. Coulomb excitation experiments were performed using accelerated beams of heavy, radioactive ions. Our data on (220)Rn and (224)Ra show clear evidence for stronger octupole deformation in the latter. The results enable discrimination between differing theoretical approaches to octupole correlations, and help to constrain suitable candidates for experimental studies of atomic electric-dipole moments that might reveal extensions to the standard model.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gaffney, L P -- Butler, P A -- Scheck, M -- Hayes, A B -- Wenander, F -- Albers, M -- Bastin, B -- Bauer, C -- Blazhev, A -- Bonig, S -- Bree, N -- Cederkall, J -- Chupp, T -- Cline, D -- Cocolios, T E -- Davinson, T -- De Witte, H -- Diriken, J -- Grahn, T -- Herzan, A -- Huyse, M -- Jenkins, D G -- Joss, D T -- Kesteloot, N -- Konki, J -- Kowalczyk, M -- Kroll, Th -- Kwan, E -- Lutter, R -- Moschner, K -- Napiorkowski, P -- Pakarinen, J -- Pfeiffer, M -- Radeck, D -- Reiter, P -- Reynders, K -- Rigby, S V -- Robledo, L M -- Rudigier, M -- Sambi, S -- Seidlitz, M -- Siebeck, B -- Stora, T -- Thoele, P -- Van Duppen, P -- Vermeulen, M J -- von Schmid, M -- Voulot, D -- Warr, N -- Wimmer, K -- Wrzosek-Lipska, K -- Wu, C Y -- Zielinska, M -- England -- Nature. 2013 May 9;497(7448):199-204. doi: 10.1038/nature12073.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oliver Lodge Laboratory, University of Liverpool, Liverpool L69 7ZE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23657348" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    Publication Date: 2011-06-17
    Description: The identification of intestinal stem cells as well as their malignant counterparts, colon cancer stem cells, has undergone rapid development in recent years. Under physiological conditions, intestinal homeostasis is a carefully balanced and efficient interplay between stem cells, their progeny and the microenvironment. These interactions regulate the astonishingly rapid renewal of the intestinal epithelial layer, which consequently puts us at serious risk of developing cancer. Here we highlight the microenvironment-derived signals that regulate stem-cell fate and epithelial differentiation. As our understanding of normal intestinal crypt homeostasis grows, these developments may point towards new insights into the origin of cancer and the maintenance and regulation of cancer stem cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Medema, Jan Paul -- Vermeulen, Louis -- England -- Nature. 2011 Jun 15;474(7351):318-26. doi: 10.1038/nature10212.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Experimental Oncology and Radiobiology, Center for Experimental Molecular Medicine, Academic Medical Center, Amsterdam 1105AZ, The Netherlands. j.p.medema@amc.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21677748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Homeostasis ; Humans ; Intestinal Neoplasms/genetics/*pathology ; Intestines/cytology/*pathology/*physiology/physiopathology ; Neoplastic Stem Cells/metabolism/pathology ; Signal Transduction ; Stem Cells/*cytology/pathology/*physiology ; *Tumor Microenvironment/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Publication Date: 2012-09-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Houweling, Sander -- Badawy, Bakr -- Baker, David F -- Basu, Sourish -- Belikov, Dmitry -- Bergamaschi, Peter -- Bousquet, Philippe -- Broquet, Gregoire -- Butler, Tim -- Canadell, Josep G -- Chen, Jing -- Chevallier, Frederic -- Ciais, Philippe -- Collatz, G James -- Denning, Scott -- Engelen, Richard -- Enting, Ian G -- Fischer, Marc L -- Fraser, Annemarie -- Gerbig, Christoph -- Gloor, Manuel -- Jacobson, Andrew R -- Jones, Dylan B A -- Heimann, Martin -- Khalil, Aslam -- Kaminski, Thomas -- Kasibhatla, Prasad S -- Krakauer, Nir Y -- Krol, Maarten -- Maki, Takashi -- Maksyutov, Shamil -- Manning, Andrew -- Meesters, Antoon -- Miller, John B -- Palmer, Paul I -- Patra, Prabir -- Peters, Wouter -- Peylin, Philippe -- Poussi, Zegbeu -- Prather, Michael J -- Randerson, James T -- Rockmann, Thomas -- Rodenbeck, Christian -- Sarmiento, Jorge L -- Schimel, David S -- Scholze, Marko -- Schuh, Andrew -- Suntharalingam, Parv -- Takahashi, Taro -- Turnbull, Jocelyn -- Yurganov, Leonid -- Vermeulen, Alex -- New York, N.Y. -- Science. 2012 Aug 31;337(6098):1038-40. doi: 10.1126/science.337.6098.1038-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22936755" target="_blank"〉PubMed〈/a〉
    Keywords: Atmosphere/*chemistry ; Carbon Dioxide/*analysis ; *Climate Change
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    Publication Date: 2013-11-23
    Description: Cancer is a disease in which cells accumulate genetic aberrations that are believed to confer a clonal advantage over cells in the surrounding tissue. However, the quantitative benefit of frequently occurring mutations during tumor development remains unknown. We quantified the competitive advantage of Apc loss, Kras activation, and P53 mutations in the mouse intestine. Our findings indicate that the fate conferred by these mutations is not deterministic, and many mutated stem cells are replaced by wild-type stem cells after biased, but still stochastic events. Furthermore, P53 mutations display a condition-dependent advantage, and especially in colitis-affected intestines, clones harboring mutations in this gene are favored. Our work confirms the previously theoretical notion that the tissue architecture of the intestine suppresses the accumulation of mutated lineages.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vermeulen, Louis -- Morrissey, Edward -- van der Heijden, Maartje -- Nicholson, Anna M -- Sottoriva, Andrea -- Buczacki, Simon -- Kemp, Richard -- Tavare, Simon -- Winton, Douglas J -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):995-8. doi: 10.1126/science.1243148.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK, Cambridge Institute, University of Cambridge, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24264992" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein/genetics ; Animals ; Cell Transformation, Neoplastic/*genetics/*pathology ; *Gene Expression Regulation, Neoplastic ; Intestinal Neoplasms/*genetics/*pathology ; Mice ; Mice, Mutant Strains ; Models, Biological ; Mutation ; Neoplastic Stem Cells/metabolism/*pathology ; Proto-Oncogene Proteins p21(ras)/genetics ; Transcriptional Activation ; Tumor Suppressor Protein p53/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    Publication Date: 2013-07-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garnett, T -- Appleby, M C -- Balmford, A -- Bateman, I J -- Benton, T G -- Bloomer, P -- Burlingame, B -- Dawkins, M -- Dolan, L -- Fraser, D -- Herrero, M -- Hoffmann, I -- Smith, P -- Thornton, P K -- Toulmin, C -- Vermeulen, S J -- Godfray, H C J -- New York, N.Y. -- Science. 2013 Jul 5;341(6141):33-4. doi: 10.1126/science.1234485.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Oxford, Oxford, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23828927" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture/*trends ; Food Supply/*methods ; Goals ; Policy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    Publication Date: 2014-05-23
    Description: Deregulation of lysine methylation signalling has emerged as a common aetiological factor in cancer pathogenesis, with inhibitors of several histone lysine methyltransferases (KMTs) being developed as chemotherapeutics. The largely cytoplasmic KMT SMYD3 (SET and MYND domain containing protein 3) is overexpressed in numerous human tumours. However, the molecular mechanism by which SMYD3 regulates cancer pathways and its relationship to tumorigenesis in vivo are largely unknown. Here we show that methylation of MAP3K2 by SMYD3 increases MAP kinase signalling and promotes the formation of Ras-driven carcinomas. Using mouse models for pancreatic ductal adenocarcinoma and lung adenocarcinoma, we found that abrogating SMYD3 catalytic activity inhibits tumour development in response to oncogenic Ras. We used protein array technology to identify the MAP3K2 kinase as a target of SMYD3. In cancer cell lines, SMYD3-mediated methylation of MAP3K2 at lysine 260 potentiates activation of the Ras/Raf/MEK/ERK signalling module and SMYD3 depletion synergizes with a MEK inhibitor to block Ras-driven tumorigenesis. Finally, the PP2A phosphatase complex, a key negative regulator of the MAP kinase pathway, binds to MAP3K2 and this interaction is blocked by methylation. Together, our results elucidate a new role for lysine methylation in integrating cytoplasmic kinase-signalling cascades and establish a pivotal role for SMYD3 in the regulation of oncogenic Ras signalling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4122675/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4122675/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mazur, Pawel K -- Reynoird, Nicolas -- Khatri, Purvesh -- Jansen, Pascal W T C -- Wilkinson, Alex W -- Liu, Shichong -- Barbash, Olena -- Van Aller, Glenn S -- Huddleston, Michael -- Dhanak, Dashyant -- Tummino, Peter J -- Kruger, Ryan G -- Garcia, Benjamin A -- Butte, Atul J -- Vermeulen, Michiel -- Sage, Julien -- Gozani, Or -- DP2 OD007447/OD/NIH HHS/ -- R01 CA172560/CA/NCI NIH HHS/ -- T32 GM007276/GM/NIGMS NIH HHS/ -- U19 AI109662/AI/NIAID NIH HHS/ -- England -- Nature. 2014 Jun 12;510(7504):283-7. doi: 10.1038/nature13320. Epub 2014 May 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Pediatrics, Stanford University School of Medicine, California 94305, USA [2] Department of Genetics, Stanford University School of Medicine, California 94305, USA [3]. ; 1] Department of Biology, Stanford University, California 94305, USA [2]. ; Institute for Immunity, Transplantation and Infection, and Department of Medicine, Stanford University School of Medicine, California 94305, USA. ; Department of Molecular Cancer Research and Department of Medical Oncology, University Medical Center Utrecht, 3508 AB Utrecht, The Netherlands. ; Department of Biology, Stanford University, California 94305, USA. ; Epigenetics Program and Department of Biochemistry and Biophysics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Cancer Epigenetics DPU, Oncology R&D, GlaxoSmithKline, Collegeville, Pennsylvania 19426 USA. ; 1] Cancer Epigenetics DPU, Oncology R&D, GlaxoSmithKline, Collegeville, Pennsylvania 19426 USA [2] Janssen Research and Development, 1400 McKean Road, Spring House, Pennsylvania 19477, USA (D.D.); Department of Molecular Biology, Faculty of Science, Radboud Institute for Molecular Life Sciences (RIMLS), Radboud University, 6525GA Nijmegen, The Netherlands (M.V.). ; 1] Department of Pediatrics, Stanford University School of Medicine, California 94305, USA [2] Department of Genetics, Stanford University School of Medicine, California 94305, USA. ; 1] Department of Molecular Cancer Research and Department of Medical Oncology, University Medical Center Utrecht, 3508 AB Utrecht, The Netherlands [2] Janssen Research and Development, 1400 McKean Road, Spring House, Pennsylvania 19477, USA (D.D.); Department of Molecular Biology, Faculty of Science, Radboud Institute for Molecular Life Sciences (RIMLS), Radboud University, 6525GA Nijmegen, The Netherlands (M.V.).〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24847881" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/enzymology/genetics/metabolism/pathology ; Animals ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics/*metabolism/pathology ; Disease Models, Animal ; Histone-Lysine N-Methyltransferase/*metabolism ; Humans ; Lung Neoplasms/enzymology/genetics/metabolism/pathology ; Lysine/*metabolism ; MAP Kinase Kinase Kinase 2/chemistry/*metabolism ; MAP Kinase Kinase Kinases/chemistry/*metabolism ; Methylation ; Mice ; Mitogen-Activated Protein Kinases/metabolism ; Oncogene Protein p21(ras)/genetics/*metabolism ; Pancreatic Neoplasms/enzymology/genetics/metabolism/pathology ; Protein Phosphatase 2/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins A-raf/metabolism ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...