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  • 1
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    P2 × 7 receptor stimulation reduces glucose absorption by down-regulating glucose transporter 2 expression at the membrane of intestinal epithelial cells (2012)
    Wiley
    Details
    Publication Date: 2012-05-08
    Description: With the diabetes epidemic affecting the world population, there is an increasing demand for means to regulate glycaemia. Dietary glucose is first absorbed by the intestine before entering the blood stream. Thus, the regulation of glucose absorption by intestinal epithelial cells (IECs) could represent a way to regulate glycaemia. Among the molecules involved in glycaemia homeostasis, extracellular ATP, a paracrine signaling molecule, was reported to induce insulin secretion from pancreatic β cells by activating P2Y and P2X receptors. In rat's jejunum, P2 × 7 expression was previously immunolocalized to the apex of villi, where it has been suspected to play a role in apoptosis. However, using an antibody recognizing the receptor extracellular domain and thus most of the P2 × 7 isoforms, we showed that expression of the receptor is apparent in the top two-thirds of villi. These data suggest a different role for this receptor in IECs. Using the non-cancerous IEC-6 cells and differentiated Caco-2 cells, glucose transport was reduced by more than 30% following P2 × 7 stimulation. This effect on glucose transport was not due to P2 × 7-induced cell apoptosis, but rather was the consequence of glucose transporter 2 (Glut2)'s internalization. The signaling pathway leading to P2 × 7-dependent Glut2 internalization involved the calcium-independent activation of phospholipase Cγ1 (PLCγ1), PKCδ and PKD1. Although the complete mechanism regulating Glut2 internalization following P2 × 7 activation is not fully understood, modulation of P2 × 7 receptor activation could represent an interesting approach to regulate intestinal glucose absorption. J. Cell. Physiol. © 2012 Wiley Periodicals, Inc.
    Electronic ISSN: 1097-4652
    Topics: Biology , Medicine
    Published by Wiley
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  • 2
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    The histone methyltransferase SETDB1 is recurrently amplified in melanoma and accelerates its onset (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-25
    Description: The most common mutation in human melanoma, BRAF(V600E), activates the serine/threonine kinase BRAF and causes excessive activity in the mitogen-activated protein kinase pathway. BRAF(V600E) mutations are also present in benign melanocytic naevi, highlighting the importance of additional genetic alterations in the genesis of malignant tumours. Such changes include recurrent copy number variations that result in the amplification of oncogenes. For certain amplifications, the large number of genes in the interval has precluded an understanding of the cooperating oncogenic events. Here we have used a zebrafish melanoma model to test genes in a recurrently amplified region of chromosome 1 for the ability to cooperate with BRAF(V600E) and accelerate melanoma. SETDB1, an enzyme that methylates histone H3 on lysine 9 (H3K9), was found to accelerate melanoma formation significantly in zebrafish. Chromatin immunoprecipitation coupled with massively parallel DNA sequencing and gene expression analyses uncovered genes, including HOX genes, that are transcriptionally dysregulated in response to increased levels of SETDB1. Our studies establish SETDB1 as an oncogene in melanoma and underscore the role of chromatin factors in regulating tumorigenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3348545/" 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/PMC3348545/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ceol, Craig J -- Houvras, Yariv -- Jane-Valbuena, Judit -- Bilodeau, Steve -- Orlando, David A -- Battisti, Valentine -- Fritsch, Lauriane -- Lin, William M -- Hollmann, Travis J -- Ferre, Fabrizio -- Bourque, Caitlin -- Burke, Christopher J -- Turner, Laura -- Uong, Audrey -- Johnson, Laura A -- Beroukhim, Rameen -- Mermel, Craig H -- Loda, Massimo -- Ait-Si-Ali, Slimane -- Garraway, Levi A -- Young, Richard A -- Zon, Leonard I -- CA103846/CA/NCI NIH HHS/ -- CA146455/CA/NCI NIH HHS/ -- DK055381/DK/NIDDK NIH HHS/ -- HG002668/HG/NHGRI NIH HHS/ -- K08 DK075432/DK/NIDDK NIH HHS/ -- K08 DK075432-04/DK/NIDDK NIH HHS/ -- K08DK075432-04/DK/NIDDK NIH HHS/ -- K99AR056899-02/AR/NIAMS NIH HHS/ -- R00 AR056899/AR/NIAMS NIH HHS/ -- R00 AR056899-02/AR/NIAMS NIH HHS/ -- R01 CA103846/CA/NCI NIH HHS/ -- R01 CA103846-09/CA/NCI NIH HHS/ -- R01 CA146445/CA/NCI NIH HHS/ -- R01 CA146445-03/CA/NCI NIH HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- R01 HG002668-08/HG/NHGRI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Mar 24;471(7339):513-7. doi: 10.1038/nature09806.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Program and Hematology/Oncology, Children's Hospital Boston, Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430779" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Amino Acid Substitution ; Animals ; Animals, Genetically Modified ; Cell Transformation, Neoplastic/genetics ; Chromatin Immunoprecipitation ; Chromosomes, Human, Pair 1/genetics ; DNA Copy Number Variations/*genetics ; Disease Models, Animal ; Gene Amplification/*genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/genetics ; Genes, Homeobox/genetics ; Histone-Lysine N-Methyltransferase/*genetics/metabolism ; Humans ; Melanocytes/cytology/enzymology/metabolism/pathology ; Melanoma/enzymology/*genetics/*pathology ; Nevus/enzymology ; Oncogenes/genetics ; Protein Methyltransferases/*genetics/*metabolism ; Proto-Oncogene Proteins B-raf/chemistry/genetics/metabolism ; Zebrafish/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Enhancer decommissioning by LSD1 during embryonic stem cell differentiation (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-02-03
    Description: Transcription factors and chromatin modifiers are important in the programming and reprogramming of cellular states during development. Transcription factors bind to enhancer elements and recruit coactivators and chromatin-modifying enzymes to facilitate transcription initiation. During differentiation a subset of these enhancers must be silenced, but the mechanisms underlying enhancer silencing are poorly understood. Here we show that the histone demethylase lysine-specific demethylase 1 (LSD1; ref. 5), which demethylates histone H3 on Lys 4 or Lys 9 (H3K4/K9), is essential in decommissioning enhancers during the differentiation of mouse embryonic stem cells (ESCs). LSD1 occupies enhancers of active genes that are critical for control of the state of ESCs. However, LSD1 is not essential for the maintenance of ESC identity. Instead, ESCs lacking LSD1 activity fail to differentiate fully, and ESC-specific enhancers fail to undergo the histone demethylation events associated with differentiation. At active enhancers, LSD1 is a component of the NuRD (nucleosome remodelling and histone deacetylase) complex, which contains additional subunits that are necessary for ESC differentiation. We propose that the LSD1-NuRD complex decommissions enhancers of the pluripotency program during differentiation, which is essential for the complete shutdown of the ESC gene expression program and the transition to new cell states.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4144424/" 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/PMC4144424/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whyte, Warren A -- Bilodeau, Steve -- Orlando, David A -- Hoke, Heather A -- Frampton, Garrett M -- Foster, Charles T -- Cowley, Shaun M -- Young, Richard A -- G0600135/Medical Research Council/United Kingdom -- HG002668/HG/NHGRI NIH HHS/ -- NS055923/NS/NINDS NIH HHS/ -- P01 NS055923/NS/NINDS NIH HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2012 Feb 1;482(7384):221-5. doi: 10.1038/nature10805.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22297846" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/*genetics ; Embryonic Stem Cells/*cytology/*metabolism ; Enhancer Elements, Genetic/*genetics ; Fibroblasts ; *Gene Silencing ; Histone Demethylases ; Mi-2 Nucleosome Remodeling and Deacetylase Complex/metabolism ; Mice ; Oxidoreductases, N-Demethylating/antagonists & inhibitors/*metabolism ; Promoter Regions, Genetic/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Mediator and cohesin connect gene expression and chromatin architecture (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-08-20
    Description: Transcription factors control cell-specific gene expression programs through interactions with diverse coactivators and the transcription apparatus. Gene activation may involve DNA loop formation between enhancer-bound transcription factors and the transcription apparatus at the core promoter, but this process is not well understood. Here we report that mediator and cohesin physically and functionally connect the enhancers and core promoters of active genes in murine embryonic stem cells. Mediator, a transcriptional coactivator, forms a complex with cohesin, which can form rings that connect two DNA segments. The cohesin-loading factor Nipbl is associated with mediator-cohesin complexes, providing a means to load cohesin at promoters. DNA looping is observed between the enhancers and promoters occupied by mediator and cohesin. Mediator and cohesin co-occupy different promoters in different cells, thus generating cell-type-specific DNA loops linked to the gene expression program of each cell.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2953795/" 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/PMC2953795/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kagey, Michael H -- Newman, Jamie J -- Bilodeau, Steve -- Zhan, Ye -- Orlando, David A -- van Berkum, Nynke L -- Ebmeier, Christopher C -- Goossens, Jesse -- Rahl, Peter B -- Levine, Stuart S -- Taatjes, Dylan J -- Dekker, Job -- Young, Richard A -- HG002668/HG/NHGRI NIH HHS/ -- HG003143/HG/NHGRI NIH HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- R01 HG002668-07/HG/NHGRI NIH HHS/ -- R01 HG003143/HG/NHGRI NIH HHS/ -- R01 HG003143-06/HG/NHGRI NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2010 Sep 23;467(7314):430-5. doi: 10.1038/nature09380. Epub 2010 Aug 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20720539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle Proteins/genetics/*metabolism ; Cells, Cultured ; Chromatin/chemistry/*genetics/*metabolism ; Chromatin Assembly and Disassembly/*genetics ; Chromosomal Proteins, Non-Histone/genetics/*metabolism ; DNA/chemistry/genetics/metabolism ; Embryonic Stem Cells/cytology/*metabolism ; Enhancer Elements, Genetic/genetics ; Fibroblasts ; Gene Expression Regulation/*genetics ; Mediator Complex/genetics/*metabolism ; Mice ; Nucleic Acid Conformation ; Organ Specificity ; Promoter Regions, Genetic/genetics ; Protein Binding
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Accommodation of excess Ti in a (Ba, Sr)TiO3 thin film with 53.4% Ti grown on Pt/SiO2/Si by metalorganic chemical-vapor deposition (1999)
    American Institute of Physics
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    Publication Date: 1999-08-30
    Print ISSN: 0003-6951
    Electronic ISSN: 1077-3118
    Topics: Physics
    Published by American Institute of Physics
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  • 6
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    Demonstration of scaled (⩾0.12 μm2) Pb(Zr,Ti)O3 capacitors on W plugs with Al interconnect (2001)
    American Institute of Physics
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    Publication Date: 2001-12-10
    Print ISSN: 0003-6951
    Electronic ISSN: 1077-3118
    Topics: Physics
    Published by American Institute of Physics
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  • 7
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    X-linked H3K27me3 demethylase Utx is required for embryonic development in a sex-specific manner (2012)
    National Academy of Sciences
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    Publication Date: 2012-07-23
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 8
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    Utx is required for embryogenesis [Developmental Biology] (2012)
    National Academy of Sciences
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    Publication Date: 2012-08-08
    Description: Embryogenesis requires the timely and coordinated activation of developmental regulators. It has been suggested that the recently discovered class of histone demethylases (UTX and JMJD3) that specifically target the repressive H3K27me3 modification play an important role in the activation of “bivalent” genes in response to specific developmental cues. To determine the requirements for UTX in pluripotency and development, we have generated Utx-null ES cells and mutant mice. The loss of UTX had a profound effect during embryogenesis. Utx-null embryos had reduced somite counts, neural tube closure defects and heart malformation that presented between E9.5 and E13.5. Unexpectedly, homozygous mutant female embryos were more severely affected than hemizygous mutant male embryos. In fact, we observed the survival of a subset of UTX-deficient males that were smaller in size and had reduced lifespan. Interestingly, these animals were fertile with normal spermatogenesis. Consistent with a midgestation lethality, UTX-null male and female ES cells gave rise to all three germ layers in teratoma assays, though sex-specific differences could be observed in the activation of developmental regulators in embryoid body assays. Lastly, ChIP-seq analysis revealed an increase in H3K27me3 in Utx-null male ES cells. In summary, our data demonstrate sex-specific requirements for this X-linked gene while suggesting a role for UTY during development.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 9
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    Second Landau level fractional quantum Hall effects in the Corbino geometry (2015)
    Elsevier
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    Publication Date: 2015-09-01
    Print ISSN: 0038-1098
    Electronic ISSN: 1879-2766
    Topics: Physics
    Published by Elsevier
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  • 10
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    Structure, soft modes, and superconductivity in Cl-doped cadmium sulfide (1988)
    American Physical Society
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    Publication Date: 1988-03-01
    Print ISSN: 0163-1829
    Electronic ISSN: 1095-3795
    Topics: Physics
    Published by American Physical Society
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