ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
Filter
  • Female  (9)
  • Mutation  (5)
  • Gene Expression Regulation, Developmental  (3)
  • 1
    facet.materialart.
    Unknown
    Chromosomal instability and tumors promoted by DNA hypomethylation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eden, Amir -- Gaudet, Francois -- Waghmare, Alpana -- Jaenisch, Rudolf -- CA87869/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 18;300(5618):455.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Nine Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Mammalian/*genetics/physiology ; DNA (Cytosine-5-)-Methyltransferase/genetics/metabolism ; *DNA Methylation ; Fibroblasts/metabolism ; Genes, Neurofibromatosis 1 ; Genes, p53 ; Humans ; *Loss of Heterozygosity ; Mice ; Mutation ; Neoplasms/genetics ; Recombination, Genetic ; Sarcoma/*genetics ; Soft Tissue Neoplasms/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Nuclear cloning and epigenetic reprogramming of the genome (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-08-11
    Description: Cloning of mammals by nuclear transfer (NT) results in gestational or neonatal failure with at most a few percent of manipulated embryos resulting in live births. Many of those that survive to term succumb to a variety of abnormalities that are likely due to inappropriate epigenetic reprogramming. Cloned embryos derived from donors, such as embryonic stem cells, that may require little or no reprogramming of early developmental genes develop substantially better beyond implantation than NT clones derived from somatic cells. Although recent experiments have demonstrated normal reprogramming of telomere length and X chromosome inactivation, epigenetic information established during gametogenesis, such as gametic imprints, cannot be restored after nuclear transfer. Survival of cloned animals to birth and beyond, despite substantial transcriptional dysregulation, is consistent with mammalian development being rather tolerant to epigenetic abnormalities, with lethality resulting only beyond a threshold of faulty gene reprogramming encompassing multiple loci.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rideout , W M 3rd -- Eggan, K -- Jaenisch, R -- New York, N.Y. -- Science. 2001 Aug 10;293(5532):1093-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research and, Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11498580" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Nucleus/*genetics/metabolism ; *Cloning, Organism ; DNA Methylation ; Dosage Compensation, Genetic ; Embryo, Mammalian/cytology/*physiology ; *Embryo, Nonmammalian ; *Embryonic and Fetal Development ; Female ; Gametogenesis ; *Gene Expression Regulation, Developmental ; Genomic Imprinting ; Germ Cells/cytology/physiology ; Male ; Nuclear Transfer Techniques ; Phenotype ; Stem Cells/cytology/physiology ; Telomere/physiology/ultrastructure
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Epigenetic instability in ES cells and cloned mice (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-07-07
    Description: Cloning by nuclear transfer (NT) is an inefficient process in which most clones die before birth and survivors often display growth abnormalities. In an effort to correlate gene expression with survival and fetal overgrowth, we have examined imprinted gene expression in both mice cloned by nuclear transfer and in the embryonic stem (ES) cell donor populations from which they were derived. The epigenetic state of the ES cell genome was found to be extremely unstable. Similarly, variation in imprinted gene expression was observed in most cloned mice, even in those derived from ES cells of the same subclone. Many of the animals survived to adulthood despite widespread gene dysregulation, indicating that mammalian development may be rather tolerant to epigenetic aberrations of the genome. These data imply that even apparently normal cloned animals may have subtle abnormalities in gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Humpherys, D -- Eggan, K -- Akutsu, H -- Hochedlinger, K -- Rideout , W M 3rd -- Biniszkiewicz, D -- Yanagimachi, R -- Jaenisch, R -- 5-R35-CA44339/CA/NCI NIH HHS/ -- R01-CA84198/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2001 Jul 6;293(5527):95-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11441181" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Birth Weight ; Cell Nucleus/*genetics ; Cesarean Section ; *Cloning, Organism/methods ; Congenital Abnormalities/genetics ; DNA Methylation ; Embryo Loss/genetics ; Embryo Transfer ; Embryo, Mammalian/*cytology/metabolism ; Female ; Fetal Death/genetics ; *Gene Expression Regulation, Developmental ; Gene Silencing ; Genomic Imprinting/*genetics ; Mice ; Oocytes/metabolism ; Placenta/metabolism ; Placentation ; Polyploidy ; Pregnancy ; RNA, Messenger/genetics/metabolism ; Respiration ; Stem Cells/*cytology/*metabolism ; Survival Rate
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Developmental biology. Don't clone humans! (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-04-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaenisch, R -- Wilmut, I -- New York, N.Y. -- Science. 2001 Mar 30;291(5513):2552.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research and Department of Biology, MIT, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11286275" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethics ; Cell Nucleus/*physiology ; Chromatin/physiology ; *Cloning, Organism/adverse effects ; Congenital Abnormalities/etiology/prevention & control ; Embryo, Mammalian/cytology ; Embryonic and Fetal Development ; Gene Expression Regulation, Developmental ; *Genome, Human ; Humans ; Nuclear Transfer Techniques ; Public Opinion ; Research ; Risk ; Stem Cells
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    X-Chromosome inactivation in cloned mouse embryos (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-25
    Description: To study whether cloning resets the epigenetic differences between the two X chromosomes of a somatic female nucleus, we monitored X inactivation in cloned mouse embryos. Both X chromosomes were active during cleavage of cloned embryos, followed by random X inactivation in the embryo proper. In the trophectoderm (TE), X inactivation was nonrandom with the inactivated X of the somatic donor being chosen for inactivation. When female embryonic stem cells with two active X chromosomes were used as donors, random X inactivation was seen in the TE and embryo. These results demonstrate that epigenetic marks can be removed and reestablished on either X chromosome during cloning. Our results also suggest that the epigenetic marks imposed on the X chromosomes during gametogenesis, responsible for normal imprinted X inactivation in the TE, are functionally equivalent to the marks imposed on the chromosomes during somatic X inactivation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eggan, K -- Akutsu, H -- Hochedlinger, K -- Rideout, W 3rd -- Yanagimachi, R -- Jaenisch, R -- 5-R35-CA44339/CA/NCI NIH HHS/ -- R01-CA84198/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1578-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11090356" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Differentiation ; *Cloning, Organism ; *Dosage Compensation, Genetic ; Embryo, Mammalian/cytology/*metabolism ; Embryonic and Fetal Development ; Female ; Gene Silencing ; Genes, Reporter ; Genomic Imprinting ; Green Fluorescent Proteins ; Luminescent Proteins/genetics ; Male ; Mice ; Muridae ; Nuclear Transfer Techniques ; Oocytes ; Placenta/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Stem Cell Transplantation ; Stem Cells/metabolism ; Transgenes ; X Chromosome/*genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    Dissecting direct reprogramming through integrative genomic analysis (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-05-30
    Description: Somatic cells can be reprogrammed to a pluripotent state through the ectopic expression of defined transcription factors. Understanding the mechanism and kinetics of this transformation may shed light on the nature of developmental potency and suggest strategies with improved efficiency or safety. Here we report an integrative genomic analysis of reprogramming of mouse fibroblasts and B lymphocytes. Lineage-committed cells show a complex response to the ectopic expression involving induction of genes downstream of individual reprogramming factors. Fully reprogrammed cells show gene expression and epigenetic states that are highly similar to embryonic stem cells. In contrast, stable partially reprogrammed cell lines show reactivation of a distinctive subset of stem-cell-related genes, incomplete repression of lineage-specifying transcription factors, and DNA hypermethylation at pluripotency-related loci. These observations suggest that some cells may become trapped in partially reprogrammed states owing to incomplete repression of transcription factors, and that DNA de-methylation is an inefficient step in the transition to pluripotency. We demonstrate that RNA inhibition of transcription factors can facilitate reprogramming, and that treatment with DNA methyltransferase inhibitors can improve the overall efficiency of the reprogramming process.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754827/" 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/PMC2754827/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mikkelsen, Tarjei S -- Hanna, Jacob -- Zhang, Xiaolan -- Ku, Manching -- Wernig, Marius -- Schorderet, Patrick -- Bernstein, Bradley E -- Jaenisch, Rudolf -- Lander, Eric S -- Meissner, Alexander -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-04/HG/NHGRI NIH HHS/ -- England -- Nature. 2008 Jul 3;454(7200):49-55. doi: 10.1038/nature07056. Epub 2008 May 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18509334" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Azacitidine/pharmacology ; Cell Line ; Cell Lineage ; Cellular Reprogramming/*genetics ; Chromatin/metabolism ; DNA (Cytosine-5-)-Methyltransferase/antagonists & inhibitors/genetics/metabolism ; DNA Methylation ; Embryonic Stem Cells/metabolism ; Enzyme Inhibitors/pharmacology ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Genome/genetics ; *Genomics ; Mice ; Pluripotent Stem Cells/cytology/*metabolism ; Transcription Factors/deficiency/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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    HDAC2 negatively regulates memory formation and synaptic plasticity (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-05-09
    Description: Chromatin modifications, especially histone-tail acetylation, have been implicated in memory formation. Increased histone-tail acetylation induced by inhibitors of histone deacetylases (HDACis) facilitates learning and memory in wild-type mice as well as in mouse models of neurodegeneration. Harnessing the therapeutic potential of HDACis requires knowledge of the specific HDAC family member(s) linked to cognitive enhancement. Here we show that neuron-specific overexpression of HDAC2, but not that of HDAC1, decreased dendritic spine density, synapse number, synaptic plasticity and memory formation. Conversely, Hdac2 deficiency resulted in increased synapse number and memory facilitation, similar to chronic treatment with HDACis in mice. Notably, reduced synapse number and learning impairment of HDAC2-overexpressing mice were ameliorated by chronic treatment with HDACis. Correspondingly, treatment with HDACis failed to further facilitate memory formation in Hdac2-deficient mice. Furthermore, analysis of promoter occupancy revealed an association of HDAC2 with the promoters of genes implicated in synaptic plasticity and memory formation. Taken together, our results suggest that HDAC2 functions in modulating synaptic plasticity and long-lasting changes of neural circuits, which in turn negatively regulates learning and memory. These observations encourage the development and testing of HDAC2-selective inhibitors for human diseases associated with memory impairment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3498958/" 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/PMC3498958/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guan, Ji-Song -- Haggarty, Stephen J -- Giacometti, Emanuela -- Dannenberg, Jan-Hermen -- Joseph, Nadine -- Gao, Jun -- Nieland, Thomas J F -- Zhou, Ying -- Wang, Xinyu -- Mazitschek, Ralph -- Bradner, James E -- DePinho, Ronald A -- Jaenisch, Rudolf -- Tsai, Li-Huei -- R01 DA028301/DA/NIDA NIH HHS/ -- R01 DA028301-02/DA/NIDA NIH HHS/ -- R01 NS051874/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 May 7;459(7243):55-60. doi: 10.1038/nature07925.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19424149" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Butyrates/pharmacology ; Dendritic Spines/physiology ; Electrical Synapses/*physiology ; Female ; Gene Expression Regulation ; Hippocampus/metabolism ; Histone Deacetylase 1 ; Histone Deacetylase 2 ; Histone Deacetylase Inhibitors ; Histone Deacetylases/deficiency/genetics/*metabolism ; Hydroxamic Acids/pharmacology ; Learning/drug effects ; Male ; Memory/drug effects/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons/metabolism ; Promoter Regions, Genetic/genetics ; Repressor Proteins/antagonists & inhibitors/genetics/*metabolism ; Sodium/pharmacology
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    Direct cell reprogramming is a stochastic process amenable to acceleration (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-11-10
    Description: Direct reprogramming of somatic cells into induced pluripotent stem (iPS) cells can be achieved by overexpression of Oct4, Sox2, Klf4 and c-Myc transcription factors, but only a minority of donor somatic cells can be reprogrammed to pluripotency. Here we demonstrate that reprogramming by these transcription factors is a continuous stochastic process where almost all mouse donor cells eventually give rise to iPS cells on continued growth and transcription factor expression. Additional inhibition of the p53/p21 pathway or overexpression of Lin28 increased the cell division rate and resulted in an accelerated kinetics of iPS cell formation that was directly proportional to the increase in cell proliferation. In contrast, Nanog overexpression accelerated reprogramming in a predominantly cell-division-rate-independent manner. Quantitative analyses define distinct cell-division-rate-dependent and -independent modes for accelerating the stochastic course of reprogramming, and suggest that the number of cell divisions is a key parameter driving epigenetic reprogramming to pluripotency.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789972/" 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/PMC2789972/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanna, Jacob -- Saha, Krishanu -- Pando, Bernardo -- van Zon, Jeroen -- Lengner, Christopher J -- Creyghton, Menno P -- van Oudenaarden, Alexander -- Jaenisch, Rudolf -- R01 CA087869/CA/NCI NIH HHS/ -- R01 CA087869-09/CA/NCI NIH HHS/ -- R01 HD045022/HD/NICHD NIH HHS/ -- R01 HD045022-06/HD/NICHD NIH HHS/ -- R01-CA087869/CA/NCI NIH HHS/ -- R01-HDO45022/PHS HHS/ -- R37 CA084198/CA/NCI NIH HHS/ -- R37 CA084198-09/CA/NCI NIH HHS/ -- R37-CA084198/CA/NCI NIH HHS/ -- U54CA143874/CA/NCI NIH HHS/ -- England -- Nature. 2009 Dec 3;462(7273):595-601. doi: 10.1038/nature08592. Epub 2009 Nov 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA. Hanna@wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19898493" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Division ; Cell Line ; *Cellular Reprogramming ; Gene Expression Regulation, Developmental ; Mice ; Mice, SCID ; Models, Biological ; Pluripotent Stem Cells/*cytology/*metabolism ; Time Factors ; Transcription Factors/genetics/metabolism
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    facet.materialart.
    Unknown
    Uracil DNA glycosylase activity is dispensable for immunoglobulin class switch (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-25
    Description: Activation-induced cytidine deaminase (AID) is required for the DNA cleavage step in immunoglobulin class switch recombination (CSR). AID is proposed to deaminate cytosine to generate uracil (U) in either mRNA or DNA. In the second instance, DNA cleavage depends on uracil DNA glycosylase (UNG) for removal of U. Using phosphorylated histone gamma-H2AX focus formation as a marker of DNA cleavage, we found that the UNG inhibitor Ugi did not inhibit DNA cleavage in immunoglobulin heavy chain (IgH) locus during CSR, even though Ugi blocked UNG binding to DNA and strongly inhibited CSR. Strikingly, UNG mutants that had lost the capability of removing U rescued CSR in UNG-/- B cells. These results indicate that UNG is involved in the repair step of CSR yet by an unknown mechanism. The dispensability of U removal in the DNA cleavage step of CSR requires a reconsideration of the model of DNA deamination by AID.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Begum, Nasim A -- Kinoshita, Kazuo -- Kakazu, Naoki -- Muramatsu, Masamichi -- Nagaoka, Hitoshi -- Shinkura, Reiko -- Biniszkiewicz, Detlev -- Boyer, Laurie A -- Jaenisch, Rudolf -- Honjo, Tasuku -- New York, N.Y. -- Science. 2004 Aug 20;305(5687):1160-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry and Molecular Biology, Graduate School of Medicine, Kyoto University, Yoshida Sakyo-ku, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15326357" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/enzymology/immunology/*physiology ; Cell Line, Tumor ; Cytidine Deaminase/metabolism ; DNA/*metabolism ; DNA Glycosylases/antagonists & inhibitors/genetics/*metabolism ; DNA Repair ; *Genes, Immunoglobulin ; *Immunoglobulin Class Switching ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Switch Region ; Mice ; Mutation ; Precipitin Tests ; Recombination, Genetic ; Transfection ; Uracil/metabolism ; Uracil-DNA Glycosidase ; Viral Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 10
    facet.materialart.
    Unknown
    Antigen-specific B-cell receptor sensitizes B cells to infection by influenza virus (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-10-22
    Description: Influenza A virus-specific B lymphocytes and the antibodies they produce protect against infection. However, the outcome of interactions between an influenza haemagglutinin-specific B cell via its receptor (BCR) and virus is unclear. Through somatic cell nuclear transfer we generated mice that harbour B cells with a BCR specific for the haemagglutinin of influenza A/WSN/33 virus (FluBI mice). Their B cells secrete an immunoglobulin gamma 2b that neutralizes infectious virus. Whereas B cells from FluBI and control mice bind equivalent amounts of virus through interaction of haemagglutinin with surface-disposed sialic acids, the A/WSN/33 virus infects only the haemagglutinin-specific B cells. Mere binding of virus is not sufficient for infection of B cells: this requires interactions of the BCR with haemagglutinin, causing both disruption of antibody secretion and FluBI B-cell death within 18 h. In mice infected with A/WSN/33, lung-resident FluBI B cells are infected by the virus, thus delaying the onset of protective antibody release into the lungs, whereas FluBI cells in the draining lymph node are not infected and proliferate. We propose that influenza targets and kills influenza-specific B cells in the lung, thus allowing the virus to gain purchase before the initiation of an effective adaptive response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3863936/" 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/PMC3863936/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dougan, Stephanie K -- Ashour, Joseph -- Karssemeijer, Roos A -- Popp, Maximilian W -- Avalos, Ana M -- Barisa, Marta -- Altenburg, Arwen F -- Ingram, Jessica R -- Cragnolini, Juan Jose -- Guo, Chunguang -- Alt, Frederick W -- Jaenisch, Rudolf -- Ploegh, Hidde L -- DP1 GM106409/GM/NIGMS NIH HHS/ -- R01 AI033456/AI/NIAID NIH HHS/ -- R01 AI087879/AI/NIAID NIH HHS/ -- R01 GM100518/GM/NIGMS NIH HHS/ -- R01 HD045022/HD/NICHD NIH HHS/ -- R37 HD045022/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Nov 21;503(7476):406-9. doi: 10.1038/nature12637. Epub 2013 Oct 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24141948" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology/metabolism ; Antibody Specificity/immunology ; B-Lymphocytes/*immunology/pathology/secretion/*virology ; Cell Death ; Female ; Hemagglutinin Glycoproteins, Influenza Virus/immunology/metabolism ; Immunoglobulin G/immunology/metabolism ; Lung/cytology/immunology/secretion/virology ; Lymph Nodes/cytology/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Neutralization Tests ; Nuclear Transfer Techniques ; Orthomyxoviridae/pathogenicity/*physiology ; Receptors, Antigen, B-Cell/*immunology/metabolism ; Virus Replication
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...