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
  • Cells, Cultured  (141)
  • American Association for the Advancement of Science (AAAS)  (141)
  • Springer Science + Business Media
  • 2010-2014  (35)
  • 1990-1994  (52)
  • 1980-1984  (54)
Collection
Keywords
Publisher
Years
Year
  • 1
    facet.materialart.
    Unknown
    Reconstituting organ-level lung functions on a chip (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-26
    Description: Here, we describe a biomimetic microsystem that reconstitutes the critical functional alveolar-capillary interface of the human lung. This bioinspired microdevice reproduces complex integrated organ-level responses to bacteria and inflammatory cytokines introduced into the alveolar space. In nanotoxicology studies, this lung mimic revealed that cyclic mechanical strain accentuates toxic and inflammatory responses of the lung to silica nanoparticles. Mechanical strain also enhances epithelial and endothelial uptake of nanoparticulates and stimulates their transport into the underlying microvascular channel. Similar effects of physiological breathing on nanoparticle absorption are observed in whole mouse lung. Mechanically active "organ-on-a-chip" microdevices that reconstitute tissue-tissue interfaces critical to organ function may therefore expand the capabilities of cell culture models and provide low-cost alternatives to animal and clinical studies for drug screening and toxicology applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huh, Dongeun -- Matthews, Benjamin D -- Mammoto, Akiko -- Montoya-Zavala, Martin -- Hsin, Hong Yuan -- Ingber, Donald E -- R01-ES016665/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1662-8. doi: 10.1126/science.1188302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20576885" target="_blank"〉PubMed〈/a〉
    Keywords: Air ; Animals ; *Biomimetic Materials ; Blood-Air Barrier ; Capillaries/*physiology ; Capillary Permeability ; Cells, Cultured ; Endothelial Cells/*physiology ; Escherichia coli/immunology ; Humans ; Immunity, Innate ; Inflammation ; Lung/blood supply/physiology ; Mice ; *Microfluidic Analytical Techniques ; Microtechnology ; Nanoparticles/toxicity ; Neutrophil Infiltration ; Oxidative Stress ; Pneumocytes/*physiology ; Pulmonary Alveoli/*blood supply/cytology/immunology/*physiology ; Respiration ; Silicon Dioxide/toxicity ; Stress, Mechanical
    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
    A neutralizing antibody selected from plasma cells that binds to group 1 and group 2 influenza A hemagglutinins (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-30
    Description: The isolation of broadly neutralizing antibodies against influenza A viruses has been a long-sought goal for therapeutic approaches and vaccine design. Using a single-cell culture method for screening large numbers of human plasma cells, we isolated a neutralizing monoclonal antibody that recognized the hemagglutinin (HA) glycoprotein of all 16 subtypes and neutralized both group 1 and group 2 influenza A viruses. Passive transfer of this antibody conferred protection to mice and ferrets. Complexes with HAs from the group 1 H1 and the group 2 H3 subtypes analyzed by x-ray crystallography showed that the antibody bound to a conserved epitope in the F subdomain. This antibody may be used for passive protection and to inform vaccine design because of its broad specificity and neutralization potency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corti, Davide -- Voss, Jarrod -- Gamblin, Steven J -- Codoni, Giosiana -- Macagno, Annalisa -- Jarrossay, David -- Vachieri, Sebastien G -- Pinna, Debora -- Minola, Andrea -- Vanzetta, Fabrizia -- Silacci, Chiara -- Fernandez-Rodriguez, Blanca M -- Agatic, Gloria -- Bianchi, Siro -- Giacchetto-Sasselli, Isabella -- Calder, Lesley -- Sallusto, Federica -- Collins, Patrick -- Haire, Lesley F -- Temperton, Nigel -- Langedijk, Johannes P M -- Skehel, John J -- Lanzavecchia, Antonio -- G0600369/Medical Research Council/United Kingdom -- MC_U117584222/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Aug 12;333(6044):850-6. doi: 10.1126/science.1205669. Epub 2011 Jul 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Research in Biomedicine, 6500 Bellinzona, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21798894" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Neutralizing/*immunology/isolation & purification ; Antibodies, Viral/*immunology/isolation & purification ; Antibody Specificity ; Antigens, Viral/*immunology ; Cells, Cultured ; Cross Reactions ; Crystallography, X-Ray ; Epitopes/immunology ; Ferrets ; Glycosylation ; Hemagglutinin Glycoproteins, Influenza Virus/*immunology ; Humans ; Hydrophobic and Hydrophilic Interactions ; Immunization, Passive ; Immunoglobulin Variable Region/immunology ; Influenza A Virus, H1N1 Subtype/immunology ; Influenza A virus/*immunology ; Influenza B virus/immunology ; Influenza, Human/immunology ; Mice ; Models, Molecular ; Molecular Sequence Data ; Orthomyxoviridae Infections/immunology/prevention & control/therapy ; Plasma Cells/immunology ; Protein Multimerization ; Protein Structure, Secondary
    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
    Selective activation of the B natriuretic peptide receptor by C-type natriuretic peptide (CNP) (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-05
    Description: The natriuretic peptides are hormones that can stimulate natriuretic, diuretic, and vasorelaxant activity in vivo, presumably through the activation of two known cell surface receptor guanylyl cyclases (ANPR-A and ANPR-B). Although atrial natriuretic peptide (ANP) and, to a lesser extent, brain natriuretic peptide (BNP) are efficient activators of the ANPR-A guanylyl cyclase, neither hormone can significantly stimulate ANPR-B. A member of this hormone family, C-type natriuretic peptide (CNP), potently and selectively activated the human ANPR-B guanylyl cyclase. CNP does not increase guanosine 3',5'-monophosphate accumulation in cells expressing human ANPR-A. The affinity of CNP for ANPR-B is 50- or 500-fold higher than ANP or BNP, respectively. This ligand-receptor pair may be involved in the regulation of fluid homeostasis by the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koller, K J -- Lowe, D G -- Bennett, G L -- Minamino, N -- Kangawa, K -- Matsuo, H -- Goeddel, D V -- New York, N.Y. -- Science. 1991 Apr 5;252(5002):120-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Genentech, Inc., South San Francisco 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1672777" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atrial Natriuretic Factor/*physiology ; Cells, Cultured ; Cercopithecus aethiops ; Cloning, Molecular ; Dose-Response Relationship, Drug ; Guanylate Cyclase/metabolism ; Humans ; Natriuretic Peptide, Brain ; Natriuretic Peptide, C-Type ; Nerve Tissue Proteins/*pharmacology ; Receptors, Atrial Natriuretic Factor ; Receptors, Cell Surface/*physiology ; Recombinant Proteins ; Signal Transduction
    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
    Rel-associated pp40: an inhibitor of the rel family of transcription factors (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-23
    Description: The Rel-associated protein pp40 is functionally related to I kappa B, an inhibitor of the transcription factor NF-kappa B. Purified pp40 inhibits the DNA binding activity of the NF-kappa B protein complex (p50:p65 heterodimers), p50:c-Rel heteromers, and c-Rel homodimers. The sequence of the complementary DNA encoding pp40 revealed similarity to the gene encoding MAD-3, a protein with mammalian I kappa B-like activity. Protein sequencing of I kappa B purified from rabbit lung confirmed that MAD-3 encodes a protein similar to I kappa B. The sequence similarity between MAD-3 and pp40 includes a casein kinase II and consensus tyrosine phosphorylation site, as well as five repeats of a sequence found in the human erythrocyte protein ankyrin. These results suggest that rel-related transcription factors, which are capable of cytosolic to nuclear translocation, may be held in the cytosol by interaction with related cytoplasmic anchor molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, N -- Ghosh, S -- Simmons, D L -- Tempst, P -- Liou, H C -- Baltimore, D -- Bose, H R Jr -- CA09583/CA/NCI NIH HHS/ -- CA2616/CA/NCI NIH HHS/ -- CA33192/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Sep 13;253(5025):1268-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Texas, Austin 78712.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1891714" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cells, Cultured ; Chick Embryo ; Cloning, Molecular ; DNA Probes ; Molecular Sequence Data ; NF-kappa B/*antagonists & inhibitors ; Oligonucleotide Probes ; Oncogene Proteins v-rel ; Open Reading Frames ; Phosphoproteins/*genetics/metabolism ; Protein-Tyrosine Kinases/antagonists & inhibitors ; RNA, Messenger/genetics ; Retroviridae Proteins, Oncogenic/*antagonists & inhibitors ; Sequence Homology, Nucleic Acid ; Transcription Factors/*antagonists & inhibitors
    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
    Activation-induced ubiquitination of the T cell antigen receptor (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: The zeta subunit of the T cell antigen receptor (TCR) exists primarily as a disulfide-linked homodimer. This receptor subunit is important in TCR-mediated signal transduction and is a substrate for a TCR-activated protein tyrosine kinase. The zeta chain was found to undergo ubiquitination in response to receptor engagement. This posttranslational modification occurred in normal T cells and tumor lines. Both nonphosphorylated and phosphorylated zeta molecules were modified, and at least one other TCR subunit, CD3 delta, was also ubiquitinated after activation of the receptor. These findings suggest an expanded role for ubiquitination in transmembrane receptor function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cenciarelli, C -- Hou, D -- Hsu, K C -- Rellahan, B L -- Wiest, D L -- Smith, H T -- Fried, V A -- Weissman, A M -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):795-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1323144" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3 ; Antigens, Differentiation, T-Lymphocyte/immunology/metabolism ; Cells, Cultured ; Hybridomas/immunology ; Lymphocyte Activation/*physiology ; Macromolecular Substances ; Mice ; Mice, Inbred C57BL ; Molecular Weight ; *Protein Processing, Post-Translational ; Receptors, Antigen, T-Cell/immunology/isolation & purification/*metabolism ; Spleen/immunology ; T-Lymphocytes/*immunology ; Ubiquitins/isolation & purification/*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
    Signaling kinase AMPK activates stress-promoted transcription via histone H2B phosphorylation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-22
    Description: The mammalian adenosine monophosphate-activated protein kinase (AMPK) is a serine-threonine kinase protein complex that is a central regulator of cellular energy homeostasis. However, the mechanisms by which AMPK mediates cellular responses to metabolic stress remain unclear. We found that AMPK activates transcription through direct association with chromatin and phosphorylation of histone H2B at serine 36. AMPK recruitment and H2B Ser36 phosphorylation colocalized within genes activated by AMPK-dependent pathways, both in promoters and in transcribed regions. Ectopic expression of H2B in which Ser36 was substituted by alanine reduced transcription and RNA polymerase II association to AMPK-dependent genes, and lowered cell survival in response to stress. Our results place AMPK-dependent H2B Ser36 phosphorylation in a direct transcriptional and chromatin regulatory pathway leading to cellular adaptation to stress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3922052/" 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/PMC3922052/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bungard, David -- Fuerth, Benjamin J -- Zeng, Ping-Yao -- Faubert, Brandon -- Maas, Nancy L -- Viollet, Benoit -- Carling, David -- Thompson, Craig B -- Jones, Russell G -- Berger, Shelley L -- CA078831/CA/NCI NIH HHS/ -- CA09171/CA/NCI NIH HHS/ -- CA105463/CA/NCI NIH HHS/ -- MC_U120027537/Medical Research Council/United Kingdom -- MOP-93799/Canadian Institutes of Health Research/Canada -- P01 AG031862/AG/NIA NIH HHS/ -- P01 CA104838/CA/NCI NIH HHS/ -- R01 CA078831/CA/NCI NIH HHS/ -- R01 CA105463/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1201-5. doi: 10.1126/science.1191241. Epub 2010 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Developmental Biology, University of Pennsylvania Medical School, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647423" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/chemistry/*metabolism ; Adaptation, Physiological ; Amino Acid Motifs ; Amino Acid Substitution ; Animals ; Cell Line ; Cell Line, Tumor ; Cell Survival ; Cells, Cultured ; Chromatin/*metabolism ; Chromatin Immunoprecipitation ; Enzyme Activation ; Gene Expression Regulation ; Histones/chemistry/*metabolism ; Humans ; Mice ; Phosphorylation ; Promoter Regions, Genetic ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Serine/metabolism ; Signal Transduction ; *Stress, Physiological ; *Transcription, Genetic ; Tumor Suppressor Protein p53/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
  • 7
    facet.materialart.
    Unknown
    Mammalian genes are transcribed with widely different bursting kinetics (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-19
    Description: In prokaryotes and eukaryotes, most genes appear to be transcribed during short periods called transcriptional bursts, interspersed by silent intervals. We describe how such bursts generate gene-specific temporal patterns of messenger RNA (mRNA) synthesis in mammalian cells. To monitor transcription at high temporal resolution, we established various gene trap cell lines and transgenic cell lines expressing a short-lived luciferase protein from an unstable mRNA, and recorded bioluminescence in real time in single cells. Mathematical modeling identified gene-specific on- and off-switching rates in transcriptional activity and mean numbers of mRNAs produced during the bursts. Transcriptional kinetics were markedly altered by cis-regulatory DNA elements. Our analysis demonstrated that bursting kinetics are highly gene-specific, reflecting refractory periods during which genes stay inactive for a certain time before switching on again.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suter, David M -- Molina, Nacho -- Gatfield, David -- Schneider, Kim -- Schibler, Ueli -- Naef, Felix -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):472-4. doi: 10.1126/science.1198817. Epub 2011 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Sciences III, University of Geneva, 30 Quai Ernest Ansermet, 1211 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21415320" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Cells, Cultured ; Chromatin/physiology ; Circadian Rhythm/genetics ; Down-Regulation ; *Gene Expression ; Histones/metabolism ; Kinetics ; Luminescent Measurements ; Mice ; Models, Genetic ; NIH 3T3 Cells ; Promoter Regions, Genetic ; Protein Biosynthesis ; RNA, Messenger/genetics/metabolism ; Stochastic Processes ; *Transcription, Genetic ; Transcriptional Activation ; Transgenes ; Up-Regulation
    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
  • 8
    facet.materialart.
    Unknown
    Intramembrane cleavage of AMA1 triggers Toxoplasma to switch from an invasive to a replicative mode (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-06
    Description: Apicomplexan parasites invade host cells and immediately initiate cell division. The extracellular parasite discharges transmembrane proteins onto its surface to mediate motility and invasion. These are shed by intramembrane cleavage, a process associated with invasion but otherwise poorly understood. Functional analysis of Toxoplasma rhomboid 4, a surface intramembrane protease, by conditional overexpression of a catalytically inactive form produced a profound block in replication. This was completely rescued by expression of the cleaved cytoplasmic tail of Toxoplasma or Plasmodium apical membrane antigen 1 (AMA1). These results reveal an unexpected function for AMA1 in parasite replication and suggest that invasion proteins help to promote parasite switch from an invasive to a replicative mode.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santos, Joana M -- Ferguson, David J P -- Blackman, Michael J -- Soldati-Favre, Dominique -- MC_U117532063/Medical Research Council/United Kingdom -- U117532063/Medical Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):473-7. doi: 10.1126/science.1199284. Epub 2010 Dec 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Faculty of Medicine, University of Geneva, 1 rue-Michel Servet, 1211 Geneva 4, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21205639" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Protozoan/chemistry/genetics/*metabolism ; Cell Cycle ; Cell Division ; Cell Membrane/metabolism ; Cells, Cultured ; Fibroblasts/parasitology ; Humans ; Membrane Proteins/chemistry/genetics/*metabolism ; Movement ; Mutant Proteins/metabolism ; Plasmodium falciparum ; Protozoan Proteins/chemistry/genetics/*metabolism ; Serine Proteases/genetics/metabolism ; Signal Transduction ; Toxoplasma/cytology/growth & development/*physiology
    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
  • 9
    facet.materialart.
    Unknown
    BRCA1 tumor suppression depends on BRCT phosphoprotein binding, but not its E3 ligase activity (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-29
    Description: Germline mutations of the breast cancer 1 (BRCA1) gene are a major cause of familial breast and ovarian cancer. The BRCA1 protein displays E3 ubiquitin ligase activity, and this enzymatic function is thought to be required for tumor suppression. To test this hypothesis, we generated mice that express an enzymatically defective Brca1. We found that this mutant Brca1 prevents tumor formation to the same degree as does wild-type Brca1 in three different genetically engineered mouse (GEM) models of cancer. In contrast, a mutation that ablates phosphoprotein recognition by the BRCA C terminus (BRCT) domains of BRCA1 elicits tumors in each of the three GEM models. Thus, BRCT phosphoprotein recognition, but not the E3 ligase activity, is required for BRCA1 tumor suppression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3904783/" 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/PMC3904783/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shakya, Reena -- Reid, Latarsha J -- Reczek, Colleen R -- Cole, Francesca -- Egli, Dieter -- Lin, Chyuan-Sheng -- deRooij, Dirk G -- Hirsch, Steffen -- Ravi, Kandasamy -- Hicks, James B -- Szabolcs, Matthias -- Jasin, Maria -- Baer, Richard -- Ludwig, Thomas -- F31-CA132626/CA/NCI NIH HHS/ -- F32-HD51392/HD/NICHD NIH HHS/ -- P01 CA097403/CA/NCI NIH HHS/ -- P01-CA97403/CA/NCI NIH HHS/ -- R01 CA137023/CA/NCI NIH HHS/ -- R01 HD040916/HD/NICHD NIH HHS/ -- R01 HD040916-10/HD/NICHD NIH HHS/ -- R01-CA137023/CA/NCI NIH HHS/ -- R01-HD40916/HD/NICHD NIH HHS/ -- T32-CA09503/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2011 Oct 28;334(6055):525-8. doi: 10.1126/science.1209909.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22034435" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/chemistry/*metabolism ; Basic-Leucine Zipper Transcription Factors/genetics/metabolism ; Cells, Cultured ; Disease Models, Animal ; Embryonic Stem Cells/metabolism ; *Genes, BRCA1 ; Ligands ; Mammary Neoplasms, Experimental/*genetics/metabolism ; Mice ; Mutant Proteins/chemistry/genetics/metabolism ; Pancreatic Neoplasms/*genetics/metabolism ; Phosphoproteins/*metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Multimerization ; RING Finger Domains ; Tumor Suppressor Proteins/chemistry/metabolism ; Ubiquitin-Protein Ligases/chemistry/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
    A single progenitor population switches behavior to maintain and repair esophageal epithelium (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-24
    Description: Diseases of the esophageal epithelium (EE), such as reflux esophagitis and cancer, are rising in incidence. Despite this, the cellular behaviors underlying EE homeostasis and repair remain controversial. Here, we show that in mice, EE is maintained by a single population of cells that divide stochastically to generate proliferating and differentiating daughters with equal probability. In response to challenge with all-trans retinoic acid (atRA), the balance of daughter cell fate is unaltered, but the rate of cell division increases. However, after wounding, cells reversibly switch to producing an excess of proliferating daughters until the wound has closed. Such fate-switching enables a single progenitor population to both maintain and repair tissue without the need for a "reserve" slow-cycling stem cell pool.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3527005/" 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/PMC3527005/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doupe, David P -- Alcolea, Maria P -- Roshan, Amit -- Zhang, Gen -- Klein, Allon M -- Simons, Benjamin D -- Jones, Philip H -- 079249/Wellcome Trust/United Kingdom -- 092096/Wellcome Trust/United Kingdom -- G0601740/Medical Research Council/United Kingdom -- G0700600/1/National Centre for the Replacement, Refinement and Reduction of Animals in Research/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- MC_U105370181/Medical Research Council/United Kingdom -- U.1053.00.010(70181)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Aug 31;337(6098):1091-3. doi: 10.1126/science.1218835. Epub 2012 Jul 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Cancer Cell Unit, Hutchison-MRC Research Centre, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22821983" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cell Proliferation/drug effects ; Cells, Cultured ; Doxycycline/pharmacology ; Epithelial Cells/*physiology ; Epithelium/drug effects/metabolism/*physiology ; Esophagus/*cytology/*physiology ; Green Fluorescent Proteins/biosynthesis ; Histones/biosynthesis ; Mice ; Mice, Inbred C57BL ; Recombinant Fusion Proteins/biosynthesis ; *Regeneration ; Stem Cells/metabolism/*physiology
    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
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...