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  • Cells, Cultured  (64)
  • American Association for the Advancement of Science (AAAS)  (64)
  • Hindawi
  • Wiley
  • 2010-2014  (22)
  • 1980-1984  (42)
  • 2013  (22)
  • 1981  (42)
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  • 2010-2014  (22)
  • 1980-1984  (42)
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  • 1
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    Interfollicular epidermal stem cells self-renew via autocrine Wnt signaling (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-07
    Description: The skin is a classical example of a tissue maintained by stem cells. However, the identity of the stem cells that maintain the interfollicular epidermis and the source of the signals that control their activity remain unclear. Using mouse lineage tracing and quantitative clonal analyses, we showed that the Wnt target gene Axin2 marks interfollicular epidermal stem cells. These Axin2-expressing cells constitute the majority of the basal epidermal layer, compete neutrally, and require Wnt/beta-catenin signaling to proliferate. The same cells contribute robustly to wound healing, with no requirement for a quiescent stem cell subpopulation. By means of double-labeling RNA in situ hybridization in mice, we showed that the Axin2-expressing cells themselves produce Wnt signals as well as long-range secreted Wnt inhibitors, suggesting an autocrine mechanism of stem cell self-renewal.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4081860/" 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/PMC4081860/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lim, Xinhong -- Tan, Si Hui -- Koh, Winston Lian Chye -- Chau, Rosanna Man Wah -- Yan, Kelley S -- Kuo, Calvin J -- van Amerongen, Renee -- Klein, Allon Moshe -- Nusse, Roel -- 1R01DK085720/DK/NIDDK NIH HHS/ -- 1U01DK085527/DK/NIDDK NIH HHS/ -- 5K08DK096048/DK/NIDDK NIH HHS/ -- K08 DK096048/DK/NIDDK NIH HHS/ -- P30 DK026743/DK/NIDDK NIH HHS/ -- R01 DK085720/DK/NIDDK NIH HHS/ -- U01 DK085527/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Dec 6;342(6163):1226-30. doi: 10.1126/science.1239730.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Howard Hughes Medical Institute (HHMI), Institute for Stem Cell Biology and Regenerative Medicine, School of Medicine, Stanford University, Stanford, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24311688" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autocrine Communication ; Axin Protein/genetics/metabolism ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Epidermis/*cytology/injuries/metabolism ; Epithelial Cells/cytology/metabolism ; Gene Expression ; Homeostasis ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Keratinocytes/cytology/metabolism ; Mice ; Regeneration ; Skin/injuries ; Stem Cell Niche ; Stem Cells/cytology/*physiology ; Wnt Proteins/metabolism ; *Wnt Signaling Pathway ; Wound Healing ; beta Catenin/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    B cells use mechanical energy to discriminate antigen affinities (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-05-21
    Description: The generation of high-affinity antibodies depends on the ability of B cells to extract antigens from the surfaces of antigen-presenting cells. B cells that express high-affinity B cell receptors (BCRs) acquire more antigen and obtain better T cell help. However, the mechanisms by which B cells extract antigen remain unclear. Using fluid and flexible membrane substrates to mimic antigen-presenting cells, we showed that B cells acquire antigen by dynamic myosin IIa-mediated contractions that pull out and invaginate the presenting membranes. The forces generated by myosin IIa contractions ruptured most individual BCR-antigen bonds and promoted internalization of only high-affinity, multivalent BCR microclusters. Thus, B cell contractility contributes to affinity discrimination by mechanically testing the strength of antigen binding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3713314/" 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/PMC3713314/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Natkanski, Elizabeth -- Lee, Wing-Yiu -- Mistry, Bhakti -- Casal, Antonio -- Molloy, Justin E -- Tolar, Pavel -- MC_U117570592/Medical Research Council/United Kingdom -- MC_U117597138/Medical Research Council/United Kingdom -- U117570592/Medical Research Council/United Kingdom -- U117597138/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 Jun 28;340(6140):1587-90. doi: 10.1126/science.1237572. Epub 2013 May 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immune Cell Biology, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23686338" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Affinity ; *Antigen Presentation ; Antigens/*immunology ; B-Lymphocytes/*immunology ; Cells, Cultured ; Mechanical Processes ; Mice ; Mice, Inbred C57BL ; Microscopy, Atomic Force ; Nonmuscle Myosin Type IIA/*physiology ; Receptors, Antigen, B-Cell/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Targeted inhibition of mutant IDH2 in leukemia cells induces cellular differentiation (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-04-06
    Description: A number of human cancers harbor somatic point mutations in the genes encoding isocitrate dehydrogenases 1 and 2 (IDH1 and IDH2). These mutations alter residues in the enzyme active sites and confer a gain-of-function in cancer cells, resulting in the accumulation and secretion of the oncometabolite (R)-2-hydroxyglutarate (2HG). We developed a small molecule, AGI-6780, that potently and selectively inhibits the tumor-associated mutant IDH2/R140Q. A crystal structure of AGI-6780 complexed with IDH2/R140Q revealed that the inhibitor binds in an allosteric manner at the dimer interface. The results of steady-state enzymology analysis were consistent with allostery and slow-tight binding by AGI-6780. Treatment with AGI-6780 induced differentiation of TF-1 erythroleukemia and primary human acute myelogenous leukemia cells in vitro. These data provide proof-of-concept that inhibitors targeting mutant IDH2/R140Q could have potential applications as a differentiation therapy for cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Fang -- Travins, Jeremy -- DeLaBarre, Byron -- Penard-Lacronique, Virginie -- Schalm, Stefanie -- Hansen, Erica -- Straley, Kimberly -- Kernytsky, Andrew -- Liu, Wei -- Gliser, Camelia -- Yang, Hua -- Gross, Stefan -- Artin, Erin -- Saada, Veronique -- Mylonas, Elena -- Quivoron, Cyril -- Popovici-Muller, Janeta -- Saunders, Jeffrey O -- Salituro, Francesco G -- Yan, Shunqi -- Murray, Stuart -- Wei, Wentao -- Gao, Yi -- Dang, Lenny -- Dorsch, Marion -- Agresta, Sam -- Schenkein, David P -- Biller, Scott A -- Su, Shinsan M -- de Botton, Stephane -- Yen, Katharine E -- New York, N.Y. -- Science. 2013 May 3;340(6132):622-6. doi: 10.1126/science.1234769. Epub 2013 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Agios Pharmaceuticals, Cambridge, MA 02139-4169, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23558173" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Site ; Antineoplastic Agents/chemistry/metabolism/pharmacology ; Catalytic Domain ; Cell Line, Tumor ; Cell Proliferation ; Cells, Cultured ; Crystallography, X-Ray ; Enzyme Inhibitors/chemistry/metabolism/*pharmacology ; Erythropoiesis/drug effects ; Gene Expression Regulation, Leukemic ; Glutarates/metabolism ; Hematopoiesis/*drug effects ; Humans ; Isocitrate Dehydrogenase/*antagonists & inhibitors/chemistry/*genetics/metabolism ; Leukemia, Erythroblastic, Acute ; Leukemia, Myeloid, Acute/drug therapy/*enzymology/genetics/pathology ; Molecular Targeted Therapy ; Mutant Proteins/antagonists & inhibitors/chemistry/metabolism ; Phenylurea Compounds/chemistry/metabolism/*pharmacology ; Point Mutation ; Protein Multimerization ; Protein Structure, Secondary ; Small Molecule Libraries ; Sulfonamides/chemistry/metabolism/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 4
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    Erythropoietin derived by chemical synthesis (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-18
    Description: Erythropoietin is a signaling glycoprotein that controls the fundamental process of erythropoiesis, orchestrating the production and maintenance of red blood cells. As administrated clinically, erythropoietin has a polypeptide backbone with complex dishomogeneity in its carbohydrate domains. Here we describe the total synthesis of homogeneous erythropoietin with consensus carbohydrate domains incorporated at all of the native glycosylation sites. The oligosaccharide sectors were built by total synthesis and attached stereospecifically to peptidyl fragments of the wild-type primary sequence, themselves obtained by solid-phase peptide synthesis. The glycopeptidyl constructs were joined by chemical ligation, followed by metal-free dethiylation, and subsequently folded. This homogeneous erythropoietin glycosylated at the three wild-type aspartates with N-linked high-mannose sialic acid-containing oligosaccharides and O-linked glycophorin exhibits Procrit-level in vivo activity in mice.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4080428/" 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/PMC4080428/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Ping -- Dong, Suwei -- Shieh, Jae-Hung -- Peguero, Elizabeth -- Hendrickson, Ronald -- Moore, Malcolm A S -- Danishefsky, Samuel J -- HL025848/HL/NHLBI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R01 GM109760/GM/NIGMS NIH HHS/ -- R01 HL025848/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2013 Dec 13;342(6164):1357-60. doi: 10.1126/science.1245095.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Bioorganic Chemistry, Sloan-Kettering Institute for Cancer Research, 1275 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24337294" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Aspartic Acid/chemistry ; Cells, Cultured ; Consensus Sequence ; Dose-Response Relationship, Drug ; Erythrocyte Count ; Erythropoietin/*administration & dosage/*chemical synthesis/chemistry ; Glycophorin/chemistry ; Glycosylation ; Injections, Subcutaneous ; Mannose/chemistry ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; N-Acetylneuraminic Acid/chemistry ; Oligosaccharides/chemistry ; Reticulocytes/drug effects
    Print ISSN: 0036-8075
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  • 5
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    An erythroid enhancer of BCL11A subject to genetic variation determines fetal hemoglobin level (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-10-12
    Description: Genome-wide association studies (GWASs) have ascertained numerous trait-associated common genetic variants, frequently localized to regulatory DNA. We found that common genetic variation at BCL11A associated with fetal hemoglobin (HbF) level lies in noncoding sequences decorated by an erythroid enhancer chromatin signature. Fine-mapping uncovers a motif-disrupting common variant associated with reduced transcription factor (TF) binding, modestly diminished BCL11A expression, and elevated HbF. The surrounding sequences function in vivo as a developmental stage-specific, lineage-restricted enhancer. Genome engineering reveals the enhancer is required in erythroid but not B-lymphoid cells for BCL11A expression. These findings illustrate how GWASs may expose functional variants of modest impact within causal elements essential for appropriate gene expression. We propose the GWAS-marked BCL11A enhancer represents an attractive target for therapeutic genome engineering for the beta-hemoglobinopathies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4018826/" 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/PMC4018826/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bauer, Daniel E -- Kamran, Sophia C -- Lessard, Samuel -- Xu, Jian -- Fujiwara, Yuko -- Lin, Carrie -- Shao, Zhen -- Canver, Matthew C -- Smith, Elenoe C -- Pinello, Luca -- Sabo, Peter J -- Vierstra, Jeff -- Voit, Richard A -- Yuan, Guo-Cheng -- Porteus, Matthew H -- Stamatoyannopoulos, John A -- Lettre, Guillaume -- Orkin, Stuart H -- 123382/Canadian Institutes of Health Research/Canada -- K08 DK093705/DK/NIDDK NIH HHS/ -- K08DK093705/DK/NIDDK NIH HHS/ -- P01HL032262/HL/NHLBI NIH HHS/ -- P30 DK049216/DK/NIDDK NIH HHS/ -- P30DK049216/DK/NIDDK NIH HHS/ -- R01 HG005085/HG/NHGRI NIH HHS/ -- R01 HL032259/HL/NHLBI NIH HHS/ -- R01HL032259/HL/NHLBI NIH HHS/ -- U54HG004594/HG/NHGRI NIH HHS/ -- U54HG007010/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Oct 11;342(6155):253-7. doi: 10.1126/science.1242088.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24115442" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/*genetics ; Cell Line, Tumor ; Cells, Cultured ; Chromatin/genetics/metabolism ; Chromatin Immunoprecipitation ; Chromosome Mapping ; *Enhancer Elements, Genetic ; Erythroid Cells/*metabolism ; Fetal Hemoglobin/*biosynthesis/genetics ; *Gene Expression Regulation ; Gene Targeting ; Genetic Engineering ; Genetic Variation ; Genome-Wide Association Study ; Hemoglobinopathies/*genetics/therapy ; Humans ; Mice ; Nuclear Proteins/*genetics ; Precursor Cells, B-Lymphoid/metabolism ; Transcription Factors/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Mice genetically deficient in vasopressin V1a and V1b receptors are resistant to jet lag (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-10-05
    Description: Jet-lag symptoms arise from temporal misalignment between the internal circadian clock and external solar time. We found that circadian rhythms of behavior (locomotor activity), clock gene expression, and body temperature immediately reentrained to phase-shifted light-dark cycles in mice lacking vasopressin receptors V1a and V1b (V1a(-/-)V1b(-/-)). Nevertheless, the behavior of V1a(-/-)V1b(-/-) mice was still coupled to the internal clock, which oscillated normally under standard conditions. Experiments with suprachiasmatic nucleus (SCN) slices in culture suggested that interneuronal communication mediated by V1a and V1b confers on the SCN an intrinsic resistance to external perturbation. Pharmacological blockade of V1a and V1b in the SCN of wild-type mice resulted in accelerated recovery from jet lag, which highlights the potential of vasopressin signaling as a therapeutic target for management of circadian rhythm misalignment, such as jet lag and shift work.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamaguchi, Yoshiaki -- Suzuki, Toru -- Mizoro, Yasutaka -- Kori, Hiroshi -- Okada, Kazuki -- Chen, Yulin -- Fustin, Jean-Michel -- Yamazaki, Fumiyoshi -- Mizuguchi, Naoki -- Zhang, Jing -- Dong, Xin -- Tsujimoto, Gozoh -- Okuno, Yasushi -- Doi, Masao -- Okamura, Hitoshi -- New York, N.Y. -- Science. 2013 Oct 4;342(6154):85-90. doi: 10.1126/science.1238599.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Systems Biology, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24092737" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antidiuretic Hormone Receptor Antagonists ; Body Temperature/genetics ; CLOCK Proteins/genetics ; Cell Communication/drug effects/genetics ; Cells, Cultured ; Circadian Rhythm/genetics ; Gene Expression Regulation ; Jet Lag Syndrome/*genetics/physiopathology ; Mice ; Mice, Knockout ; Motor Activity/genetics ; Receptors, Vasopressin/*genetics ; Suprachiasmatic Nucleus/physiopathology
    Print ISSN: 0036-8075
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  • 7
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    53BP1 regulates DSB repair using Rif1 to control 5' end resection (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-01-12
    Description: The choice between double-strand break (DSB) repair by either homology-directed repair (HDR) or nonhomologous end joining (NHEJ) is tightly regulated. Defects in this regulation can induce genome instability and cancer. 53BP1 is critical for the control of DSB repair, promoting NHEJ, and inhibiting the 5' end resection needed for HDR. Using dysfunctional telomeres and genome-wide DSBs, we identify Rif1 as the main factor used by 53BP1 to impair 5' end resection. Rif1 inhibits resection involving CtIP, BLM, and Exo1; limits accumulation of BRCA1/BARD1 complexes at sites of DNA damage; and defines one of the mechanisms by which 53BP1 causes chromosomal abnormalities in Brca1-deficient cells. These data establish Rif1 as an important contributor to the control of DSB repair by 53BP1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3664841/" 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/PMC3664841/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimmermann, Michal -- Lottersberger, Francisca -- Buonomo, Sara B -- Sfeir, Agnel -- de Lange, Titia -- R37 GM049046/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 8;339(6120):700-4. doi: 10.1126/science.1231573. Epub 2013 Jan 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23306437" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/metabolism ; Cells, Cultured ; Chromosomal Proteins, Non-Histone/chemistry/genetics/*metabolism ; DNA/metabolism ; *DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; *DNA Repair ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Mice ; Replication Protein A/metabolism ; Telomere/*metabolism ; Telomere-Binding Proteins/*metabolism ; Telomeric Repeat Binding Protein 2/genetics/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Rif1 prevents resection of DNA breaks and promotes immunoglobulin class switching (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-01-12
    Description: DNA double-strand breaks (DSBs) represent a threat to the genome because they can lead to the loss of genetic information and chromosome rearrangements. The DNA repair protein p53 binding protein 1 (53BP1) protects the genome by limiting nucleolytic processing of DSBs by a mechanism that requires its phosphorylation, but whether 53BP1 does so directly is not known. Here, we identify Rap1-interacting factor 1 (Rif1) as an ATM (ataxia-telangiectasia mutated) phosphorylation-dependent interactor of 53BP1 and show that absence of Rif1 results in 5'-3' DNA-end resection in mice. Consistent with enhanced DNA resection, Rif1 deficiency impairs DNA repair in the G(1) and S phases of the cell cycle, interferes with class switch recombination in B lymphocytes, and leads to accumulation of chromosome DSBs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815530/" 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/PMC3815530/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Virgilio, Michela -- Callen, Elsa -- Yamane, Arito -- Zhang, Wenzhu -- Jankovic, Mila -- Gitlin, Alexander D -- Feldhahn, Niklas -- Resch, Wolfgang -- Oliveira, Thiago Y -- Chait, Brian T -- Nussenzweig, Andre -- Casellas, Rafael -- Robbiani, Davide F -- Nussenzweig, Michel C -- AI037526/AI/NIAID NIH HHS/ -- GM007739/GM/NIGMS NIH HHS/ -- GM103314/GM/NIGMS NIH HHS/ -- R01 AI037526/AI/NIAID NIH HHS/ -- RR00862/RR/NCRR NIH HHS/ -- RR022220/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 8;339(6120):711-5. doi: 10.1126/science.1230624. Epub 2013 Jan 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23306439" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; B-Lymphocytes/immunology/metabolism ; Cell Cycle Proteins/antagonists & inhibitors/metabolism ; Cells, Cultured ; Chromosomal Proteins, Non-Histone/*metabolism ; DNA/*metabolism ; *DNA Breaks, Double-Stranded ; DNA Repair ; DNA-Binding Proteins/antagonists & inhibitors/*metabolism ; G1 Phase ; G2 Phase ; Genomic Instability ; *Immunoglobulin Class Switching ; Mice ; Phosphorylation ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; S Phase ; Telomere-Binding Proteins/*metabolism ; Tumor Suppressor Proteins/antagonists & inhibitors/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Neuroscience. Neural stem cells, excited (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-03-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsieh, Jenny -- Schneider, Jay W -- New York, N.Y. -- Science. 2013 Mar 29;339(6127):1534-5. doi: 10.1126/science.1237576.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. jenny.hsieh@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23539589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*cytology/*physiology ; Calcium Channels/physiology ; Cells, Cultured ; Humans ; Neural Stem Cells/*physiology ; *Neurogenesis ; Receptors, N-Methyl-D-Aspartate/physiology ; *Synaptic Transmission ; gamma-Aminobutyric Acid/physiology
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Evidence for a common mechanism of SIRT1 regulation by allosteric activators (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-03-09
    Description: A molecule that treats multiple age-related diseases would have a major impact on global health and economics. The SIRT1 deacetylase has drawn attention in this regard as a target for drug design. Yet controversy exists around the mechanism of sirtuin-activating compounds (STACs). We found that specific hydrophobic motifs found in SIRT1 substrates such as PGC-1alpha and FOXO3a facilitate SIRT1 activation by STACs. A single amino acid in SIRT1, Glu(230), located in a structured N-terminal domain, was critical for activation by all previously reported STAC scaffolds and a new class of chemically distinct activators. In primary cells reconstituted with activation-defective SIRT1, the metabolic effects of STACs were blocked. Thus, SIRT1 can be directly activated through an allosteric mechanism common to chemically diverse STACs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799917/" 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/PMC3799917/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hubbard, Basil P -- Gomes, Ana P -- Dai, Han -- Li, Jun -- Case, April W -- Considine, Thomas -- Riera, Thomas V -- Lee, Jessica E -- E, Sook Yen -- Lamming, Dudley W -- Pentelute, Bradley L -- Schuman, Eli R -- Stevens, Linda A -- Ling, Alvin J Y -- Armour, Sean M -- Michan, Shaday -- Zhao, Huizhen -- Jiang, Yong -- Sweitzer, Sharon M -- Blum, Charles A -- Disch, Jeremy S -- Ng, Pui Yee -- Howitz, Konrad T -- Rolo, Anabela P -- Hamuro, Yoshitomo -- Moss, Joel -- Perni, Robert B -- Ellis, James L -- Vlasuk, George P -- Sinclair, David A -- P01 AG027916/AG/NIA NIH HHS/ -- R01 AG019719/AG/NIA NIH HHS/ -- R01 AG028730/AG/NIA NIH HHS/ -- R37 AG028730/AG/NIA NIH HHS/ -- ZIA HL000659-20/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 8;339(6124):1216-9. doi: 10.1126/science.1231097.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23471411" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Amino Acid Motifs ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Cells, Cultured ; Enzyme Activation ; Forkhead Transcription Factors/chemistry/genetics ; Glutamic Acid/chemistry/genetics ; Heterocyclic Compounds with 4 or More Rings/chemistry/pharmacology ; Humans ; Hydrophobic and Hydrophilic Interactions ; Mice ; Molecular Sequence Data ; Myoblasts/drug effects/enzymology ; Protein Structure, Tertiary ; Sirtuin 1/*chemistry/genetics/*metabolism ; Stilbenes/chemistry/*pharmacology ; Substrate Specificity
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Staphylococcus aureus degrades neutrophil extracellular traps to promote immune cell death (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-11-16
    Description: Bacterial invasion of host tissues triggers polymorphonuclear leukocytes to release DNA [neutrophil extracellular traps (NETs)], thereby immobilizing microbes for subsequent clearance by innate defenses including macrophage phagocytosis. We report here that Staphylococcus aureus escapes these defenses by converting NETs to deoxyadenosine, which triggers the caspase-3-mediated death of immune cells. Conversion of NETs to deoxyadenosine requires two enzymes, nuclease and adenosine synthase, that are secreted by S. aureus and are necessary for the exclusion of macrophages from staphylococcal abscesses. Thus, the pathogenesis of S. aureus infections has evolved to anticipate host defenses and to repurpose them for the destruction of the immune system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4026193/" 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/PMC4026193/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thammavongsa, Vilasack -- Missiakas, Dominique M -- Schneewind, Olaf -- AI038897/AI/NIAID NIH HHS/ -- AI052474/AI/NIAID NIH HHS/ -- AI057153/AI/NIAID NIH HHS/ -- R01 AI038897/AI/NIAID NIH HHS/ -- R01 AI052474/AI/NIAID NIH HHS/ -- T32 AI007090/AI/NIAID NIH HHS/ -- U54 AI057153/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Nov 15;342(6160):863-6. doi: 10.1126/science.1242255.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Chicago, 920 East 58th Street, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24233725" target="_blank"〉PubMed〈/a〉
    Keywords: Abscess/immunology/microbiology ; Animals ; Apoptosis/*immunology ; Cells, Cultured ; Cytotoxicity, Immunologic ; Deoxyadenosines/*metabolism ; Deoxyribonucleases/metabolism ; Host-Pathogen Interactions/*immunology ; Humans ; Macrophages/immunology/microbiology ; Mice, Inbred BALB C ; Neutrophils/*immunology/*microbiology ; Staphylococcal Infections/*immunology ; Staphylococcus aureus/enzymology/*pathogenicity
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    Positive feedback between PU.1 and the cell cycle controls myeloid differentiation (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-07-23
    Description: Regulatory gene circuits with positive-feedback loops control stem cell differentiation, but several mechanisms can contribute to positive feedback. Here, we dissect feedback mechanisms through which the transcription factor PU.1 controls lymphoid and myeloid differentiation. Quantitative live-cell imaging revealed that developing B cells decrease PU.1 levels by reducing PU.1 transcription, whereas developing macrophages increase PU.1 levels by lengthening their cell cycles, which causes stable PU.1 accumulation. Exogenous PU.1 expression in progenitors increases endogenous PU.1 levels by inducing cell cycle lengthening, implying positive feedback between a regulatory factor and the cell cycle. Mathematical modeling showed that this cell cycle-coupled feedback architecture effectively stabilizes a slow-dividing differentiated state. These results show that cell cycle duration functions as an integral part of a positive autoregulatory circuit to control cell fate.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3913367/" 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/PMC3913367/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kueh, Hao Yuan -- Champhekar, Ameya -- Nutt, Stephen L -- Elowitz, Michael B -- Rothenberg, Ellen V -- R01 AI083514/AI/NIAID NIH HHS/ -- R01 CA090233/CA/NCI NIH HHS/ -- R01 CA90233/CA/NCI NIH HHS/ -- R33 HL089123/HL/NHLBI NIH HHS/ -- RC2 CA148278/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Aug 9;341(6146):670-3. doi: 10.1126/science.1240831. Epub 2013 Jul 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA, USA. kueh@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23868921" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/*genetics ; Cell Differentiation/*genetics ; Cells, Cultured ; Feedback, Physiological ; *Gene Expression Regulation ; *Gene Regulatory Networks ; Macrophages/cytology ; Mice ; Mice, Inbred Strains ; Myeloid Cells/*cytology ; Precursor Cells, B-Lymphoid/*cytology ; Proto-Oncogene Proteins/genetics/*physiology ; Trans-Activators/genetics/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Mucus enhances gut homeostasis and oral tolerance by delivering immunoregulatory signals (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-09-28
    Description: A dense mucus layer in the large intestine prevents inflammation by shielding the underlying epithelium from luminal bacteria and food antigens. This mucus barrier is organized around the hyperglycosylated mucin MUC2. Here we show that the small intestine has a porous mucus layer, which permitted the uptake of MUC2 by antigen-sampling dendritic cells (DCs). Glycans associated with MUC2 imprinted DCs with anti-inflammatory properties by assembling a galectin-3-Dectin-1-FcgammaRIIB receptor complex that activated beta-catenin. This transcription factor interfered with DC expression of inflammatory but not tolerogenic cytokines by inhibiting gene transcription through nuclear factor kappaB. MUC2 induced additional conditioning signals in intestinal epithelial cells. Thus, mucus does not merely form a nonspecific physical barrier, but also constrains the immunogenicity of gut antigens by delivering tolerogenic signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005805/" 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/PMC4005805/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shan, Meimei -- Gentile, Maurizio -- Yeiser, John R -- Walland, A Cooper -- Bornstein, Victor U -- Chen, Kang -- He, Bing -- Cassis, Linda -- Bigas, Anna -- Cols, Montserrat -- Comerma, Laura -- Huang, Bihui -- Blander, J Magarian -- Xiong, Huabao -- Mayer, Lloyd -- Berin, Cecilia -- Augenlicht, Leonard H -- Velcich, Anna -- Cerutti, Andrea -- AI073899/AI/NIAID NIH HHS/ -- AI095245/AI/NIAID NIH HHS/ -- AI57653/AI/NIAID NIH HHS/ -- AI61093/AI/NIAID NIH HHS/ -- AI74378/AI/NIAID NIH HHS/ -- AI95613/AI/NIAID NIH HHS/ -- AI96187/AI/NIAID NIH HHS/ -- DK072201/DK/NIDDK NIH HHS/ -- P01 AI061093/AI/NIAID NIH HHS/ -- P01 DK072201/DK/NIDDK NIH HHS/ -- P60 DK020541/DK/NIDDK NIH HHS/ -- R01 AI057653/AI/NIAID NIH HHS/ -- R01 AI093577/AI/NIAID NIH HHS/ -- U01 AI095613/AI/NIAID NIH HHS/ -- U19 AI096187/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Oct 25;342(6157):447-53. doi: 10.1126/science.1237910. Epub 2013 Sep 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24072822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dendritic Cells/immunology ; Galectin 3/genetics/metabolism ; Glycosylation ; *Homeostasis ; Humans ; Immune Tolerance/genetics/*immunology ; Inflammation/immunology ; Intestinal Mucosa/immunology ; Intestine, Small/*immunology ; Lectins, C-Type/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mouth/*immunology ; Mucin-2/genetics/physiology ; Mucus/*immunology ; NF-kappa B/metabolism ; Receptors, IgG/genetics/metabolism ; Transcription, Genetic ; beta Catenin/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    BTBD3 controls dendrite orientation toward active axons in mammalian neocortex (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-11-02
    Description: Experience-dependent structural changes in the developing brain are fundamental for proper neural circuit formation. Here, we show that during the development of the sensory cortex, dendritic field orientation is controlled by the BTB/POZ domain-containing 3 (BTBD3). In developing mouse somatosensory cortex, endogenous Btbd3 translocated to the cell nucleus in response to neuronal activity and oriented primary dendrites toward active axons in the barrel hollow. Btbd3 also directed dendrites toward active axon terminals when ectopically expressed in mouse visual cortex or normally expressed in ferret visual cortex. BTBD3 regulation of dendrite orientation is conserved across species and cortical areas and shows how high-acuity sensory function may be achieved by the tuning of subcellular polarity to sources of high sensory activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsui, Asuka -- Tran, May -- Yoshida, Aya C -- Kikuchi, Satomi S -- U, Mami -- Ogawa, Masaharu -- Shimogori, Tomomi -- New York, N.Y. -- Science. 2013 Nov 29;342(6162):1114-8. doi: 10.1126/science.1244505. Epub 2013 Oct 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉RIKEN Brain Science Institute, Laboratory for Molecular Mechanisms of Thalamus Development, 2-1 Hirosawa Wako, Saitama 351-0198, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24179155" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; Axons/*physiology ; Cell Nucleus/metabolism ; *Cell Polarity ; Cells, Cultured ; Dendrites/*physiology ; Ferrets ; Gene Knockdown Techniques ; Mice ; Mice, Mutant Strains ; Neocortex/*embryology ; Nerve Net/*growth & development ; Nerve Tissue Proteins/genetics/*metabolism ; Visual Cortex/*embryology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    A localized Wnt signal orients asymmetric stem cell division in vitro (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-03-23
    Description: Developmental signals such as Wnts are often presented to cells in an oriented manner. To examine the consequences of local Wnt signaling, we immobilized Wnt proteins on beads and introduced them to embryonic stem cells in culture. At the single-cell level, the Wnt-bead induced asymmetric distribution of Wnt-beta-catenin signaling components, oriented the plane of mitotic division, and directed asymmetric inheritance of centrosomes. Before cytokinesis was completed, the Wnt-proximal daughter cell expressed high levels of nuclear beta-catenin and pluripotency genes, whereas the distal daughter cell acquired hallmarks of differentiation. We suggest that a spatially restricted Wnt signal induces an oriented cell division that generates distinct cell fates at predictable positions relative to the Wnt source.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3966430/" 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/PMC3966430/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habib, Shukry J -- Chen, Bi-Chang -- Tsai, Feng-Chiao -- Anastassiadis, Konstantinos -- Meyer, Tobias -- Betzig, Eric -- Nusse, Roel -- 102513/Wellcome Trust/United Kingdom -- GM063702/GM/NIGMS NIH HHS/ -- NS069375/NS/NINDS NIH HHS/ -- R01 GM030179/GM/NIGMS NIH HHS/ -- R01 GM063702/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Mar 22;339(6126):1445-8. doi: 10.1126/science.1231077.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Howard Hughes Medical Institute, Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive, Stanford, CA 94305, USA. shabib@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23520113" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Asymmetric Cell Division ; *Cell Differentiation ; Cells, Cultured ; Centrosome/physiology ; Cytokinesis ; Embryonic Stem Cells/*cytology/*metabolism ; Gene Expression ; Homeodomain Proteins/genetics/metabolism ; Mice ; Mitosis ; Octamer Transcription Factor-3/genetics/metabolism ; Pluripotent Stem Cells/physiology ; Recombinant Proteins/metabolism ; Single-Cell Analysis ; Transcription Factors/genetics/metabolism ; Wnt Proteins/metabolism ; *Wnt Signaling Pathway ; Wnt3A Protein/*metabolism ; beta Catenin/metabolism
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  • 16
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    Yeast reveal a "druggable" Rsp5/Nedd4 network that ameliorates alpha-synuclein toxicity in neurons (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-10-26
    Description: alpha-Synuclein (alpha-syn) is a small lipid-binding protein implicated in several neurodegenerative diseases, including Parkinson's disease, whose pathobiology is conserved from yeast to man. There are no therapies targeting these underlying cellular pathologies, or indeed those of any major neurodegenerative disease. Using unbiased phenotypic screens as an alternative to target-based approaches, we discovered an N-aryl benzimidazole (NAB) that strongly and selectively protected diverse cell types from alpha-syn toxicity. Three chemical genetic screens in wild-type yeast cells established that NAB promoted endosomal transport events dependent on the E3 ubiquitin ligase Rsp5/Nedd4. These same steps were perturbed by alpha-syn itself. Thus, NAB identifies a druggable node in the biology of alpha-syn that can correct multiple aspects of its underlying pathology, including dysfunctional endosomal and endoplasmic reticulum-to-Golgi vesicle trafficking.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993916/" 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/PMC3993916/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tardiff, Daniel F -- Jui, Nathan T -- Khurana, Vikram -- Tambe, Mitali A -- Thompson, Michelle L -- Chung, Chee Yeun -- Kamadurai, Hari B -- Kim, Hyoung Tae -- Lancaster, Alex K -- Caldwell, Kim A -- Caldwell, Guy A -- Rochet, Jean-Christophe -- Buchwald, Stephen L -- Lindquist, Susan -- 5R01GM069530/GM/NIGMS NIH HHS/ -- F32GM099817/GM/NIGMS NIH HHS/ -- F32NS061419/NS/NINDS NIH HHS/ -- GM58160/GM/NIGMS NIH HHS/ -- K01 AG038546/AG/NIA NIH HHS/ -- R01 GM058160/GM/NIGMS NIH HHS/ -- R15 NS075684/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):979-83. doi: 10.1126/science.1245321. Epub 2013 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research (WIBR), Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24158909" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzimidazoles/chemistry/*pharmacology ; Caenorhabditis elegans ; Cells, Cultured ; *Cytoprotection ; Drug Evaluation, Preclinical ; Endosomal Sorting Complexes Required for Transport/*genetics ; Gene Regulatory Networks/*drug effects ; Neurodegenerative Diseases/*metabolism ; Neurons/*drug effects/metabolism ; Neuroprotective Agents/*pharmacology ; Parkinson Disease/metabolism ; Rats ; Saccharomyces cerevisiae/drug effects ; Saccharomyces cerevisiae Proteins/*genetics ; Small Molecule Libraries/chemistry/pharmacology ; Ubiquitin-Protein Ligase Complexes/*genetics ; Ubiquitin-Protein Ligases/*genetics ; alpha-Synuclein/*metabolism
    Print ISSN: 0036-8075
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  • 17
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    Supercomplex assembly determines electron flux in the mitochondrial electron transport chain (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-07-03
    Description: The textbook description of mitochondrial respiratory complexes (RCs) views them as free-moving entities linked by the mobile carriers coenzyme Q (CoQ) and cytochrome c (cyt c). This model (known as the fluid model) is challenged by the proposal that all RCs except complex II can associate in supercomplexes (SCs). The proposed SCs are the respirasome (complexes I, III, and IV), complexes I and III, and complexes III and IV. The role of SCs is unclear, and their existence is debated. By genetic modulation of interactions between complexes I and III and III and IV, we show that these associations define dedicated CoQ and cyt c pools and that SC assembly is dynamic and organizes electron flux to optimize the use of available substrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lapuente-Brun, Esther -- Moreno-Loshuertos, Raquel -- Acin-Perez, Rebeca -- Latorre-Pellicer, Ana -- Colas, Carmen -- Balsa, Eduardo -- Perales-Clemente, Ester -- Quiros, Pedro M -- Calvo, Enrique -- Rodriguez-Hernandez, M A -- Navas, Placido -- Cruz, Raquel -- Carracedo, Angel -- Lopez-Otin, Carlos -- Perez-Martos, Acisclo -- Fernandez-Silva, Patricio -- Fernandez-Vizarra, Erika -- Enriquez, Jose Antonio -- New York, N.Y. -- Science. 2013 Jun 28;340(6140):1567-70. doi: 10.1126/science.1230381.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23812712" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Cytochromes c/*metabolism ; Electron Transport ; Electron Transport Complex I/genetics/*metabolism ; Electron Transport Complex III/genetics/*metabolism ; Electron Transport Complex IV/genetics/*metabolism ; Gene Knockdown Techniques ; HEK293 Cells ; Humans ; Mice ; Mice, Inbred C57BL ; Mitochondria/*enzymology ; Molecular Sequence Data ; Ubiquinone/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Long-distance integration of nuclear ERK signaling triggered by activation of a few dendritic spines (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-11-30
    Description: The late phase of long-term potentiation (LTP) at glutamatergic synapses, which is thought to underlie long-lasting memory, requires gene transcription in the nucleus. However, the mechanism by which signaling initiated at synapses is transmitted into the nucleus to induce transcription has remained elusive. Here, we found that induction of LTP in only three to seven dendritic spines in rat CA1 pyramidal neurons was sufficient to activate extracellular signal-regulated kinase (ERK) in the nucleus and regulate downstream transcription factors. Signaling from individual spines was integrated over a wide range of time (〉30 minutes) and space (〉80 micrometers). Spatially dispersed inputs over multiple branches activated nuclear ERK much more efficiently than clustered inputs over one branch. Thus, biochemical signals from individual dendritic spines exert profound effects on nuclear signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4318497/" 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/PMC4318497/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhai, Shenyu -- Ark, Eugene D -- Parra-Bueno, Paula -- Yasuda, Ryohei -- R01 MH080047/MH/NIMH NIH HHS/ -- R01 NS068410/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Nov 29;342(6162):1107-11. doi: 10.1126/science.1245622.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24288335" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CA1 Region, Hippocampal/enzymology/*physiology ; Cells, Cultured ; Dendritic Spines/enzymology/*physiology ; Extracellular Signal-Regulated MAP Kinases/*metabolism ; Glutamates/metabolism ; *Long-Term Potentiation ; Rats ; Signal Transduction ; Transcription Factors/metabolism
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  • 19
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    Hedgehog signaling controls T cell killing at the immunological synapse (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-07
    Description: The centrosome is essential for cytotoxic T lymphocyte (CTL) function, contacting the plasma membrane and directing cytotoxic granules for secretion at the immunological synapse. Centrosome docking at the plasma membrane also occurs during cilia formation. The primary cilium, formed in nonhematopoietic cells, is essential for vertebrate Hedgehog (Hh) signaling. Lymphocytes do not form primary cilia, but we found and describe here that Hh signaling played an important role in CTL killing. T cell receptor activation, which "prearms" CTLs with cytotoxic granules, also initiated Hh signaling. Hh pathway activation occurred intracellularly and triggered Rac1 synthesis. These events "prearmed" CTLs for action by promoting the actin remodeling required for centrosome polarization and granule release. Thus, Hh signaling plays a role in CTL function, and the immunological synapse may represent a modified cilium.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4022134/" 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/PMC4022134/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de la Roche, Maike -- Ritter, Alex T -- Angus, Karen L -- Dinsmore, Colin -- Earnshaw, Charles H -- Reiter, Jeremy F -- Griffiths, Gillian M -- 075880/Wellcome Trust/United Kingdom -- 100140/Wellcome Trust/United Kingdom -- R01 AR054396/AR/NIAMS NIH HHS/ -- R01 GM095941/GM/NIGMS NIH HHS/ -- R01AR05439/AR/NIAMS NIH HHS/ -- R01GM095941/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Dec 6;342(6163):1247-50. doi: 10.1126/science.1244689.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cambridge Institute for Medical Research, University of Cambridge, Hills Road, Cambridge CB2 0XY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24311692" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/*immunology/metabolism ; Cell Polarity ; Cells, Cultured ; Centrosome/metabolism ; *Cytotoxicity, Immunologic ; Hedgehog Proteins/*metabolism ; *Immunological Synapses ; Kruppel-Like Transcription Factors/genetics/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Immunological ; Neuropeptides/genetics/metabolism ; Receptors, Antigen, T-Cell/immunology/metabolism ; Receptors, Cell Surface/metabolism ; Receptors, G-Protein-Coupled/metabolism ; *Signal Transduction ; T-Lymphocytes, Cytotoxic/*immunology/metabolism ; rac1 GTP-Binding Protein/genetics/metabolism
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  • 20
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    Quantitative phosphoproteomics reveal mTORC1 activates de novo pyrimidine synthesis (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-02-23
    Description: The Ser-Thr kinase mammalian target of rapamycin (mTOR) controls cell growth and metabolism by stimulating glycolysis and synthesis of proteins and lipids. To further understand the central role of mTOR in cell physiology, we used quantitative phosphoproteomics to identify substrates or downstream effectors of the two mTOR complexes. mTOR controlled the phosphorylation of 335 proteins, including CAD (carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, and dihydroorotase). CAD catalyzes the first three steps in de novo pyrimidine synthesis. mTORC1 indirectly phosphorylated CAD-S1859 through S6 kinase (S6K). CAD-S1859 phosphorylation promoted CAD oligomerization and thereby stimulated de novo synthesis of pyrimidines and progression through S phase of the cell cycle in mammalian cells. Thus, mTORC1 also stimulates the synthesis of nucleotides to control cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robitaille, Aaron M -- Christen, Stefan -- Shimobayashi, Mitsugu -- Cornu, Marion -- Fava, Luca L -- Moes, Suzette -- Prescianotto-Baschong, Cristina -- Sauer, Uwe -- Jenoe, Paul -- Hall, Michael N -- New York, N.Y. -- Science. 2013 Mar 15;339(6125):1320-3. doi: 10.1126/science.1228771. Epub 2013 Feb 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biozentrum, University of Basel, Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23429704" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspartate Carbamoyltransferase/genetics/*metabolism ; Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)/genetics/*metabolism ; Cells, Cultured ; Dihydroorotase/genetics/*metabolism ; HeLa Cells ; Humans ; Mice ; Mice, Knockout ; Multiprotein Complexes/*metabolism ; Phosphoproteins/*metabolism ; Proteome/metabolism ; Pyrimidines/*biosynthesis ; TOR Serine-Threonine Kinases/*metabolism
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  • 21
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    A secreted disulfide catalyst controls extracellular matrix composition and function (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-05-25
    Description: Disulfide bond formation in secretory proteins occurs primarily in the endoplasmic reticulum (ER), where multiple enzyme families catalyze cysteine cross-linking. Quiescin sulfhydryl oxidase 1 (QSOX1) is an atypical disulfide catalyst, localized to the Golgi apparatus or secreted from cells. We examined the physiological function for extracellular catalysis of de novo disulfide bond formation by QSOX1. QSOX1 activity was required for incorporation of laminin into the extracellular matrix (ECM) synthesized by fibroblasts, and ECM produced without QSOX1 was defective in supporting cell-matrix adhesion. We developed an inhibitory monoclonal antibody against QSOX1 that could modulate ECM properties and undermine cell migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ilani, Tal -- Alon, Assaf -- Grossman, Iris -- Horowitz, Ben -- Kartvelishvily, Elena -- Cohen, Sidney R -- Fass, Deborah -- New York, N.Y. -- Science. 2013 Jul 5;341(6141):74-6. doi: 10.1126/science.1238279. Epub 2013 May 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Structural Biology, Weizmann Institute of Science, Rehovot, Israel. tal.ilani@weizmann.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23704371" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Cell Adhesion ; Cell Line, Tumor ; Cell Movement ; Cells, Cultured ; Cysteine/metabolism ; Disulfides/metabolism ; Extracellular Matrix/enzymology/*physiology/ultrastructure ; Fibroblasts/enzymology/ultrastructure ; Humans ; Laminin/metabolism ; Oxidoreductases Acting on Sulfur Group Donors/antagonists & ; inhibitors/*metabolism
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  • 22
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    IFI16 DNA sensor is required for death of lymphoid CD4 T cells abortively infected with HIV (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-21
    Description: The progressive depletion of quiescent "bystander" CD4 T cells, which are nonpermissive to HIV infection, is a principal driver of the acquired immunodeficiency syndrome (AIDS). These cells undergo abortive infection characterized by the cytosolic accumulation of incomplete HIV reverse transcripts. These viral DNAs are sensed by an unidentified host sensor that triggers an innate immune response, leading to caspase-1 activation and pyroptosis. Using unbiased proteomic and targeted biochemical approaches, as well as two independent methods of lentiviral short hairpin RNA-mediated gene knockdown in primary CD4 T cells, we identify interferon-gamma-inducible protein 16 (IFI16) as a host DNA sensor required for CD4 T cell death due to abortive HIV infection. These findings provide insights into a key host pathway that plays a central role in CD4 T cell depletion during disease progression to AIDS.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3976200/" 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/PMC3976200/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monroe, Kathryn M -- Yang, Zhiyuan -- Johnson, Jeffrey R -- Geng, Xin -- Doitsh, Gilad -- Krogan, Nevan J -- Greene, Warner C -- 1DP1036502/DP/NCCDPHP CDC HHS/ -- DP1 DA036502/DA/NIDA NIH HHS/ -- P01 AI090935/AI/NIAID NIH HHS/ -- P30 AI027763/AI/NIAID NIH HHS/ -- P50 GM081879/GM/NIGMS NIH HHS/ -- P50 GM082250/GM/NIGMS NIH HHS/ -- R21 AI102782/AI/NIAID NIH HHS/ -- U19 AI096113/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 24;343(6169):428-32. doi: 10.1126/science.1243640. Epub 2013 Dec 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Virology and Immunology, 1650 Owens Street, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24356113" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*immunology ; Apoptosis/*immunology ; CD4-Positive T-Lymphocytes/*immunology/*virology ; Cells, Cultured ; DNA, Viral/*immunology ; DNA-Binding Proteins/genetics/immunology ; Gene Knockdown Techniques ; HEK293 Cells ; HIV-1/*immunology ; Humans ; Immunity, Innate ; Lymphocyte Depletion ; Nuclear Proteins/genetics/*immunology ; Palatine Tonsil/immunology ; Phosphoproteins/genetics/*immunology ; RNA, Small Interfering/genetics ; Spleen/immunology
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  • 23
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    Malignant potential of murine stromal cells after transplantation of human tumors into nude mice (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-04-03
    Description: Human malignant cancer tumors grafted into nude mice produce tumors containing both human cancer cells and the host's stromal cells. After short-term propagation of these tumors in vitro, the murine mesenchymal cells appear transformed and are tumorigenic in nude mice. However, established human cancer cell lines fail to similarly after adjacent murine stromal cells when used to produce tumors in nude mice. These experiments suggest that cancer cells may recruit normal cells to become malignant, qualifying the view of the clonal (unicellular) origin of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldenberg, D M -- Pavia, R A -- 1R01 CA17198/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1981 Apr 3;212(4490):65-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7209521" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/pathology ; Animals ; Cell Line ; Cells, Cultured ; Colonic Neoplasms/pathology ; Fibrosarcoma/*etiology ; Humans ; Karyotyping ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Neoplasm Transplantation ; Neoplasms, Experimental/*etiology ; Transplantation, Heterologous
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 24
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    Radiosensitivity of human cells in vitro (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-04-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Furcinitti, P S -- Todd, P -- New York, N.Y. -- Science. 1981 Apr 3;212(4490):6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7209518" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Survival/*radiation effects ; Cells, Cultured ; Dose-Response Relationship, Radiation ; HeLa Cells/radiation effects ; Humans
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  • 25
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    Voltage clamp studies in macrophages from mouse spleen cultures (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-10-23
    Description: Voltage clamp studies of macrophages from cultures of mouse spleen macrophages produced N-shaped steady-state current-voltage curves containing a region of negative slope resistance. Some macrophages exhibit two stable states of membrane potential, having current-voltage relationships that cross the voltage axis at three points. Outward currents that turn on at voltages of +15 millivolts or greater were noted in several cells. The addition of barium chloride to the bathing medium abolished the negative slope resistance and reduced the inward currents in response to hyperpolarizing voltage steps. These data provide direct evidence that macrophages exhibit at least tow different voltage-dependent conductances and demonstrate that voltage clamp techniques can be useful in studying the membrane properties of leukocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallin, E K -- New York, N.Y. -- Science. 1981 Oct 23;214(4519):458-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7291986" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Barium/pharmacology ; Cell Membrane/physiology ; Cells, Cultured ; Electric Conductivity ; Macrophages/*physiology ; Membrane Potentials ; Mice ; Spleen/cytology
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  • 26
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    Multiple opiate receptors: alcohol selectively inhibits binding to delta receptors (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-10-23
    Description: The addition of ethanol or other aliphatic alcohols to rat brain membranes strongly inhibits binding of enkephalins at concentrations at which little inhibition of opiate alkaloids is seen. Inhibition is reversible, and potency increases with chain length of the alcohol. The results suggest that delta receptors are considerably more sensitive to alcohols than mu receptors. This is the first demonstration of selective inhibition of one of the postulated classes of opiate receptors by a reagent that is not a ligand for the receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hiller, J M -- Angel, L M -- Simon, E J -- DA-00017/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1981 Oct 23;214(4519):468-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6270788" target="_blank"〉PubMed〈/a〉
    Keywords: Alcohols/*pharmacology ; Animals ; Brain/metabolism ; Cells, Cultured ; In Vitro Techniques ; Neuroblastoma/metabolism ; Rats ; Receptors, Opioid/classification/*drug effects/metabolism ; Structure-Activity Relationship
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  • 27
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    Divalent cation ionophores stimulate resorption and inhibit DNA synthesis in cultured fetal rat bone (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-06-05
    Description: Two divalent cation ionophores, A23187 and Ionomycin, which are selective for calcium, stimulated the resorption of fetal rat long bones in organ culture at 0.1 to 1 micromolar but not at higher concentrations. Both agents inhibited DNA synthesis at concentrations that stimulated resorption. These results might explain the differences in ionophore effects on bone previously reported, and they imply that cell replication is not required for osteoclast formation in fetal rat long bone cultures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lorenzo, J A -- Raisz, L G -- AM 07290/AM/NIADDK NIH HHS/ -- AM 18063/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Jun 5;212(4499):1157-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6785885" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/*pharmacology ; Bone Resorption/*drug effects ; Bone and Bones/drug effects/*metabolism ; Calcimycin/*pharmacology ; Calcium/metabolism ; Calcium Radioisotopes ; Cells, Cultured ; DNA/*biosynthesis ; DNA Replication/*drug effects ; Ethers/pharmacology ; Fetus ; Ionomycin ; Ionophores/pharmacology ; Kinetics ; Mice ; Parathyroid Hormone/pharmacology
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  • 28
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    Falciparum malaria-infected erythrocytes specifically bind to cultured human endothelial cells (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-07-31
    Description: Erythrocytes infected with the late stages of the human malarial parasite Plasmodium falciparum became attached to a subpopulation of cultured human endothelial cells by knoblike protrusions on the surface of the infected erythrocytes. Infected erythrocytes did not bind to cultured fibroblasts; uninfected erythrocytes did not bind to either endothelial cells or fibroblasts. The results suggest a specific receptor-ligand interaction between endothelial cells and a component, components, in the knobs of the infected erythrocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Udeinya, I J -- Schmidt, J A -- Aikawa, M -- Miller, L H -- Green, I -- New York, N.Y. -- Science. 1981 Jul 31;213(4507):555-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7017935" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aotus trivirgatus ; Cells, Cultured ; Endothelium/microbiology ; Erythrocytes/*microbiology/ultrastructure ; Female ; Humans ; Microscopy, Electron ; Plasmodium falciparum/*pathogenicity ; Pregnancy ; Umbilical Veins
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  • 29
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    Hormonal requirements for growth of arterial smooth muscle cells in vitro: and endocrine approach to atherosclerosis (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-05-15
    Description: In this study the hormonal requirements for the growth of arterial smooth muscle cells in vitro were determined. A serum-free, biochemically defined medium, supplemented with the relevant hormones, permitted proliferation and propagation of normal diploid mammalian arterial smooth muscle cells. Serum-free, hormone-supplemented cultures spontaneously formed atherosclerotic plaque-like nodules. Thus atherosclerosis may be mediated by a complex endocrine system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weinstein, R -- Stemerman, M B -- Maciag, T -- AM 07026/AM/NIADDK NIH HHS/ -- HL 06197/HL/NHLBI NIH HHS/ -- HL 07374/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1981 May 15;212(4496):818-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7013068" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta, Abdominal/cytology ; Cell Division/drug effects ; Cells, Cultured ; Culture Media ; Growth Substances/pharmacology ; Hormones/*pharmacology ; Insulin/pharmacology ; Muscle, Smooth, Vascular/*cytology ; Rats ; Transferrin/pharmacology
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  • 30
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    Diethylstilbestrol induces neoplastic transformation without measurable gene mutation at two loci (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-06-19
    Description: The frequency with which diethylstilbestrol induces neoplastic transformation and somatic mutation was measured concomitantly in Syrian hamster embryo cells. While diethylstilbestrol was as active as benzo[a]pyrene in inducing transformation, it failed to induce mutations at two conventionally studied loci. These results suggest that diethylstilbestrol may transform cells in the absence of gene mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barrett, J C -- Wong, A -- McLachlan, J A -- New York, N.Y. -- Science. 1981 Jun 19;212(4501):1402-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6262919" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzo(a)pyrene ; Benzopyrenes ; Carcinogens ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Cricetinae ; Diethylstilbestrol/*pharmacology ; Embryo, Mammalian ; Genes/*drug effects ; Mesocricetus ; *Mutation
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  • 31
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    Conversion of 3T3-L1 fibroblasts to fat cells by an inhibitor of methylation: effect of 3-deazaadenosine (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-03-13
    Description: 3-Deazaadenosine, an inhibitor of methylation, increased the frequency of conversion of 3T3-L1 fibroblasts to fat cells in a dose-dependent manner. Once converted, the 3T3-L1 fat cells retained their adipose morphology and accumulated triglycerides even when 3-deazaadenosine was removed from the culture medium. 3-Deazaadenosine may perturb cellular methylation and thereby lead to an increase in the frequency of differentiation of 3T3-L1 fibroblasts to fat cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chiang, P K -- New York, N.Y. -- Science. 1981 Mar 13;211(4487):1164-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7466386" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*cytology ; Animals ; Carnitine/pharmacology ; Cell Differentiation/*drug effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Fibroblasts/cytology ; Methylation ; Mice ; Ribonucleosides/*pharmacology ; Tubercidin/*pharmacology
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    A conjugate of alpha-amanitin and monoclonal immunoglobulin G to Thy 1.2 antigen is selectively toxic to T lymphoma cells (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-09-18
    Description: A covalent conjugate of an alpha-amanitin azo derivative and a monoclonal immunoglobulin G to the Thy 1.2 antigen on murine T lymphocytes was synthesized. The conjugate was 375- to 750-fold more inhibitory to murine T lymphoma S49.1 cells than the unconjugated derivative. At 0.7 X 10(-7) to 1.5 X 10(-7) M and at 4 X 10(-7) M amanitin equivalents, the conjugate inhibited protein synthesis in S49.1 cells by 50 percent and 80 to 96 percent, respectively. At these concentrations, mutant Thy l-deficient S49 cells and other murine lymphoma lacking Thy l altogether or carrying Thy 1.1 antigens were unaffected. This result demonstrated the potential for targeting amanitin to specific cell types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, M T -- Preston, J F 3rd -- R01 CA 19043/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1981 Sep 18;213(4514):1385-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6115471" target="_blank"〉PubMed〈/a〉
    Keywords: Amanitins/*administration & dosage ; Amino Acids/metabolism ; Animals ; Antibodies/administration & dosage ; Antibodies, Monoclonal ; Antigens, Surface/*immunology ; Antigens, Thy-1 ; Cells, Cultured ; Clone Cells/immunology ; Hybrid Cells/immunology ; Immunoglobulin G/*administration & dosage ; Lymphoma/*drug therapy ; Membrane Proteins/*immunology ; Mice ; Neoplasms, Experimental/drug therapy ; T-Lymphocytes/drug effects
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    Lateral diffusion of surface molecules in animal cells and tissues (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-08-21
    Description: When bound to cell surfaces, certain lectins such as concanavalin A induce a drop in the average diffusion coefficients (D) of a number of cell surface molecules. To find whether such anchorage modulation occurs naturally, D of surface antigens on different cell and tissue types were measured by fluorescence photobleaching recovery. Values for cells of the same tissue origin under different conditions of growth and association - in tissues, in small aggregates, and as isolated cells - varied by less than twofold when polyspecific monovalent antibodies to cell surface antigens were used, a range much less than the sixfold decrease in D observed after lectin-induced anchorage modulation. Thus, if reversible modulation of the diffusion rate is used naturally as a means of cell signaling, it must involve only a few kinds of surface receptors not detected by the antibodies used in this study. In certain tissues, however, a significant proportion of cells showed no apparent receptor mobility. This "all or none" modulation of lateral diffusion may reflect relatively long-lasting alterations in the states of a single cell type or differentiation among the cells of the particular tissue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gall, W E -- Edelman, G M -- AI-09273/AI/NIAID NIH HHS/ -- AI-11378/AI/NIAID NIH HHS/ -- AM-04256/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1981 Aug 21;213(4510):903-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7196087" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/physiology ; Cell Adhesion ; Cell Division ; Cells, Cultured ; Chick Embryo ; Cytoskeleton/physiology ; Diffusion ; *Membrane Fluidity ; Mice
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    Phase locking, period-doubling bifurcations, and irregular dynamics in periodically stimulated cardiac cells (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-12-18
    Description: The spontaneous rhythmic activity of aggregates of embryonic chick heart cells was perturbed by the injection of single current pulses and periodic trains of current pulses. The regular and irregular dynamics produced by periodic stimulation were predicted theoretically from a mathematical analysis of the response to single pulses. Period-doubling bifurcations, in which the period of a regular oscillation doubles, were predicted theoretically and observed experimentally.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guevara, M R -- Glass, L -- Shrier, A -- New York, N.Y. -- Science. 1981 Dec 18;214(4527):1350-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7313693" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Chick Embryo ; Electric Stimulation ; Heart/*physiology ; In Vitro Techniques ; Membrane Potentials ; Models, Biological ; *Myocardial Contraction ; Periodicity
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    Epidermal growth factors enhances viral transformation of granulosa cells (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-07-10
    Description: Kirsten sarcoma virus produced a low incidence of transient morphological transformation in primary cultures of rat ovarian granulosa cells. In the presence of epidermal growth factor, the incidence of transient transformation increased severalfold and two continuous cell lines were established. Epidermal growth factor, a naturally occurring polypeptide hormone, appears to act here as a tumor promoter in the retrovirus-induced transformation of a mesodermally derived epithelium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harrison, J -- Auersperg, N -- New York, N.Y. -- Science. 1981 Jul 10;213(4504):218-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6264597" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Transformation, Viral/*drug effects ; Cells, Cultured ; Epidermal Growth Factor/*pharmacology ; Female ; Granulosa Cells/*cytology/drug effects ; Kirsten murine sarcoma virus/drug effects/*genetics ; Peptides/*pharmacology ; Rats ; Sarcoma Viruses, Murine/*genetics
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    Somatomedin B: mitogenic activity derived from contaminant epidermal growth factor (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-09-04
    Description: The mitogenic effect of somatomedin B on human cultured glial cells was neutralized by the addition of antibodies to mouse epidermal growth factor. Somatomedin B contained epidermal growth factor--like activity, competing for binding to the epidermal growth factor receptor. It is concluded that contaminating epidermal growth factor may explain the entire mitogenic activity of somatomedin B.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heldin, C H -- Wasteson, A -- Fryklund, L -- Westermark, B -- New York, N.Y. -- Science. 1981 Sep 4;213(4512):1122-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6973821" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division/drug effects ; Cells, Cultured ; Epidermal Growth Factor/*pharmacology ; Growth Substances/*pharmacology ; Humans ; Neuroglia ; Peptides/*pharmacology ; Somatomedins/*pharmacology ; Structure-Activity Relationship
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    Calcium spike electrogenesis and other electrical activity in continuously cultured small cell carcinoma of the lung (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-06-05
    Description: Spike electrogenesis, local depolarizing and hyperpolarizing responses, spontaneous rhythmic firing, and alternating resting potentials were measured in cells from a continuously cultured small cell carcinoma of the lung. Spike generation was blocked by MnCl2. In view of this evidence for calcium-spike electrogenesis and previous evidence of secretory activity in these cells, this cell line (DMS 53) can provide a model for the study of excitation-secretion behavior in human neoplastic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCann, F V -- Pettengill, O S -- Cole, J J -- Russell, J A -- Sorenson, G D -- CA 25845/CA/NCI NIH HHS/ -- DA 23108/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1981 Jun 5;212(4499):1155-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6262914" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Calcium/pharmacology ; Carcinoma, Small Cell/*physiopathology ; Cells, Cultured ; Electric Conductivity ; Humans ; Lung Neoplasms/*physiopathology ; Manganese/pharmacology ; Membrane Potentials/drug effects
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    Fc and C3b receptors on pulmonary endothelial cells: induction by injury (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-10-30
    Description: Receptors for the activated third component of complement and for the Fc portion of immunoglobulin G are not expressed by apparently normal bovine pulmonary endothelial cells, but are expressed when the cells are exposed to white cell lysates or are infected with influenza or cytomegalovirus. The unmasking of these latent receptors may contribute to the pulmonary inflammatory response characteristic of, for example, anaphylaxis and to those lung diseases characterized by the deposition of immune complexes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryan, U S -- Schultz, D R -- Ruan, J W -- HL 21568/HL/NHLBI NIH HHS/ -- HL 22087/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1981 Oct 30;214(4520):557-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6270789" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cells, Cultured ; Complement C3b/metabolism ; Cytomegalovirus Infections/physiopathology ; Endothelium/metabolism ; Orthomyxoviridae Infections/physiopathology ; Pulmonary Artery/*cytology ; Receptors, Complement/*metabolism ; Receptors, Fc/*metabolism
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    Somatomedin-C mediates growth hormone negative feedback by effects on both the hypothalamus and the pituitary (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-06-12
    Description: Somatomedin-C stimulates somatostatin release to a maximum of 390 percent of basal release during short-term (20-minute) incubation of rat hypothalamus. It has no effect on basal or stimulated growth hormone release from primary cultures of rat adenohypophyseal cells during a 4-hour incubation, but inhibits stimulated release by more that 90 percent after 24 hours. These findings suggest that somatomedin-C participates in the growth hormone negative feedback loop with an immediate effect on hypothalamic somatostatin and a delayed effect on the anterior pituitary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berelowitz, M -- Szabo, M -- Frohman, L A -- Firestone, S -- Chu, L -- Hintz, R L -- AM 18722/AM/NIADDK NIH HHS/ -- AM 24085/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Jun 12;212(4500):1279-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6262917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bucladesine/pharmacology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Feedback ; Growth Hormone/pharmacology/*secretion ; Hypothalamus/drug effects/*physiology ; Insulin-Like Growth Factor I ; Kinetics ; Pituitary Gland, Anterior/drug effects/*secretion ; Rats ; Somatomedins/*pharmacology
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    Regeneration of neurites on long-term cultures of sympathetic neurons deprived of nerve growth factor (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-10-30
    Description: Sympathetic neurons from newborn rats, cultured for 1 month or longer in the virtual absence of nonneuronal cells, were capable of regenerating neurites after neuritotomy. Regeneration occurred even after nerve growth factor was withdrawn from the cultures, although it was much less extensive and appeared limited to a few days following neuritotomy. Even after 29 days of nerve growth factor deprivation, reintroduction of the protein prompted a resumption of neurite growth. Possible roles of both nerve growth factor-independent and -dependent components in adult nerve regeneration are discussed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Campenot, R B -- NS15559/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1981 Oct 30;214(4520):579-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7292000" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cells, Cultured ; Ganglia, Sympathetic/*cytology ; Nerve Growth Factors/*pharmacology ; Nerve Regeneration/*drug effects ; Neurons/*cytology ; Rats ; Time Factors
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    DNA synthesis in cultured adult cardiocytes (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-10-30
    Description: Trypsin-dissociated atrial cardiocytes from adult rats were exposed to [3H]thymidine for sequential 24-hour periods from day 2 to day 12 of culture. On day 3 and each day thereafter, cells were prepared for ultrastructural radioautography and examined with an electron microscope. Maximal incorporation occurred on day 5, when 63 percent of the cardiocytes were labeled. Mitotic activity was never present in more than 0.5 percent of the cardiocytes examined. Incorporation of [3H]thymidine and mitosis occurred only in immature cardiocytes characterized by subsarcolemmal primary filaments and Z bands with or without specific granules; more mature cardiocytes were never labeled.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cantin, M -- Ballak, M -- Beuzeron-Mangina, J -- Anand-Srivastava, M B -- Tautu, C -- New York, N.Y. -- Science. 1981 Oct 30;214(4520):569-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7291996" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; Cell Division ; Cells, Cultured ; DNA/*biosynthesis ; Female ; Mitosis ; Myocardium/*cytology ; Rats ; Rats, Inbred Strains ; Time Factors
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    Growth arrest and morphological change of human breast cancer cells by dibutyryl cyclic AMP and L-arginine (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-10-02
    Description: The growth in vitro of human breast cancer cells, line MCF-7, was inhibited by a daily supplement of L-arginine (1 milligram per milliliter). Arginine acted synergistically with dibutyryl adenosine 3',5'-monophosphate (cyclic AMP) (10(-6) molar) to enhance the growth inhibitory effect: the cell replication ceased completely within 2 days after treatment. The growth arrest accompanied a change in cell morphology and was preceded by increases in the cellular concentration of cyclic AMP, adenylate cyclase, and type II cyclic AMP-dependent protein kinase activities as well as a decrease of estrogen binding activity. The results suggest that growth of human breast cancer cells is subject to cyclic AMP-mediated regulation and that arginine may play a specific role in this process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho-Chung, Y S -- Clair, T -- Bodwin, J S -- Berghoffer, B -- New York, N.Y. -- Science. 1981 Oct 2;214(4516):77-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6269181" target="_blank"〉PubMed〈/a〉
    Keywords: Arginine/*pharmacology ; Breast Neoplasms/metabolism/*pathology ; Bucladesine/*pharmacology ; Cell Division/*drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Cyclic AMP/metabolism ; Drug Synergism ; Female ; *Growth Inhibitors ; Humans
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    Interferon-resistant cell line lacks fatty acid cyclooxygenase activity (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-04-17
    Description: A clone of L1210 mouse leukemia cells selected for resistance to both the antiviral and anticellular properties of mouse interferon were essentially devoid of fatty acid cyclooxygenase activity. Experiments in which broken cell preparations were mixed or the two cell types were cultivated together failed to indicate the presence of a diffusible enzyme inhibitor. Fatty acid lipoxygenase activity of similar magnitude was detectable in both cell types. A selective impairment of fatty acid cyclooxygenase in interferon-resistant cells is consistent with recently described data suggesting that this enzyme may play a crucial role in mediating the antiviral and anticellular effects of interferon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandrabose, K A -- Cuatrecasas, P -- Pottathil, R -- Lang, D J -- New York, N.Y. -- Science. 1981 Apr 17;212(4492):329-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6163214" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonic Acids/metabolism ; Cells, Cultured ; Clone Cells/drug effects/enzymology ; Cyclooxygenase Inhibitors ; Interferons/*pharmacology ; Leukemia L1210 ; Lipoxygenase/metabolism ; Lipoxygenase Inhibitors ; Mice ; Prostaglandin-Endoperoxide Synthases/*deficiency ; Prostaglandins/biosynthesis
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    Elastin fragments attract macrophage precursors to diseased sites in pulmonary emphysema (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-05-22
    Description: This study suggests one mechanism by which alveolar macrophages accumulate in the lung in pulmonary emphysema: elastin fragments generated at the diseased sites are potent chemoattractants for monocytes, the precursors of the macrophages. The most chemotactic elastin fragments have a molecular weight between 10,000 and 50,000 and are active at concentrations as low as 3 nanograms per milliliter. By comparison, elastin fragments with higher molecular weights and desmosines are active at concentrations greater than 0.3 microgram per milliliter. In addition, preincubation of monocytes with the 10,000- to 50,000-dalton elastin impairs the ability of the cells to migrate toward elastin fragments but not toward activated serum. Fragments of tropoelastin are not chemotactic for monocytes. Because elastin, but not tropoelastin, contains lysyl-derived cross-links, these structures may be the active chemotactic site on the elastin fragments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hunninghake, G W -- Davidson, J M -- Rennard, S -- Szapiel, S -- Gadek, J E -- Crystal, R G -- New York, N.Y. -- Science. 1981 May 22;212(4497):925-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7233186" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Chemotaxis, Leukocyte/*drug effects ; Dose-Response Relationship, Drug ; Elastin/*analogs & derivatives/*pharmacology ; Humans ; Macrophages/physiology ; Monocytes/*physiology ; Peptide Fragments/pharmacology ; Pulmonary Emphysema/*physiopathology ; Structure-Activity Relationship ; Tropoelastin/*pharmacology
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    Binding and mobility of the cell surface receptors for 3,3',5-triiodo-L-thyronine (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-01-02
    Description: A fluorescent derivative of the thyroid hormone 3,3'-triiodo-L-thyronine binds to cultured mouse fibroblasts; such binding is saturable. Video intensification fluorescence microscopy indicates that binding occurs at the plasma membrane. Diffusion coefficients, obtained by fluorescence photobleaching recovery, are consistent with binding to a protein receptor on the cell surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maxfield, F R -- Willingham, M C -- Pastan, I -- Dragsten, P -- Cheng, S Y -- New York, N.Y. -- Science. 1981 Jan 2;211(4477):63-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6255563" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/*metabolism ; Cells, Cultured ; Cytoplasmic Granules/metabolism ; Diffusion ; Endocytosis ; Kinetics ; Membrane Fluidity ; Membrane Proteins/metabolism ; Mice ; Microscopy, Fluorescence ; Receptors, Cell Surface/*metabolism ; Receptors, Thyroid Hormone ; Triiodothyronine/*metabolism
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    The posterior pituitary: regulation of anterior pituitary prolactin secretion (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-08-07
    Description: Removal of the posterior pituitary from anesthetized male rats results in a prompt and significant increase in circulating prolactin that is reversed by the injection of dopamine. Posterior pituitary extracts, which contain high concentrations of endogenous dopamine, inhibit prolactin secretion from isolated anterior pituitary cells. This inhibition is prevented by incubation of the cells with the dopamine receptor antagonist (+)-butaclamol. The data show that posterior pituitary dopamine reaches the anterior pituitary via the short hypophysial portal vessels and participates in the regulation of prolactin secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, L L -- Hoefer, M T -- Ben-Jonathan, N -- HD 14348/HD/NICHD NIH HHS/ -- NS-13234/NS/NINDS NIH HHS/ -- NS-219/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1981 Aug 7;213(4508):659-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7256264" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dopamine/pharmacology/*physiology ; Luteinizing Hormone/secretion ; Male ; Pituitary Gland, Posterior/*physiology ; Prolactin/*secretion ; Rats ; Secretory Rate/drug effects
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    Compartmentalization of cyclic AMP during phagocytosis by human neutrophilic granulocytes (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-01-23
    Description: Immunocytochemistry shows that early during phagocytosis of zymosan, adenosine 3',5'-monophosphate (cyclic AMP) appears on the cell surface before the phagosome is internalized. The appearance of cyclic AMP on the cell surface is coincident with that of granule products and regulatory subunit of type I cyclic AMP-dependent protein kinase. Guanosine 3',5'-monophosphate is not associated with the initiation site of phagocytosis, but is observed throughout the granular cytoplasmic region. This sharply localized accumulation of cyclic AMP may serve as a signal for the initiation of phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pryzwansky, K B -- Steiner, A L -- Spitznagel, J K -- Kapoor, C L -- 02430-22/PHS HHS/ -- AM17438/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Jan 23;211(4480):407-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6261328" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Compartmentation ; Cells, Cultured ; Cyclic AMP/*metabolism ; Cyclic GMP/metabolism ; Cytoplasmic Granules/metabolism ; Humans ; Lactoferrin/metabolism ; Macromolecular Substances ; Neutrophils/*physiology/ultrastructure ; Peroxidase/metabolism ; *Phagocytosis ; Protein Kinases/metabolism
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    Lectins mimic insulin in the induction of tyrosine aminotransferase (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-11-13
    Description: Various lectins were found to induce tyrosine aminotransferase in H-35 rat hepatoma cells grown in monolayer culture. Wheat germ agglutinin gave a maximal induction of tyrosine aminotransferase 6 hours after its addition. The induction time course was similar to that elicited by insulin. Fourteen micrograms of wheat germ agglutinin per milliliter gave half-maximal enzyme induction and 50 micrograms per milliliter gave the maximal response. The induction of tyrosine aminotransferase by wheat germ agglutinin was additive with the induction by either dexamethasone or dibutyryl adenosine 3',5'-monophosphate, but was not additive with the tyrosine amino transferase induction by insulin. Wheat germ agglutinin also mimicked insulin in the inhibition of cellular protein degradation in the absence of serum. The insulin-like effects of lectins should be considered in lectin-mediated manipulations such as agglutination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, J D -- Liu, A Y -- AM20274/AM/NIADDK NIH HHS/ -- GM 07258/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1981 Nov 13;214(4522):799-800.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6117128" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bucladesine/pharmacology ; Cells, Cultured ; Dexamethasone/pharmacology ; Enzyme Induction/drug effects ; Insulin/*pharmacology ; Lectins/*pharmacology ; Liver/*enzymology ; Liver Neoplasms, Experimental/enzymology ; Peptide Hydrolases/metabolism ; Rats ; Receptor, Insulin/drug effects ; Tyrosine Transaminase/*biosynthesis
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    Activation of the transforming potential of a normal cell sequence: a molecular model for oncogenesis (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-05-22
    Description: The molecularly cloned, long terminal repeat (LTR) of the Moloney sarcoma virus (M-MSV) provirus has been covalently linked to c-mos, the cellular homolog of the M-MSV-specific sequence, v-mos. These newly constructed clones lack any M-MSV-derived sequences other than the LTR, but in DNA transfection assays they transform cells as efficiently as cloned subgenomic M-MSV fragments containing both v-mos and LTR. Cells transformed by LTR:c-mos hybrid molecules contain additional copies of mos DNA, and several size classes of polyadenylated RNA's with sequence homology to mos. The activation of the transforming potential of c-mos by the proviral LTR suggests a model whereby LTR-like elements could activate other normal cell sequences with oncogenic potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blair, D G -- Oskarsson, M -- Wood, T G -- McClements, W L -- Fischinger, P J -- Vande Woude, G G -- New York, N.Y. -- Science. 1981 May 22;212(4497):941-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7233190" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Viral ; Cells, Cultured ; DNA, Recombinant ; Defective Viruses/genetics ; Gene Expression Regulation ; *Genes, Viral ; Mice ; Moloney murine leukemia virus/*genetics ; Nucleic Acid Hybridization ; Operon ; Plasmids
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    Regulation of muscle differentiation: stimulation of myoblast fusion in vitro by catecholamines (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-12-18
    Description: Epinephrine and isoproterenol provoke primary chick myoblasts to initiate precocious cell fusion. Both the rise in intracellular adenosine 3' ,5-monophosphate (cyclic AMP) and cell fusion generated by these effectors are prevented by propranolol, which is a specific blocker of the beta-adrenergic receptor. Propranolol has no effect either on the precocious cell fusion provoked by prostaglandin E or on cell fusion in control cultures. The results support the idea that a rise in cyclic AMP is the critical intracellular change responsible for initiating events that culminate in myoblast differentiation 4 to 5 hours later. They also indicate that the culminate in myoblast differentiation 4 to 5 hours later. They also indicate that the hormone responsible for the positive regulation of myoblast differentiation in vitro is not acting through the beta-adrenergic receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curtis, D H -- Zalin, R J -- New York, N.Y. -- Science. 1981 Dec 18;214(4527):1355-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6274017" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catecholamines/*pharmacology ; Cell Differentiation/drug effects ; Cell Fusion/*drug effects ; Cells, Cultured ; Chick Embryo ; Cyclic AMP/metabolism ; Epinephrine/pharmacology ; Isoproterenol/pharmacology ; Muscles/*cytology ; Propranolol/pharmacology ; Prostaglandins E/pharmacology ; Receptors, Adrenergic, beta/drug effects ; Stimulation, Chemical
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    Tritiated thymidine incorporation does not measure DNA synthesis in ribavirin-treated human cells (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-05-01
    Description: When the incorporation of tritiated thymidine into acid insoluble material was measured, ribavirin appeared to be a potent inhibitor of DNA synthesis in KB cells and human lymphocytes. Inhibition was nearly 100-fold less, however, when DNA synthesis was measured by incorporation of phosphorus-32-labeled phosphate or by DNA fluorescence. The potent inhibition detected by incorporation of tritiated thymidine into DNA actually was the result of a potent effect on the labeling of deoxythymidine triphosphate, not on the synthesis of DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drach, J C -- Thomas, M A -- Barnett, J W -- Smith, S H -- Shipman, C Jr -- DE 02731/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 1981 May 1;212(4494):549-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7209549" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; DNA/*biosynthesis ; DNA Replication/*drug effects ; Humans ; Lymphocytes/metabolism ; Phosphates/metabolism ; Ribavirin/*pharmacology ; Ribonucleosides/*pharmacology ; Thymidine/*metabolism ; Thymine Nucleotides/biosynthesis
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    Optical recording of calcium action potentials from growth cones of cultured neurons with a laser microbeam (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-06-05
    Description: Simultaneous recordings of calcium action potentials directly from growth cones and from somata of neuroblastoma cells indicated that they could be generated in the neurites at or near growth cones. Growth cone responses were measured with a fluorescent voltage-sensitive dye and a 5-milliwatt helium-neon laser microbeam as a monitoring light source.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grinvald, A -- Farber, I C -- NS14716/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1981 Jun 5;212(4499):1164-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7233210" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Calcium/*pharmacology ; Cells, Cultured ; Chickens ; Evoked Potentials/drug effects ; Kinetics ; Lasers ; Microscopy, Fluorescence ; Neurons/drug effects/*physiology
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    Suppression of immunity by stress: effect of a graded series of stressors on lymphocyte stimulation in the rat (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-09-18
    Description: In rats a graded series of stressors produced progressively greater suppression of lymphocyte function, as measured by the number of circulating lymphocytes and by phytohemagglutinin stimulation of lymphocytes in whole blood and isolated cultures. This evidence suggests that stress suppresses immunity in proportion to the intensity of the stressor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keller, S E -- Weiss, J M -- Schleifer, S J -- Miller, N E -- Stein, M -- New York, N.Y. -- Science. 1981 Sep 18;213(4514):1397-400.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6973822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Electroshock ; *Immune Tolerance ; Leukocyte Count ; Lymphocyte Activation ; Phytohemagglutinins/pharmacology ; Rats ; Stress, Physiological/*immunology ; T-Lymphocytes/immunology
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  • 54
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    Gonadotropin-releasing hormone: regulation of adenosine 3',5'-monophosphate in ovarian granulosa cells (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-12-18
    Description: The antigonadal effects of gonadotropin-releasing hormone in ovarian granulosa cells are due to attenuation of the adenosine 3',5'-monophosphate (cyclic AMP) response to follicle-stimulating hormone. Agonists of gonadotropin-releasing hormone progressively inhibit adenylate cyclase and stimulate phosphodiesterase activities in cultured granulosa cells, indicating that blockade of gonadotropin action is attributable to the combined effects of decreased production and increased degradation of cyclic AMP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knecht, M -- Catt, K J -- 5 F32 HDO5801/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1981 Dec 18;214(4527):1346-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6274016" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cyclic AMP/*metabolism ; Enzyme Activation/drug effects ; Female ; Follicle Stimulating Hormone/antagonists & inhibitors ; *Granulosa Cells/*drug effects/metabolism ; *Hypophysectomy ; Phosphodiesterase Inhibitors/*pharmacology ; Phosphoric Diester Hydrolases/*metabolism ; Pituitary Hormone-Releasing Hormones/*pharmacology ; Rats
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    Specific antigen in serum of patients with colon carcinoma (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-04-03
    Description: The binding of monoclonal antibody specific for colon carcinoma was inhibited by serum from patients with adenocarcinoma of the colon but not by serum from patients with other bowel diseases or from healthy volunteers. Of other malignancies studied, serum from two patients with gastric carcinoma and two patients with pancreatic carcinoma also inhibited the specific binding of monoclonal antibody. The levels of carcinoembryonic antigen in these serum samples were not correlated with their levels of binding inhibition. Such monoclonal antibodies may prove useful for the detection of colorectal carcinoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koprowski, H -- Herlyn, M -- Steplewski, Z -- Sears, H F -- CA-21124/CA/NCI NIH HHS/ -- RR-05540/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1981 Apr 3;212(4490):53-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6163212" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/*immunology ; Adult ; Aged ; Antibodies, Neoplasm/immunology ; Antibody Specificity ; Antigens, Neoplasm/*analysis ; Binding, Competitive ; Carcinoembryonic Antigen/analysis ; Cells, Cultured ; Colonic Neoplasms/*immunology ; Epitopes ; Female ; Humans ; Intestinal Diseases/immunology ; Male ; Middle Aged ; Neoplasms/immunology
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    Increased pyrophosphate in fibroblasts and lymphoblasts from patients with hereditary diffuse articular chondrocalcinosis (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-11-13
    Description: The metabolic and genetic factors leading to deposition of calcium pyrophosphate crystals in cartilage of patients with chondrocalcinosis are not well understood. Analysis of cultured fibroblasts and lymphoblasts from 12 affected members of a large kindred showed a mean concentration of intracellular inorganic pyrophosphate two times greater than that in cells from unaffected family members or normal, unrelated volunteers. Increased intracellular pyrophosphate may, therefore, be a biochemical marker for the heterozygous expression of the chondrocalcinosis gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lust, G -- Faure, G -- Netter, P -- Seegmiller, J E -- AM13622/AM/NIADDK NIH HHS/ -- GM17702/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1981 Nov 13;214(4522):809-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6270793" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Chondrocalcinosis/genetics/*metabolism ; Diphosphates/*metabolism ; Fibroblasts/*metabolism ; Humans ; Lymphocytes/*metabolism
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    Cellular aging: further evidence for the commitment theory (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-09-25
    Description: A large, transient reduction in the population size of human fibroblasts in early passages significantly increases the variability of the life-spans of cultures in comparison to control cultures, as predicted by the commitment theory of cellular aging. The theory also predicts that a constant population of noncycling cells will appear in the later part of the culture life-span. This was confirmed by labeling the cells in culture with tritiated thymidine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holliday, R -- Huschtscha, L I -- Kirkwood, T B -- New York, N.Y. -- Science. 1981 Sep 25;213(4515):1505-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7280670" target="_blank"〉PubMed〈/a〉
    Keywords: *Cell Division ; *Cell Survival ; Cells, Cultured ; Fibroblasts/*physiology ; Humans ; Lung/cytology ; Probability
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    Choline stimulates nicotinic receptors on adrenal medullary chromaffin cells to induce catecholamine secretion (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-10-23
    Description: Choline stimulated secretion of catecholamines from primary dissociated cultures of bovine adrenal medullary chromaffin cells by interacting with nicotinic receptors. Secretion was readily detected at a choline concentration of 1 millimole per liter and was maximal at 3 to 10 millimoles per liter; it was completely calcium-dependent. Further analysis suggested that choline acts as a partial nicotinic agonist.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holz, R W -- Senter, R A -- 1 ROAM-27959-01/OA/SAMHSA HHS/ -- New York, N.Y. -- Science. 1981 Oct 23;214(4519):466-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7291988" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/antagonists & inhibitors ; Adrenal Medulla/*physiology ; Animals ; Catecholamines/*secretion ; Cattle ; Cells, Cultured ; Choline/*pharmacology ; Chromaffin System/*physiology ; Exocytosis/drug effects ; Receptors, Cholinergic/*drug effects ; Receptors, Nicotinic/*drug effects
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    Contractility of bile canaliculi: implications for liver function (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-05-29
    Description: Dynamic contractions of bile canaliculi were observed in groups of cultured hepatocytes by time-lapse cinephotomicrography during the early stages of monolayer formation. The contractions, which were forceful and appeared to have a pumping action, may facilitate the flow of bile in the liver's canalicular system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oshio, C -- Phillips, M J -- New York, N.Y. -- Science. 1981 May 29;212(4498):1041-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7015506" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile/*physiology ; Cells, Cultured ; Cytoskeleton/*physiology/ultrastructure ; Liver/*physiology ; Male ; Microscopy, Phase-Contrast ; Rats
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    Journey to the center of the cell: role of the receptosome (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-10-30
    Description: Fibroblasts contain a specific internalization pathway that carries hormones as well as some proteins and viruses from the cell surface to the cell interior. Initially, the ligands bind to mobile receptors that are randomly distributed on the cell surface. Next the ligand-receptor complexes are trapped and concentrated in specialized regions of the membrane termed bristle-coated pits. From the pit a smooth-walled vesicle containing the ligand forms and carries the ligand to the cell interior. Because of its role in receptor-mediated endocytosis, this vesicle has been termed a "receptosome."〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pastan, I H -- Willingham, M C -- New York, N.Y. -- Science. 1981 Oct 30;214(4520):504-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6170111" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Compartmentation ; Cells, Cultured ; Clathrin ; Cytoplasm/physiology ; *Endocytosis ; Exocytosis ; Fibroblasts/*physiology ; Ligands ; Membrane Fluidity ; Membrane Proteins/metabolism ; Mice ; Microscopy, Fluorescence ; Receptors, Drug/*physiology ; alpha-Macroglobulins/metabolism ; gamma-Glutamyltransferase/metabolism
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    Ganglioside stimulation of axonal sprouting in vitro (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-10-30
    Description: Bovine brain gangliosides were applied to primary and established neuronal cultures to examine the role of gangliosides in neuronal development. Media containing gangliosides enhanced the degree of axonal elongation exhibited by sensory ganglia neurons and increased the length and number of Neuro-2a neuroblastoma cell processes. Ganglioside-supplemented media caused a twofold increase in ornithine decarboxylase activity in both culture systems. These experiments suggest that gangliosides function as acceptor molecules for growth-promoting substances in embryonic and tumor-derived neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roisen, F J -- Bartfeld, H -- Nagele, R -- Yorke, G -- NS 11299/NS/NINDS NIH HHS/ -- NS 11605/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1981 Oct 30;214(4520):577-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7291999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cells, Cultured ; Chick Embryo ; Enzyme Induction/drug effects ; Ganglia, Spinal/embryology ; Gangliosides/*physiology ; Microscopy, Electron, Scanning ; Neurons/*cytology/ultrastructure ; Ornithine Decarboxylase/biosynthesis
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    Alcohol-dependent liver cell necrosis in vitro: a new model (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-04-17
    Description: In alcoholic liver injury, necrosis is involved in the progression from benign fatty liver to alcoholic hepatitis and cirrhosis. However, there is no practical model of alcohol-dependent liver cell necrosis. The calcium-dependent killing of cultured rat hepatocytes by two different membrane-active hepatotoxins, galactosamine and phalloidin, is potentiated by ethyl alcohol. This indicates that some general physical effect of alcohol on cellular membranes renders cells susceptible to otherwise nonlethal injuries. The in vitro model described in this report may thus be used to search for a general mechanism underlying alcohol-related tissue injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schanne, F A -- Zucker, A H -- Farber, J L -- Rubin, E -- AA 03442/AA/NIAAA NIH HHS/ -- AM 19154/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Apr 17;212(4492):338-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7209533" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/pharmacology ; Cell Membrane/drug effects ; Cells, Cultured ; Drug Synergism ; Ethanol/pharmacology ; Female ; Galactosamine/pharmacology ; In Vitro Techniques ; Liver/drug effects ; Liver Diseases, Alcoholic/*pathology ; Necrosis ; Phalloidine/pharmacology ; Rats
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    Normalization by cell fusion of sister chromatid exchange in Bloom syndrome lymphocytes (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-05-15
    Description: Fusion of fresh lymphocytes from a Bloom syndrome (BS) patient with those of normal subjects or a BS heterozygote resulted in complete normalization of the frequency of sister chromatid exchanges in the chromosomes of BS cells. This normalization took place by the first mitosis in hybrid cells. In contrast, cultivation of BS lymphocytes with those of normal subjects or the BS heterozygote had no effect on sister chromatid exchanges. The cell fusion experiments suggest that the normalization on the sister chromatid exchanges. The cell fusion experiments suggest that the normalization of the sister chromatid exchange frequencies in BS cells can be achieved by factors conserved in the cells of various mammalian species. These findings are compatible with the concept that BS is a recessive genetic mutation at regulatory levels of the DNA repair function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shiraishi, Y -- Matsui, S -- Sandberg, A A -- CA-14555/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1981 May 15;212(4496):820-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7221565" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Fusion ; Cells, Cultured ; *Crossing Over, Genetic ; Humans ; Hybrid Cells/physiology ; Photosensitivity Disorders/*genetics ; *Sister Chromatid Exchange ; Syndrome ; Telangiectasis/*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)
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  • 64
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    Toxic injury to isolated hepatocytes is not dependent on extracellular calcium (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-09-11
    Description: Freshly isolated hepatocytes from phenobarbital-treated rats were incubated in the presence or absence of extracellular calcium with three differently acting liver cell toxins, namely carbon tetrachloride, bromobenzene, and ethylmethanesulfonate. In the absence of extracellular calcium these three compounds were far more toxic to the cells than in its presence. This result is inconsistent with the hypothesis that an influx of extracellular calcium is required as the final step in toxic liver cell injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, M T -- Thor, H -- Orrenius, S -- New York, N.Y. -- Science. 1981 Sep 11;213(4513):1257-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7268433" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bromobenzenes/*toxicity ; Calcium/*metabolism ; Carbon Tetrachloride Poisoning/*physiopathology ; Cell Survival ; Cells, Cultured ; Ethyl Methanesulfonate/*toxicity ; Extracellular Space/metabolism ; Humans ; Liver/*drug effects/pathology ; Rats
    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)
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