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  • 1
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    Hepatic fibrosis in schistosomiasis: egg granulomas secrete fibroblast stimulating factor in vitro (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-10-27
    Description: Cytosol extracts and culture supernatants of isolated egg granulomas obtained from livers of mice with Schistosoma mansoni infection stimulated fibroblasts to incorporate tritiated thymidine and to proliferate in vitro. This finding suggests that hepatic granulomas may play a role in regulating hepatic fibrosis in Schistosoma mansoni infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wyler, D J -- Wahl, S M -- Wahl, L M -- New York, N.Y. -- Science. 1978 Oct 27;202(4366):438-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/705337" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Fibroblasts/pathology ; Granuloma/complications/*etiology/metabolism ; Growth Substances/*secretion ; Inflammation/physiopathology ; Liver Cirrhosis/*etiology ; Mice ; Schistosoma mansoni ; Schistosomiasis/complications/*pathology/physiopathology
    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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  • 2
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    Benzodiazepine receptor-mediated chemotaxis of human monocytes (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-09-20
    Description: Benzodiazepines, which are widely prescribed for their antianxiety effects, are shown to be potent stimulators of human monocyte chemotaxis. The chemotactic effects of benzodiazepine receptor agonists were blocked by the peripheral benzodiazepine receptor antagonist PK-11195, suggesting that these effects are mediated by the peripheral-type benzodiazepine receptor. Diazepam was also active in inducing chemotaxis. Binding studies on purified monocytes revealed high-affinity peripheral benzodiazepine receptors, and the displacement potencies of various benzodiazepines correlated with their relative potencies in mediating chemotaxis. The demonstration of functional benzodiazepine receptors on human monocytes, together with recent evidence of receptor-mediated monocyte chemotaxis by other psychoactive peptides (such as opiate peptides), suggests a biochemical substrate for psychosomatic communication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ruff, M R -- Pert, C B -- Weber, R J -- Wahl, L M -- Wahl, S M -- Paul, S M -- New York, N.Y. -- Science. 1985 Sep 20;229(4719):1281-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2994216" target="_blank"〉PubMed〈/a〉
    Keywords: Benzodiazepinones/metabolism/pharmacology ; Binding, Competitive ; Chemotaxis, Leukocyte/*drug effects ; Clonazepam/pharmacology ; Humans ; Isoquinolines/pharmacology ; Monocytes/metabolism/*physiology ; Receptors, GABA-A/analysis/drug effects/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Establishment of human iPSC-based models for the study and targeting of glioma initiating cells (2016)
    Springer Nature
    Details
    Publication Date: 2016-02-24
    Description: Article Glioma can originate from the transformation of neural progenitor cells into glioma initiating cells. Here, the authors demonstrate the use of induced pluripotent stem cells as a suitable model for generating neural progenitor cells, which can be subsequently transformed to glioma initiating cells that are able to the generate human glioma-like tumours in mice. Nature Communications doi: 10.1038/ncomms10743 Authors: Ignacio Sancho-Martinez, Emmanuel Nivet, Yun Xia, Tomoaki Hishida, Aitor Aguirre, Alejandro Ocampo, Li Ma, Robert Morey, Marie N. Krause, Andreas Zembrzycki, Olaf Ansorge, Eric Vazquez-Ferrer, Ilir Dubova, Pradeep Reddy, David Lam, Yuriko Hishida, Min-Zu Wu, Concepcion Rodriguez Esteban, Dennis O’Leary, Geoffrey M. Wahl, Inder M. Verma, Louise C. Laurent, Juan Carlos Izpisua Belmonte
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 4
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    3D reconstruction of free-formed line-like objects using NURBS representation (2003)
    Elsevier
    Details
    Publication Date: 2003-06-01
    Print ISSN: 0031-3203
    Electronic ISSN: 1873-5142
    Topics: Computer Science
    Published by Elsevier
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  • 5
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    Peripherin-2 couples rhodopsin to the CNG channel in outer segments of rod photoreceptors (2014)
    Oxford University Press
    Details
    Publication Date: 2014-10-22
    Description: Outer segments (OSs) of rod photoreceptors are cellular compartments specialized in the conversion of light into electrical signals. This process relies on the light-triggered change in the intracellular levels of cyclic guanosine monophosphate, which in turn controls the activity of cyclic nucleotide-gated (CNG) channels in the rod OS plasma membrane. The rod CNG channel is a macromolecular complex that in its core harbors the ion-conducting CNGA1 and CNGB1a subunits. To identify additional proteins of the complex that interact with the CNGB1a core subunit, we applied affinity purification of mouse retinal proteins followed by mass spectrometry. In combination with in vitro and in vivo co-immunoprecipitation and fluorescence resonance energy transfer (FRET), we found that the tetraspanin peripherin-2 links CNGB1a to the light-detector rhodopsin. Using immunoelectron microscopy, we found that this peripherin-2/rhodopsin/CNG channel complex localizes to the contact region between the disk rims and the plasma membrane. FRET measurements revealed that the fourth transmembrane domain (TM4) of peripherin-2 is required for the interaction with rhodopsin. Quantitatively, the binding affinity of the peripherin-2/rhodopsin interaction was in a similar range as that observed for rhodopsin dimers. Finally, we demonstrate that the p.G266D retinitis pigmentosa mutation found within TM4 selectively abolishes the binding of peripherin-2 to rhodopsin. This finding suggests that the specific disruption of the rhodopsin/peripherin-2 interaction in the p.G266D mutant might contribute to the pathophysiology in affected persons.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 6
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    Mosaic synaptopathy and functional defects in Cav1.4 heterozygous mice and human carriers of CSNB2 (2014)
    Oxford University Press
    Details
    Publication Date: 2014-02-20
    Description: Mutations in CACNA1F encoding the α 1 -subunit of the retinal Cav1.4 L-type calcium channel have been linked to Cav1.4 channelopathies including incomplete congenital stationary night blindness type 2A (CSNB2), Åland Island eye disease (AIED) and cone-rod dystrophy type 3 (CORDX3). Since CACNA1F is located on the X chromosome, Cav1.4 channelopathies are typically affecting male patients via X-chromosomal recessive inheritance. Occasionally, clinical symptoms have been observed in female carriers, too. It is currently unknown how these mutations lead to symptoms in carriers and how the retinal network in these females is affected. To investigate these clinically important issues, we compared retinal phenotypes in Cav1.4-deficient and Cav1.4 heterozygous mice and in human female carrier patients. Heterozygous Cacna1f carrier mice have a retinal mosaic consistent with differential X-chromosomal inactivation, characterized by adjacent vertical columns of affected and non-affected wild-type-like retinal network. Vertical columns in heterozygous mice are well comparable to either the wild-type retinal network of normal mice or to the retina of homozygous mice. Affected retinal columns display pronounced rod and cone photoreceptor synaptopathy and cone degeneration. These changes lead to vastly impaired vision-guided navigation under dark and normal light conditions and reduced retinal electroretinography (ERG) responses in Cacna1f carrier mice. Similar abnormal ERG responses were found in five human CACNA1F carriers, four of which had novel mutations. In conclusion, our data on Cav1.4 deficient mice and human female carriers of mutations in CACNA1F are consistent with a phenotype of mosaic CSNB2.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 7
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    Genetic dissection of a mammalian replicator in the human beta-globin locus (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-14
    Description: The timing and localization of DNA replication initiation in mammalian cells are heritable traits, but it is not known whether initiation requires specific DNA sequences. A site-specific recombination strategy was used to show that DNA sequences previously identified as replication initiation sites could initiate replication when transferred to new chromosomal locations. An 8-kilobase DNA sequence encompassing the origin of DNA replication in the human beta-globin locus initiated replication in the simian genome. Specific deletions within the globin origin did not initiate replication in these chromosomal sites. These data suggest that initiation of DNA replication in mammalian cells requires specific sequence information and extend the replicon hypothesis to higher eukaryotes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aladjem, M I -- Rodewald, L W -- Kolman, J L -- Wahl, G M -- CA48405/CA/NCI NIH HHS/ -- GM51104/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 14;281(5379):1005-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, The Salk Institute, San Diego, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9703500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cercopithecus aethiops ; DNA/genetics ; DNA Nucleotidyltransferases/metabolism ; *DNA Replication ; Gene Targeting ; Globins/*genetics ; Humans ; Integrases/metabolism ; Polymerase Chain Reaction ; *Replication Origin ; S Phase ; Sequence Deletion ; *Viral Proteins
    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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  • 8
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    Mouse engineering (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Gorman, S -- Wahl, G M -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1025.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9289845" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Nucleotidyltransferases/*metabolism ; *Genetic Engineering ; Integrases/metabolism ; Licensure ; Mice ; *Mice, Transgenic ; *Viral Proteins
    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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  • 9
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    Linking the p53 tumour suppressor pathway to somatic cell reprogramming (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-08-12
    Description: Reprogramming somatic cells to induced pluripotent stem (iPS) cells has been accomplished by expressing pluripotency factors and oncogenes, but the low frequency and tendency to induce malignant transformation compromise the clinical utility of this powerful approach. We address both issues by investigating the mechanisms limiting reprogramming efficiency in somatic cells. Here we show that reprogramming factors can activate the p53 (also known as Trp53 in mice, TP53 in humans) pathway. Reducing signalling to p53 by expressing a mutated version of one of its negative regulators, by deleting or knocking down p53 or its target gene, p21 (also known as Cdkn1a), or by antagonizing reprogramming-induced apoptosis in mouse fibroblasts increases reprogramming efficiency. Notably, decreasing p53 protein levels enabled fibroblasts to give rise to iPS cells capable of generating germline-transmitting chimaeric mice using only Oct4 (also known as Pou5f1) and Sox2. Furthermore, silencing of p53 significantly increased the reprogramming efficiency of human somatic cells. These results provide insights into reprogramming mechanisms and suggest new routes to more efficient reprogramming while minimizing the use of oncogenes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2735889/" 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/PMC2735889/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawamura, Teruhisa -- Suzuki, Jotaro -- Wang, Yunyuan V -- Menendez, Sergio -- Morera, Laura Batlle -- Raya, Angel -- Wahl, Geoffrey M -- Izpisua Belmonte, Juan Carlos -- 5 R01 CA061449/CA/NCI NIH HHS/ -- 5 R01 CA100845/CA/NCI NIH HHS/ -- R01 CA061449/CA/NCI NIH HHS/ -- R01 CA061449-30/CA/NCI NIH HHS/ -- R01 CA100845/CA/NCI NIH HHS/ -- R01 CA100845-05/CA/NCI NIH HHS/ -- R33 HL088293/HL/NHLBI NIH HHS/ -- R33 HL088293-03/HL/NHLBI NIH HHS/ -- England -- Nature. 2009 Aug 27;460(7259):1140-4. doi: 10.1038/nature08311. Epub 2009 Aug 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19668186" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cellular Reprogramming/*physiology ; Cyclin-Dependent Kinase Inhibitor p21/deficiency/genetics/metabolism ; Down-Regulation ; Embryo, Mammalian/cytology ; Female ; Fibroblasts/cytology/metabolism ; Humans ; Keratinocytes ; Male ; Mice ; Mice, Inbred C57BL ; Pluripotent Stem Cells/*cytology/*metabolism ; Tumor Suppressor Protein p53/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 10
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    Recombinase-mediated gene activation and site-specific integration in mammalian cells (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-15
    Description: A binary system for gene activation and site-specific integration, based on the conditional recombination of transfected sequences mediated by the FLP recombinase from yeast, was implemented in mammalian cells. In several cell lines, FLP rapidly and precisely recombined copies of its specific target sequence to activate an otherwise silent beta-galactosidase reporter gene. Clones of marked cells were generated by excisional recombination within a chromosomally integrated copy of the silent reporter. By the reverse reaction, integration of transfected DNA was targeted to a specific chromosomal site. The results suggest that FLP could be used to mosaically activate or inactivate transgenes for analysis of vertebrate development, and to efficiently integrate transfected DNA at predetermined chromosomal locations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Gorman, S -- Fox, D T -- Wahl, G M -- New York, N.Y. -- Science. 1991 Mar 15;251(4999):1351-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1900642" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Cell Line ; DNA Nucleotidyltransferases/genetics/*metabolism ; In Vitro Techniques ; Mammals/*genetics ; *Recombination, Genetic ; Restriction Mapping ; *Transfection ; beta-Galactosidase/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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