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  • 1
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    Genetic dissection of plexin signaling in vivo [Developmental Biology] (2014)
    National Academy of Sciences
    Details
    Publication Date: 2014-02-12
    Description: Mammalian plexins constitute a family of transmembrane receptors for semaphorins and represent critical regulators of various processes during development of the nervous, cardiovascular, skeletal, and renal system. In vitro studies have shown that plexins exert their effects via an intracellular R-Ras/M-Ras GTPase-activating protein (GAP) domain or by activation of RhoA...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 2
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    CDK8 is a colorectal cancer oncogene that regulates beta-catenin activity (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-09-17
    Description: Aberrant activation of the canonical WNT/beta-catenin pathway occurs in almost all colorectal cancers and contributes to their growth, invasion and survival. Although dysregulated beta-catenin activity drives colon tumorigenesis, further genetic perturbations are required to elaborate full malignant transformation. To identify genes that both modulate beta-catenin activity and are essential for colon cancer cell proliferation, we conducted two loss-of-function screens in human colon cancer cells and compared genes identified in these screens with an analysis of copy number alterations in colon cancer specimens. One of these genes, CDK8, which encodes a member of the mediator complex, is located at 13q12.13, a region of recurrent copy number gain in a substantial fraction of colon cancers. Here we show that the suppression of CDK8 expression inhibits proliferation in colon cancer cells characterized by high levels of CDK8 and beta-catenin hyperactivity. CDK8 kinase activity was necessary for beta-catenin-driven transformation and for expression of several beta-catenin transcriptional targets. Together these observations suggest that therapeutic interventions targeting CDK8 may confer a clinical benefit in beta-catenin-driven malignancies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587138/" 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/PMC2587138/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Firestein, Ron -- Bass, Adam J -- Kim, So Young -- Dunn, Ian F -- Silver, Serena J -- Guney, Isil -- Freed, Ellen -- Ligon, Azra H -- Vena, Natalie -- Ogino, Shuji -- Chheda, Milan G -- Tamayo, Pablo -- Finn, Stephen -- Shrestha, Yashaswi -- Boehm, Jesse S -- Jain, Supriya -- Bojarski, Emeric -- Mermel, Craig -- Barretina, Jordi -- Chan, Jennifer A -- Baselga, Jose -- Tabernero, Josep -- Root, David E -- Fuchs, Charles S -- Loda, Massimo -- Shivdasani, Ramesh A -- Meyerson, Matthew -- Hahn, William C -- K08 CA134931/CA/NCI NIH HHS/ -- P50CA127003/CA/NCI NIH HHS/ -- R33 CA128625/CA/NCI NIH HHS/ -- R33 CA128625-01A1/CA/NCI NIH HHS/ -- R33CA128625/CA/NCI NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 Sep 25;455(7212):547-51. doi: 10.1038/nature07179. Epub 2008 Sep 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18794900" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic ; Colorectal Neoplasms/*genetics/*metabolism/pathology ; Cyclin-Dependent Kinase 8 ; Cyclin-Dependent Kinases/deficiency/*genetics/*metabolism ; Gene Dosage ; *Gene Expression Regulation, Neoplastic ; Humans ; Oncogene Proteins/deficiency/genetics/metabolism ; *Oncogenes ; RNA Interference ; Transcription, Genetic ; beta Catenin/*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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  • 3
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    Platelet factor 4 and Duffy antigen required for platelet killing of Plasmodium falciparum (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-12
    Description: Platelets restrict the growth of intraerythrocytic malaria parasites by binding to parasitized cells and killing the parasite within. Here, we show that the platelet molecule platelet factor 4 (PF4 or CXCL4) and the erythrocyte Duffy-antigen receptor (Fy) are necessary for platelet-mediated killing of Plasmodium falciparum parasites. PF4 is released by platelets on contact with parasitized red cells, and the protein directly kills intraerythrocytic parasites. This function for PF4 is critically dependent on Fy, which binds PF4. Genetic disruption of Fy expression inhibits binding of PF4 to parasitized cells and concomitantly prevents parasite killing by both human platelets and recombinant human PF4. The protective function afforded by platelets during a malarial infection may therefore be compromised in Duffy-negative individuals, who do not express Fy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McMorran, Brendan J -- Wieczorski, Laura -- Drysdale, Karen E -- Chan, Jo-Anne -- Huang, Hong Ming -- Smith, Clare -- Mitiku, Chalachew -- Beeson, James G -- Burgio, Gaetan -- Foote, Simon J -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Dec 7;338(6112):1348-51. doi: 10.1126/science.1228892.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Australian School of Advanced Medicine, Macquarie University, Sydney, NSW 2109, Australia. brendan.mcmorran@mq.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23224555" target="_blank"〉PubMed〈/a〉
    Keywords: Blood Platelets/*immunology ; Cells, Cultured ; Duffy Blood-Group System/genetics/*immunology ; Erythrocytes/*parasitology ; Humans ; *Malaria, Falciparum/blood/immunology/parasitology ; Plasmodium falciparum/drug effects/growth & development/*immunology ; Platelet Factor 4/genetics/*immunology/pharmacology ; Receptors, Cell Surface/genetics/*immunology ; Recombinant Proteins/pharmacology
    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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  • 4
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    PTEX is an essential nexus for protein export in malaria parasites (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-07-22
    Description: During the blood stages of malaria, several hundred parasite-encoded proteins are exported beyond the double-membrane barrier that separates the parasite from the host cell cytosol. These proteins have a variety of roles that are essential to virulence or parasite growth. There is keen interest in understanding how proteins are exported and whether common machineries are involved in trafficking the different classes of exported proteins. One potential trafficking machine is a protein complex known as the Plasmodium translocon of exported proteins (PTEX). Although PTEX has been linked to the export of one class of exported proteins, there has been no direct evidence for its role and scope in protein translocation. Here we show, through the generation of two parasite lines defective for essential PTEX components (HSP101 or PTEX150), and analysis of a line lacking the non-essential component TRX2 (ref. 12), greatly reduced trafficking of all classes of exported proteins beyond the double membrane barrier enveloping the parasite. This includes proteins containing the PEXEL motif (RxLxE/Q/D) and PEXEL-negative exported proteins (PNEPs). Moreover, the export of proteins destined for expression on the infected erythrocyte surface, including the major virulence factor PfEMP1 in Plasmodium falciparum, was significantly reduced in PTEX knockdown parasites. PTEX function was also essential for blood-stage growth, because even a modest knockdown of PTEX components had a strong effect on the parasite's capacity to complete the erythrocytic cycle both in vitro and in vivo. Hence, as the only known nexus for protein export in Plasmodium parasites, and an essential enzymic machine, PTEX is a prime drug target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elsworth, Brendan -- Matthews, Kathryn -- Nie, Catherine Q -- Kalanon, Ming -- Charnaud, Sarah C -- Sanders, Paul R -- Chisholm, Scott A -- Counihan, Natalie A -- Shaw, Philip J -- Pino, Paco -- Chan, Jo-Anne -- Azevedo, Mauro F -- Rogerson, Stephen J -- Beeson, James G -- Crabb, Brendan S -- Gilson, Paul R -- de Koning-Ward, Tania F -- England -- Nature. 2014 Jul 31;511(7511):587-91. doi: 10.1038/nature13555. Epub 2014 Jul 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, 3004, Australia [2] Monash University, Clayton, Victoria, 3800, Australia [3]. ; 1] Deakin University, Waurn Ponds, 3216, Australia [2]. ; Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, 3004, Australia. ; Deakin University, Waurn Ponds, 3216, Australia. ; 1] Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, 3004, Australia [2] Monash University, Clayton, Victoria, 3800, Australia. ; National Center for Genetic Engineering and Biotechnology (BIOTEC), Pathum Thani 12120, Thailand. ; The University of Geneva, 1211 Geneva 4, Switzerland. ; The University of Melbourne, Parkville, Victoria, 3010 Australia. ; 1] Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, 3004, Australia [2] Monash University, Clayton, Victoria, 3800, Australia [3] The University of Melbourne, Parkville, Victoria, 3010 Australia. ; 1] Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, 3004, Australia [2] Monash University, Clayton, Victoria, 3800, Australia [3] The University of Melbourne, Parkville, Victoria, 3010 Australia [4].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25043043" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Erythrocytes/metabolism/parasitology ; Heat-Shock Proteins/genetics/*metabolism ; Humans ; Life Cycle Stages/physiology ; Malaria/*parasitology ; Multiprotein Complexes/metabolism ; Plasmodium falciparum/*genetics/*metabolism ; Protein Transport/genetics ; Protozoan Proteins/genetics/*metabolism ; Vacuoles/metabolism/parasitology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Subgroup-specific structural variation across 1,000 medulloblastoma genomes (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-07-27
    Description: Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4alpha. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kappaB signalling in Group 4, suggest future avenues for rational, targeted therapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3683624/" 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/PMC3683624/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Northcott, Paul A -- Shih, David J H -- Peacock, John -- Garzia, Livia -- Morrissy, A Sorana -- Zichner, Thomas -- Stutz, Adrian M -- Korshunov, Andrey -- Reimand, Juri -- Schumacher, Steven E -- Beroukhim, Rameen -- Ellison, David W -- Marshall, Christian R -- Lionel, Anath C -- Mack, Stephen -- Dubuc, Adrian -- Yao, Yuan -- Ramaswamy, Vijay -- Luu, Betty -- Rolider, Adi -- Cavalli, Florence M G -- Wang, Xin -- Remke, Marc -- Wu, Xiaochong -- Chiu, Readman Y B -- Chu, Andy -- Chuah, Eric -- Corbett, Richard D -- Hoad, Gemma R -- Jackman, Shaun D -- Li, Yisu -- Lo, Allan -- Mungall, Karen L -- Nip, Ka Ming -- Qian, Jenny Q -- Raymond, Anthony G J -- Thiessen, Nina T -- Varhol, Richard J -- Birol, Inanc -- Moore, Richard A -- Mungall, Andrew J -- Holt, Robert -- Kawauchi, Daisuke -- Roussel, Martine F -- Kool, Marcel -- Jones, David T W -- Witt, Hendrick -- Fernandez-L, Africa -- Kenney, Anna M -- Wechsler-Reya, Robert J -- Dirks, Peter -- Aviv, Tzvi -- Grajkowska, Wieslawa A -- Perek-Polnik, Marta -- Haberler, Christine C -- Delattre, Olivier -- Reynaud, Stephanie S -- Doz, Francois F -- Pernet-Fattet, Sarah S -- Cho, Byung-Kyu -- Kim, Seung-Ki -- Wang, Kyu-Chang -- Scheurlen, Wolfram -- Eberhart, Charles G -- Fevre-Montange, Michelle -- Jouvet, Anne -- Pollack, Ian F -- Fan, Xing -- Muraszko, Karin M -- Gillespie, G Yancey -- Di Rocco, Concezio -- Massimi, Luca -- Michiels, Erna M C -- Kloosterhof, Nanne K -- French, Pim J -- Kros, Johan M -- Olson, James M -- Ellenbogen, Richard G -- Zitterbart, Karel -- Kren, Leos -- Thompson, Reid C -- Cooper, Michael K -- Lach, Boleslaw -- McLendon, Roger E -- Bigner, Darell D -- Fontebasso, Adam -- Albrecht, Steffen -- Jabado, Nada -- Lindsey, Janet C -- Bailey, Simon -- Gupta, Nalin -- Weiss, William A -- Bognar, Laszlo -- Klekner, Almos -- Van Meter, Timothy E -- Kumabe, Toshihiro -- Tominaga, Teiji -- Elbabaa, Samer K -- Leonard, Jeffrey R -- Rubin, Joshua B -- Liau, Linda M -- Van Meir, Erwin G -- Fouladi, Maryam -- Nakamura, Hideo -- Cinalli, Giuseppe -- Garami, Miklos -- Hauser, Peter -- Saad, Ali G -- Iolascon, Achille -- Jung, Shin -- Carlotti, Carlos G -- Vibhakar, Rajeev -- Ra, Young Shin -- Robinson, Shenandoah -- Zollo, Massimo -- Faria, Claudia C -- Chan, Jennifer A -- Levy, Michael L -- Sorensen, Poul H B -- Meyerson, Matthew -- Pomeroy, Scott L -- Cho, Yoon-Jae -- Bader, Gary D -- Tabori, Uri -- Hawkins, Cynthia E -- Bouffet, Eric -- Scherer, Stephen W -- Rutka, James T -- Malkin, David -- Clifford, Steven C -- Jones, Steven J M -- Korbel, Jan O -- Pfister, Stefan M -- Marra, Marco A -- Taylor, Michael D -- AT1-112286/Canadian Institutes of Health Research/Canada -- CA116804/CA/NCI NIH HHS/ -- CA138292/CA/NCI NIH HHS/ -- CA159859/CA/NCI NIH HHS/ -- CA86335/CA/NCI NIH HHS/ -- K08 NS059790/NS/NINDS NIH HHS/ -- P20 CA151129/CA/NCI NIH HHS/ -- P30 CA138292/CA/NCI NIH HHS/ -- P30 HD018655/HD/NICHD NIH HHS/ -- P41 GM103504/GM/NIGMS NIH HHS/ -- R01 CA086335/CA/NCI NIH HHS/ -- R01 CA109467/CA/NCI NIH HHS/ -- R01 CA114567/CA/NCI NIH HHS/ -- R01 CA116804/CA/NCI NIH HHS/ -- R01 CA148621/CA/NCI NIH HHS/ -- R01 CA155360/CA/NCI NIH HHS/ -- R01 CA159859/CA/NCI NIH HHS/ -- R01 CA163737/CA/NCI NIH HHS/ -- R01 NS061070/NS/NINDS NIH HHS/ -- England -- Nature. 2012 Aug 2;488(7409):49-56. doi: 10.1038/nature11327.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental & Stem Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario M5G 1L7, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22832581" target="_blank"〉PubMed〈/a〉
    Keywords: Carrier Proteins/genetics ; Cerebellar Neoplasms/*classification/*genetics/metabolism ; Child ; DNA Copy Number Variations/genetics ; Gene Duplication/genetics ; Genes, myc/genetics ; Genome, Human/*genetics ; Genomic Structural Variation/*genetics ; Genomics ; Hedgehog Proteins/metabolism ; Humans ; Medulloblastoma/*classification/*genetics/metabolism ; NF-kappa B/metabolism ; Nerve Tissue Proteins/genetics ; Oncogene Proteins, Fusion/genetics ; Proteins/genetics ; RNA, Long Noncoding ; Signal Transduction ; Transforming Growth Factor beta/metabolism ; Translocation, Genetic/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
    Electronic Resource
    Electronic Resource
    Novel phloroglucinols from the plant Melicope sessilifloro (Rutaceae) (1989)
    s.l. : American Chemical Society
    The @journal of organic chemistry 54 (1989), S. 2098-2103 
    Details
    ISSN: 1520-6904
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jo00270a018
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  • 7
    Electronic Resource
    Electronic Resource
    A carbon-13 nuclear magnetic resonance study of N-acetyldaunorubicinol (1977)
    s.l. : American Chemical Society
    The @journal of organic chemistry 42 (1977), S. 2344-2345 
    Details
    ISSN: 1520-6904
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jo00433a039
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  • 8
    Electronic Resource
    Electronic Resource
    Structure of lycorenine and the 7-hydroxy alkaloids derived from the [2]benzopyrano[3,4g]indole nucleus (1972)
    s.l. : American Chemical Society
    The @journal of organic chemistry 37 (1972), S. 49-51 
    Details
    ISSN: 1520-6904
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jo00966a013
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  • 9
    Electronic Resource
    Electronic Resource
    Structure of hymenoratin (1992)
    Oxford [u.a.] : International Union of Crystallography (IUCr)
    Acta crystallographica 48 (1992), S. 211-213 
    Details
    ISSN: 1600-5759
    Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001
    Topics: Chemistry and Pharmacology , Geosciences , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1107/S0108270191008867
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  • 10
    Electronic Resource
    Electronic Resource
    Paucin methanolate (1991)
    Oxford [u.a.] : International Union of Crystallography (IUCr)
    Acta crystallographica 47 (1991), S. 1253-1256 
    Details
    ISSN: 1600-5759
    Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001
    Topics: Chemistry and Pharmacology , Geosciences , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1107/S0108270190014068
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