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  • 1
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    Abscisic acid controls calcium-dependent egress and development in Toxoplasma gondii (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-01-11
    Beschreibung: Calcium controls a number of critical events, including motility, secretion, cell invasion and egress by apicomplexan parasites. Compared to animal and plant cells, the molecular mechanisms that govern calcium signalling in parasites are poorly understood. Here we show that the production of the phytohormone abscisic acid (ABA) controls calcium signalling within the apicomplexan parasite Toxoplasma gondii, an opportunistic human pathogen. In plants, ABA controls a number of important events, including environmental stress responses, embryo development and seed dormancy. ABA induces production of the second-messenger cyclic ADP ribose (cADPR), which controls release of intracellular calcium stores in plants. cADPR also controls intracellular calcium release in the protozoan parasite T. gondii; however, previous studies have not revealed the molecular basis of this pathway. We found that addition of exogenous ABA induced formation of cADPR in T. gondii, stimulated calcium-dependent protein secretion, and induced parasite egress from the infected host cell in a density-dependent manner. Production of endogenous ABA within the parasite was confirmed by purification (using high-performance liquid chromatography) and analysis (by gas chromatography-mass spectrometry). Selective disruption of ABA synthesis by the inhibitor fluridone delayed egress and induced development of the slow-growing, dormant cyst stage of the parasite. Thus, ABA-mediated calcium signalling controls the decision between lytic and chronic stage growth, a developmental switch that is central in pathogenesis and transmission. The pathway for ABA production was probably acquired with an algal endosymbiont that was retained as a non-photosynthetic plastid known as the apicoplast. The plant-like nature of this pathway may be exploited therapeutically, as shown by the ability of a specific inhibitor of ABA synthesis to prevent toxoplasmosis in the mouse model.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877910/" 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/PMC2877910/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nagamune, Kisaburo -- Hicks, Leslie M -- Fux, Blima -- Brossier, Fabien -- Chini, Eduardo N -- Sibley, L David -- R01 AI034036/AI/NIAID NIH HHS/ -- R01 AI034036-16/AI/NIAID NIH HHS/ -- R21 AI067051/AI/NIAID NIH HHS/ -- R21 AI067051-02/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Jan 10;451(7175):207-10. doi: 10.1038/nature06478.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Avenue, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18185591" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Abscisic Acid/analysis/biosynthesis/*metabolism/pharmacology ; Animals ; Calcium/*metabolism ; *Calcium Signaling/drug effects ; Cyclic ADP-Ribose/biosynthesis/metabolism ; Disease Models, Animal ; Mice ; Mice, Inbred BALB C ; Plant Growth Regulators ; Protozoan Proteins/secretion ; Pyridones/pharmacology ; Toxoplasma/drug effects/*growth & development/*metabolism/pathogenicity ; Toxoplasmosis/parasitology/pathology/prevention & control
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Calcium-dependent protein kinase 1 is an essential regulator of exocytosis in Toxoplasma (2010)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2010-05-21
    Beschreibung: Calcium-regulated exocytosis is a ubiquitous process in eukaryotes, whereby secretory vesicles fuse with the plasma membrane and release their contents in response to an intracellular calcium surge. This process regulates various cellular functions such as plasma membrane repair in plants and animals, the discharge of defensive spikes in Paramecium, and the secretion of insulin from pancreatic cells, immune modulators from lymphocytes, and chemical transmitters from neurons. In animal cells, serine/threonine kinases including cAMP-dependent protein kinase, protein kinase C and calmodulin kinases have been implicated in calcium-signal transduction leading to regulated secretion. Although plants and protozoa also regulate secretion by means of intracellular calcium, the method by which these signals are relayed has not been explained. Here we show that the Toxoplasma gondii calcium-dependent protein kinase 1 (TgCDPK1) is an essential regulator of calcium-dependent exocytosis in this opportunistic human pathogen. Conditional suppression of TgCDPK1 revealed that it controls calcium-dependent secretion of specialized organelles called micronemes, resulting in a block of essential phenotypes including parasite motility, host-cell invasion, and egress. These phenotypes were recapitulated by using a chemical biology approach in which pyrazolopyrimidine-derived compounds specifically inhibited TgCDPK1 and disrupted the parasite's life cycle at stages dependent on microneme secretion. Inhibition was specific to TgCDPK1, because expression of a resistant mutant kinase reversed sensitivity to the inhibitor. TgCDPK1 is conserved among apicomplexans and belongs to a family of kinases shared with plants and ciliates, suggesting that related CDPKs may have a function in calcium-regulated secretion in other organisms. Because this kinase family is absent from mammalian hosts, it represents a validated target that may be exploitable for chemotherapy against T. gondii and related apicomplexans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874977/" 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/PMC2874977/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lourido, Sebastian -- Shuman, Joel -- Zhang, Chao -- Shokat, Kevan M -- Hui, Raymond -- Sibley, L David -- R01 AI034036/AI/NIAID NIH HHS/ -- R01 AI034036-17/AI/NIAID NIH HHS/ -- England -- Nature. 2010 May 20;465(7296):359-62. doi: 10.1038/nature09022.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Avenue, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20485436" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Cells, Cultured ; *Exocytosis ; Fibroblasts/parasitology ; Foreskin ; Gene Knockout Techniques ; Host-Pathogen Interactions/physiology ; Humans ; Male ; Molecular Sequence Data ; Organelles/metabolism ; Phenotype ; Protein Kinases/deficiency/genetics/*metabolism ; Protein Phosphatase 1/chemistry/metabolism ; Toxoplasma/*cytology/*enzymology/pathogenicity/physiology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Intracellular parasite invasion strategies (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2004-04-10
    Beschreibung: Intracellular parasites use various strategies to invade cells and to subvert cellular signaling pathways and, thus, to gain a foothold against host defenses. Efficient cell entry, ability to exploit intracellular niches, and persistence make these parasites treacherous pathogens. Most intracellular parasites gain entry via host-mediated processes, but apicomplexans use a system of adhesion-based motility called "gliding" to actively penetrate host cells. Actin polymerization-dependent motility facilitates parasite migration across cellular barriers, enables dissemination within tissues, and powers invasion of host cells. Efficient invasion has brought widespread success to this group, which includes Toxoplasma, Plasmodium, and Cryptosporidium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sibley, L D -- New York, N.Y. -- Science. 2004 Apr 9;304(5668):248-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Center for Infectious Diseases, Washington University School of Medicine, St. Louis, MO 63110, USA. sibley@borcim.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15073368" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actins/physiology ; Animals ; Apicomplexa/*pathogenicity/*physiology ; Cell Adhesion ; Cell Membrane/parasitology ; Cells/*parasitology ; Cryptosporidium/pathogenicity/physiology ; Models, Biological ; Molecular Motor Proteins/physiology ; Movement ; Plasmodium/pathogenicity/physiology ; Protozoan Proteins/metabolism ; Toxoplasma/pathogenicity/physiology ; Vacuoles/parasitology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Recent expansion of Toxoplasma through enhanced oral transmission (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-01-18
    Beschreibung: The global predominance of three clonal Toxoplasma gondii lineages suggests that they are endowed with an exceptional trait responsible for their current parasitism of nearly all warm-blooded vertebrates. Genetic polymorphism analyses indicate that these clonal lineages emerged within the last 10,000 years after a single genetic cross. Comparison with ancient strains (approximately 1 million years) suggests that the success of the clonal lineages resulted from the concurrent acquisition of direct oral infectivity. This key adaptation circumvented sexual recombination, simultaneously promoting transmission through successive hosts, hence leading to clonal expansion. Thus, changes in complex life cycles can occur rapidly and can profoundly influence pathogenicity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, C -- Evans, D -- Cole, R H -- Kissinger, J C -- Ajioka, J W -- Sibley, L D -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):414-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532022" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cats ; DNA, Ribosomal/genetics ; DNA, Ribosomal Spacer/genetics ; Food Parasitology ; *Genes, Protozoan ; Introns ; Life Cycle Stages ; Mice ; Molecular Sequence Data ; Mouth ; Mutation ; Phylogeny ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Recombination, Genetic ; Reproduction ; *Selection, Genetic ; Toxoplasma/*genetics/pathogenicity/*physiology ; Toxoplasmosis/*parasitology/transmission ; Toxoplasmosis, Animal/*parasitology/transmission ; Virulence
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Compensatory dendritic cell development mediated by BATF-IRF interactions (2012)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2012-09-21
    Beschreibung: The AP1 transcription factor Batf3 is required for homeostatic development of CD8alpha(+) classical dendritic cells that prime CD8 T-cell responses against intracellular pathogens. Here we identify an alternative, Batf3-independent pathway in mice for CD8alpha(+) dendritic cell development operating during infection with intracellular pathogens and mediated by the cytokines interleukin (IL)-12 and interferon-gamma. This alternative pathway results from molecular compensation for Batf3 provided by the related AP1 factors Batf, which also functions in T and B cells, and Batf2 induced by cytokines in response to infection. Reciprocally, physiological compensation between Batf and Batf3 also occurs in T cells for expression of IL-10 and CTLA4. Compensation among BATF factors is based on the shared capacity of their leucine zipper domains to interact with non-AP1 factors such as IRF4 and IRF8 to mediate cooperative gene activation. Conceivably, manipulating this alternative pathway of dendritic cell development could be of value in augmenting immune responses to vaccines.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3482832/" 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/PMC3482832/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tussiwand, Roxane -- Lee, Wan-Ling -- Murphy, Theresa L -- Mashayekhi, Mona -- KC, Wumesh -- Albring, Jorn C -- Satpathy, Ansuman T -- Rotondo, Jeffrey A -- Edelson, Brian T -- Kretzer, Nicole M -- Wu, Xiaodi -- Weiss, Leslie A -- Glasmacher, Elke -- Li, Peng -- Liao, Wei -- Behnke, Michael -- Lam, Samuel S K -- Aurthur, Cora T -- Leonard, Warren J -- Singh, Harinder -- Stallings, Christina L -- Sibley, L David -- Schreiber, Robert D -- Murphy, Kenneth M -- AI076427-02/AI/NIAID NIH HHS/ -- P30 CA91842/CA/NCI NIH HHS/ -- R01 AI036629/AI/NIAID NIH HHS/ -- R01 AI076427/AI/NIAID NIH HHS/ -- R01 CA043059/CA/NCI NIH HHS/ -- T32 AI007163/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Oct 25;490(7421):502-7. doi: 10.1038/nature11531. Epub 2012 Sep 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22992524" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigen Presentation ; Antigens, CD/metabolism ; Antigens, CD8/immunology/metabolism ; Basic-Leucine Zipper Transcription ; Factors/chemistry/deficiency/genetics/*metabolism ; CD4-Positive T-Lymphocytes/cytology/immunology ; CTLA-4 Antigen/metabolism ; Cell Differentiation ; Cell Line, Tumor ; Cell Lineage ; Dendritic Cells/*cytology/immunology/*metabolism ; Female ; Fibrosarcoma/immunology/metabolism/pathology ; Gene Expression Regulation ; Integrin alpha Chains/metabolism ; Interferon Regulatory Factors/deficiency/genetics/*metabolism ; Interleukin-10/metabolism ; Interleukin-12/immunology/metabolism ; Leucine Zippers ; Male ; Mice ; Mice, Inbred C57BL ; Neoplasm Transplantation ; Oncogene Protein p65(gag-jun)/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Repressor Proteins/deficiency/genetics ; T-Lymphocytes, Helper-Inducer/cytology/immunology/metabolism ; Toxoplasma/immunology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Polymorphic secreted kinases are key virulence factors in toxoplasmosis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-12-16
    Beschreibung: The majority of known Toxoplasma gondii isolates from Europe and North America belong to three clonal lines that differ dramatically in their virulence, depending on the host. To identify the responsible genes, we mapped virulence in F(1) progeny derived from crosses between type II and type III strains, which we introduced into mice. Five virulence (VIR) loci were thus identified, and for two of these, genetic complementation showed that a predicted protein kinase (ROP18 and ROP16, respectively) is the key molecule. Both are hypervariable rhoptry proteins that are secreted into the host cell upon invasion. These results suggest that secreted kinases unique to the Apicomplexa are crucial in the host-pathogen interaction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2646183/" 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/PMC2646183/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saeij, J P J -- Boyle, J P -- Coller, S -- Taylor, S -- Sibley, L D -- Brooke-Powell, E T -- Ajioka, J W -- Boothroyd, J C -- 1R01AI045806-01A1/AI/NIAID NIH HHS/ -- AI05093/AI/NIAID NIH HHS/ -- AI059176/AI/NIAID NIH HHS/ -- AI21423/AI/NIAID NIH HHS/ -- AI30230/AI/NIAID NIH HHS/ -- AI36629/AI/NIAID NIH HHS/ -- AI41014/AI/NIAID NIH HHS/ -- F32AI60306/AI/NIAID NIH HHS/ -- R01 AI021423/AI/NIAID NIH HHS/ -- R01 AI021423-20/AI/NIAID NIH HHS/ -- R01 AI036629/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1780-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170306" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Amino Acid Sequence ; Animals ; Chromosome Mapping ; Chromosomes/genetics ; Crosses, Genetic ; Female ; Genes, Protozoan ; Genetic Complementation Test ; Mice ; Mice, Inbred BALB C ; Mice, Inbred CBA ; Molecular Sequence Data ; Oligonucleotide Array Sequence Analysis ; *Polymorphism, Single Nucleotide ; Protozoan Proteins/chemistry/*genetics/metabolism ; Quantitative Trait Loci ; Toxoplasma/enzymology/*genetics/*pathogenicity ; Toxoplasmosis, Animal/*parasitology ; Virulence ; Virulence Factors/chemistry/*genetics/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    A secreted serine-threonine kinase determines virulence in the eukaryotic pathogen Toxoplasma gondii (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-12-16
    Beschreibung: Toxoplasma gondii strains differ dramatically in virulence despite being genetically very similar. Genetic mapping revealed two closely adjacent quantitative trait loci on parasite chromosome VIIa that control the extreme virulence of the type I lineage. Positional cloning identified the candidate virulence gene ROP18, a highly polymorphic serine-threonine kinase that was secreted into the host cell during parasite invasion. Transfection of the virulent ROP18 allele into a nonpathogenic type III strain increased growth and enhanced mortality by 4 to 5 logs. These attributes of ROP18 required kinase activity, which revealed that secretion of effectors is a major component of parasite virulence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taylor, S -- Barragan, A -- Su, C -- Fux, B -- Fentress, S J -- Tang, K -- Beatty, W L -- Hajj, H El -- Jerome, M -- Behnke, M S -- White, M -- Wootton, J C -- Sibley, L D -- AI059176/AI/NIAID NIH HHS/ -- AI36629/AI/NIAID NIH HHS/ -- AI44600/AI/NIAID NIH HHS/ -- P20 RR-020185/RR/NCRR NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1776-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63130, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170305" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Catalytic Domain ; Chromosome Mapping ; Chromosomes/genetics ; Cloning, Molecular ; Genes, Protozoan ; Mice ; Molecular Sequence Data ; Movement ; Point Mutation ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Protozoan Proteins/chemistry/genetics/*metabolism ; Quantitative Trait Loci ; Toxoplasma/*enzymology/genetics/growth & development/*pathogenicity ; Toxoplasmosis, Animal/mortality/parasitology ; Transfection ; Virulence/genetics ; Virulence Factors/chemistry/genetics/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    Virulence differences in Toxoplasma mediated by amplification of a family of polymorphic pseudokinases (2011)
    National Academy of Sciences
    Details
    Publikationsdatum: 2011-05-17
    Print ISSN: 0027-8424
    Digitale ISSN: 1091-6490
    Thema: Biologie , Medizin , Allgemeine Naturwissenschaft
    Publiziert von National Academy of Sciences
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    Identification of quantitative trait loci controlling acute virulence in Toxoplasma gondii (2002)
    National Academy of Sciences
    Details
    Publikationsdatum: 2002-07-29
    Print ISSN: 0027-8424
    Digitale ISSN: 1091-6490
    Thema: Biologie , Medizin , Allgemeine Naturwissenschaft
    Publiziert von National Academy of Sciences
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    Globally diverse Toxoplasma gondii isolates comprise six major clades originating from a small number of distinct ancestral lineages (2012)
    National Academy of Sciences
    Details
    Publikationsdatum: 2012-03-19
    Print ISSN: 0027-8424
    Digitale ISSN: 1091-6490
    Thema: Biologie , Medizin , Allgemeine Naturwissenschaft
    Publiziert von National Academy of Sciences
    Standort Signatur Erwartet Verfügbarkeit
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