Comparisons of mutants lacking the Golgi UDP-galactose or GDP-mannose transporters establish that phosphoglycans are important for promastigote but not amastigote virulence in Leishmania major - Test2 - elhamkhani - TriplyDB

Comparisons of mutants lacking the Golgi UDP-galactose or GDP-mannose transporters establish that phosphoglycans are important for promastigote but not amastigote virulence in Leishmania major

Comparisons of mutants lacking the Golgi UDP-galactose or GDP-mannose transporters establish that phosphoglycans are important for promastigote but not amastigote virulence in Leishmania major

http://www.wikidata.org/entity/Q35947298

about

Demonstration of genetic exchange during cyclical development of Leishmania in the sand fly vector Innate immunity against Leishmania infections Golgi-located NTPDase1 of Leishmania major is required for lipophosphoglycan elongation and normal lesion development whereas secreted NTPDase2 is dispensable for virulence Leishmania major glycosylation mutants require phosphoglycans (lpg2-) but not lipophosphoglycan (lpg1-) for survival in permissive sand fly vectors.Infection with arginase-deficient Leishmania major reveals a parasite number-dependent and cytokine-independent regulation of host cellular arginase activity and disease pathogenesis.Leishmania UDP-sugar pyrophosphorylase: the missing link in galactose salvage?Genetic metabolic complementation establishes a requirement for GDP-fucose in Leishmania.Proteophosphoglycan confers resistance of Leishmania major to midgut digestive enzymes induced by blood feeding in vector sand flies.Deletion of UDP-glucose pyrophosphorylase reveals a UDP-glucose independent UDP-galactose salvage pathway in Leishmania major Inhibition of Golgi apparatus glycosylation causes endoplasmic reticulum stress and decreased protein synthesis The role of nucleotide sugar transporters in development of eukaryotes.The role of the mitochondrial glycine cleavage complex in the metabolism and virulence of the protozoan parasite Leishmania major Deficiency of Leishmania phosphoglycans influences the magnitude but does not affect the quality of secondary (memory) anti-Leishmania immunity Leishmania lipophosphoglycan: how to establish structure-activity relationships for this highly complex and multifunctional glycoconjugate?Nutrient transport and pathogenesis in selected parasitic protozoa.Evaluation of α,β-unsaturated ketones as antileishmanial agents.Differential Impact of LPG-and PG-Deficient Leishmania major Mutants on the Immune Response of Human Dendritic Cells.Transgenic Leishmania and the immune response to infection Metal-drug synergy: new ruthenium(II) complexes of ketoconazole are highly active against Leishmania major and Trypanosoma cruzi and nontoxic to human or murine normal cells Leishmania major phosphoglycans influence the host early immune response by modulating dendritic cell functions Leishmania donovani lacking the Golgi GDP-Man transporter LPG2 exhibit attenuated virulence in mammalian hosts Innate immune activation and subversion of Mammalian functions by leishmania lipophosphoglycan.Leishmania cell wall as a potent target for antiparasitic drugs. A focus on the glycoconjugates.Continual renewal and replication of persistent Leishmania major parasites in concomitantly immune hosts.Leishmania infantum Lipophosphoglycan-Deficient Mutants: A Tool to Study Host Cell-Parasite Interplay.

P2860

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P2860

Comparisons of mutants lacking the Golgi UDP-galactose or GDP-mannose transporters establish that phosphoglycans are important for promastigote but not amastigote virulence in Leishmania major

http://www.wikidata.org/entity/Q35947298

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2007 nî lūn-bûn

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Comparisons of mutants lacking ...... virulence in Leishmania major

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Comparisons of mutants lacking ...... virulence in Leishmania major

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Comparisons of mutants lacking ...... virulence in Leishmania major

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Comparisons of mutants lacking ...... virulence in Leishmania major

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Comparisons of mutants lacking ...... virulence in Leishmania major

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Infection and Immunity

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Comparisons of mutants lacking ...... virulence in Leishmania major

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Althea A Capul

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Salvatore J Turco

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Suzanne Hickerson

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Tamara Barron

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P2860

Disruption of mannose activation in Leishmania mexicana: GDP-mannose pyrophosphorylase is required for virulence, but not for viability.

Advances in leishmaniasis

The suppression of galactose metabolism in procylic form Trypanosoma brucei causes cessation of cell growth and alters procyclin glycoprotein structure and copy number.

The Leishmania GDP-mannose transporter is an autonomous, multi-specific, hexameric complex of LPG2 subunits.

Identification of genes encoding arabinosyltransferases (SCA) mediating developmental modifications of lipophosphoglycan required for sand fly transmission of leishmania major.

The structure, biosynthesis and functions of glycosylphosphatidylinositol anchors, and the contributions of trypanosome research.

Developmental modification of lipophosphoglycan during the differentiation of Leishmania major promastigotes to an infectious stage.

Secretory pathway of trypanosomatid parasites.

Galactose metabolism is essential for the African sleeping sickness parasite Trypanosoma brucei

Proteophosphoglycans of Leishmania.

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4629-4637

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scholarly article

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10.1128/IAI.00735-07

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9

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75

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Stephen M. Beverley

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6230351

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17606605

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1951182

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