2,306 Works

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host, hypothetically due to evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations, which dominate the metazoan glycophysiology. After entry of the parasite into a metazoan host, the parasite's serine residues, arising throughout its life-cycle, assumingly get exposed to glycotransferase activities, expressed by plasma proteins and surfaces of mononuclear cells. In...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host, hypothetically due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations, which dominate the metazoan glycophysiology. After entry of the parasite into the metazoan host, the parasite's serine residues, arising throughout its life-cycle, assumingly get exposed to glycotransferase activities in plasma and on surfaces of mononuclear cells. In...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host likely due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations, which dominate the metazoan glycophysiology. After entry of the parasite into the metazoan host, the parasite's serine residues, arising throughout its life-cycle, assumingly get exposed to glycotransferase activities in both the metazoan plasma and on the surfaces...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations, which dominate the metazoan glycophysiology. After entry of the parasite into the metazoan host, the parasite's serine residues, arising throughout its life-cycle, assumingly get exposed to trans-species metazoan O-GalNAc-glycosylations, which in the human blood group O occur...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host, and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host and life-threatening disease occurs especially in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host and life-threatening disease especially occurs in blood group A individuals. (How O-GalNAc glycosylation drives the evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host and life-threatening malaria tropica disease especially occurs in blood group A individuals. (How O-GalNAc glycosylation drives evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host and life-threatening malaria tropica disease especially occurs in blood group A individuals - (How O-GalNAc glycosylation drives evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Why Plasmodium falciparum does not survive outside its host and life-threatening malaria tropica disease especially occurs in blood group A individuals - (How O-GalNAc glycosylation drives evolution)

Peter Arend
The protozoan eukaryotic parasite Plasmodium falciparum, pathogen of malaria tropica, does not survive outside its metazoan host assumingly due to an evolutionary incomplete protein glycosylation, lacking the synthesis of the amino sugar N-acetylgalactosamine (GalNAc) and glucosamine (Glc)-GalNAc epimerizations. Breaking the species barrier, the host's cellular machinery most likely performs metazoan trans-species O-GalNAc glycosylation, which in the human occurs predominantly in blood group A patients and is performed on abundantly expressed serine residues, arising throughout the...

Resource Types

  • Dataset
    1,235
  • Text
    777
  • Collection
    211
  • Image
    71
  • Other
    12

Publication Year

  • 2018
    197
  • 2017
    447
  • 2016
    777
  • 2015
    435
  • 2014
    450

Registration Year

  • 2018
    194
  • 2017
    447
  • 2016
    1,639
  • 2015
    19
  • 2014
    7

Data Centers

  • figshare Academic Research System
    2,306