Exact(3)
To identify CSA-independent placental interactions, FCR3Δvar2csa mutant parasites were selected for adhesion to the human placental trophoblastic BeWo cell line.
In contrast, IE of the control parasite FCR3CSA and Gb337CSA that had been repeatedly selected for adhesion to CSA showed good differential reactivity with the plasma pool obtained from pregnant women versus those of men and was well-recognized by IgG raised to the DBL3x, the DBL5e and the DBL6e domain of VAR2CSA (Figure 5A & B and data not shown).
These cassettes are present in PfEMP1s expressed in a large proportion of tested children suffering from severe malaria (Lavstsen et al., 2012; Bertin et al., 2013) and also in parasites selected for adhesion to brain endothelial cells (Avril et al., 2012; Claessens et al., 2012), suggesting a pivotal role in severe outcomes of P. falciparum infections.
Similar(57)
The rosetting clone 3D7S8.4 transcribed the var-gene PFD0630c at onset whilst the 3D7AH1S2 clone selected for CD36 adhesion transcribed PFF0845c.
By comparison to the wild-type parasites, the FCR3Δvar2csa mutants could not be selected for HA adhesion, indicating that var2csa is not only essential for IE cytoadhesion to the placental receptor CSA, but also to HA.
ItG and IT/R29 have the same genotype but have been selected for different adhesion phenotypes and express different PfEMP1 variants (Rowe et al., 1997, Springer et al., 2004).
The P. falciparum strain FCR3CSA was selected for the adhesive phenotype every three weeks by adhesion to plastic flasks coated with 10 mg ml−1 CSA as previously described (Viebig et al., 2005).
The parasites were 3D7S8.4 and 3D7AH1S2, which had been serially selected for either rosette formation or adhesion to CD36 and then cloned by micromanipulation.
These test objects were selected for experiments to mimic the adhesion of genomic material on stainless steel surgical instruments as used in the clinical praxis.
The Capan-1 model was selected for this experiment due its higher adhesion to rh-E-selectin.
Our results support the notion that MM cells are being selected for clones with increased numbers of mutated adhesion molecules during tumor evolution.
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