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The mutation of lysine 41 to glutamic acid in SCR 1 of CR2 (K41E CR2) has previously been shown to abrogate binding to C3d.
We first used two loss-of-function alleles of Scr, the EMS-induced Scr 1 allele and Df 3R Scx4, a deficiency of the distal end of the Scr cis-regulatory regions.
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Stereochemically complete models for CR2-Ig were constructed from crystal structures for the CR2 SCR 1 2 and mouse IgG1 Fc fragments.
The modelling also confirmed that the structure of CR2 SCR 1 2 is more extended in solution than in its crystal structure.
A recombinant glycosylated human CR2 SCR 1 2 domain pair was engineered with the Fc fragment of a mouse IgG1 antibody to create a chimaera CR2-Ig containing the major ligand binding domains.
X-ray and neutron scattering and analytical ultracentrifugation identified its domain structure in solution, and provided a comparison with controversial folded-back crystal structures for deglycosylated CR2 SCR 1 2.
To examine comparative binding of recombinant human CD21 SCR 1-2 anativeive human IgE to CD23 plus the effect of CD23 on IgE production, we engineered recombinant soluble human CD23 fragments; (1) derCD23, (2) sCD23 and (3) exCD23, formed in vivo by proteolysis.
Figure 4A plots optimum total costs as a function of (C pre + C scr )−1 C pre.
For CFH, mutational hotspots were observed for the SCR-19/20 SCR-19/205/18 domands, SCR-15/18 SCR-15/18 SCR-1/4 andomains/8 domains.
CFH possessed major functional activities at its N-terminal SCR-1/4 and C-terminal SCR-19/20 SCR-19/20together with another activity at the SCR-6/8 domains [ 83].
The secondary structures of SCR-1/4, SCR-6/8, SCR-10/12 and SCR-18/19 SCR-18/19 matched against each other, apart from minor deviations seen for SCR-6/7.
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