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The NF-κB signaling pathway was suspected to be crucially involved in the development of naturally occurring Treg cells, because mice lacking molecules of proximal TCR signaling leading to NF-κB activation, such as PCKθ, Bcl10, or CARMA1, show marked defects in the thymic generation of Treg cells [48], [49], [50], [51].
However, the axonal arborizations of mutant PNs in the protocerebrum manifested marked defects.
Evidence has emerged that TLR4 defective mice do not develop LV dysfunction after LPS stimulation whereas wild type mice developed marked defects in LV contraction and relaxation [ 25].
Consistent with this idea, Pax7−/− satellite cells are specified but exhibit marked defects in their ability to both proliferate and differentiate [15], [17], [18].
Our findings indicate that abdominal sepsis results in marked defects in the ability to express important innate genes.
Taken together, these results demonstrate that ectopic HH signaling activity in proximal ureteric cells causes renal hypoplasia, characterized by marked defects in the formation of nephrogenic structures, reduced ureteric branching and a qualitative defect in early stage ureteric branch tips.
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Injection of 25 pg of full length Mef2ca 4–5–6 RNA had dramatic effects on embryonic development, inducing lethality in approximately 30% of the embryos and marked developmental defects in 49% of the surviving embryos, classified as 'severely defective' (Fig. S6A,B).
The synthetic lethal phenotypes found in double mutants of Dcas and Src or FAK56D were marked by defects in dorsal closure and in some cases by the appearance of anterior cuticle holes that suggested head involution defects.
Intriguingly, NeuN+ and/or Map2+ neurons showed marked phenotypic defects on the glass surface, characterised by an absence of migration, and poor elaboration of processes and fasciculation among neuronal colonies as compared to REST-100 and REST/KD-50 ES cells (Fig. 3F 3H and 3K 3M).
In a minority of patients on treatment there are marked functional defects, especially in killing activity.
However, at the stage of flowering, elp6 mop2 RP40p::PIN1 still exhibits marked morphological defects.
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