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Whereas the mammalian GPHR is a Golgi-only associated protein whose inactivation disturbs the Golgi apparatus, our data suggest that dGPHR is expressed in both the ER and the Golgi and that dGPHR mutant flies have defects in both organelles that lead to a defective secretory pathway.
Disruption of the ASL3 would lead to a defective chloroplast and seedling lethality, and affected expression levels of genes associated with chloroplast development and photosynthesis at early leaf stage of rice.
The TCM5 encodes chloroplast-targeted Deg protease protein which is important for chloroplast development and the maintenance of PSII function and its disruption would lead to a defective chloroplast and affected expression levels of genes associated with chloroplast development and photosynthesis of rice plants under high temperatures.
The TCM5 encodes chloroplast-targeted Deg protease protein which is important for chloroplast development and the maintenance of PSII function and its disruption would lead to a defective chloroplast and affected expression levels of genes associated with chloroplast development and photosynthesis at early rice seedling stage under high temperatures.
Either these modifications produce a proportionally damped system, or the restrictions on these modifications are rather strict which suggests that in practical cases every rank 2 or higher modification that produces repeated pairs of complex eigenvalues will lead to a defective system.
SF3B1 mutations potentially lead to a defective spliceosome complex that is incapable of performing the correct splicing steps.
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The lack of these data leads to a defective understanding of how NMNPs are transferred and accumulated in the various food chain levels.
The Disproportionate micromelia (Dmm) mouse has a deletion mutation in the C-propeptide encoding region of Col2a1, which leads to a defective cartilage matrix.
If none of the eigenvalues of the unmodified system is an eigenvalue of the modified system then every rank 1 modification that produces a pair of repeated complex eigenvalues leads to a defective system.
We directly examined whether aging led to a defective ability of recipient splenic DCs to prime and activate antigen specific T cells.
Recent reports showed that impaired sensitivity of responder T cells (including autoreactive cells) to suppression by Tregs led to a defective suppression of their proliferation in disease state in NOD mice and human subjects with SLE and T1D [16], [17], [17].
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