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The rationale behind conserving hotspots is that protecting these areas should prevent the extinction of a larger number of species than would protecting areas of same size somewhere else.
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The presented analysis suggests that structurally conserved hotspots in the kinase catalytic domain may be statistically enriched by mutations with a high probability of being cancer drivers.
Moreover, we have observed that structurally conserved hotspots of cancer driver mutations often bear mutations with a high oncogenic activity (Figure 6B).
We have determined that structurally conserved hotspots in the kinase catalytic domain can be often enriched by cancer driver mutations with a high oncogenic potential.
Functionally important subdomains of the kinase catalytic core, as in the nomenclature defined by Hanks and Hunter [7], were examined to determine the distribution of nsSNPs and identify structurally conserved hotspots of functionally important mutations.
The pathogenic role of SF3B1 mutations is not only supported by its frequent occurrence in CLL, but also by the fact that mutations cluster in evolutionarily conserved hotspots within its carboxy-terminal repeat HEAT domains, whose function remains unknown [ 34].
The study by Orjuela-Sanchéz et al. [ 3] hints at the possibility of conserved recombination hotspots within P. vivax; such hotspots, as they note, have also been observed in Plasmodium falciparum [ 8].
While ecologists and evolutionary biologists rush to study what is left of natural processes in island ecosystems, conservation practitioners pioneer management techniques and contribute significantly to the field of conservation biology by trying to conserve biodiversity hotspots that are exposed to severe environmental threats.
We have also found that structurally conserved mutational hotspots can be shared by multiple kinase genes and are often enriched by cancer driver mutations with high oncogenic activity.
The database-driven analysis of sequence and structure-based signatures of kinase SNPs has clarified salient aspects of sequence conservation patterns and structural profiles of cancer-causing mutations, including the emergence of structurally conserved tumorigenic hotspots across multiple protein kinases.
Interestingly, conserved duplication hotspots have also been previously detected between D. melanogaster and D. simulans[ 47].
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