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Since only stem cells have long enough life spans to accumulate mtDNA mutations to detectable levels of homoplasmy, a clonal population marked by a particular mtDNA mutation likely represents the progeny of a single mutated stem cell (Elson et al., 2001; Greaves et al., 2006; Fellous et al., 2009).
On the other hand, a recessive mutation likely affects only the encoded subunit, and both alleles must be mutated to cause the disease.
These features, combined with the inherent advantages of Drosophila as a model system, make the IV population an attractive study system to study the mutational process, as many of the simplifying assumptions used in models of mutation likely hold.
Despite the targeted nature of IDH inhibitors, IDH mutation likely unleashes epigenetic marks that are themselves selectable, such as DNA methylation.
No second mutation, however, was identified in NEB and this nonsense mutation likely has a modifying impact on the phenotype of the patient.
The Tm in which the biotin-binding activity becomes half of tamavidin 2-HOT was 105 °C, at least 20°CC higher than those of avidin, streptavidin, and tamavidin 2. Because a reducing agent removed the thermal stability of tamavidin 2-HOT, the N115C mutation likely created disulfide bridges that stabilized inter-subunit associations.
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Mutator mutations likely occur in a minority of premalignant lesions, but these mutator premalignant lesions are disproportionately likely to develop into malignant tumors.
As our previous study indicates, certain disease-causing mutations likely affect mutation signals just like other functionally and structurally crucial sites.
Processing mutations likely trap polytopic membrane proteins like P-gp and CFTR in protease-sensitive conformations with incomplete packing of the TM segments.
This is expected; the mutations likely disrupt KAE609 binding, thereby reducing its potency.
Together, these mutations likely account for perhaps 5%to10%0% of all stuttering cases worldwide, Drayna estimates.
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