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Recently, mutations of the additional sex comb-like 1 (ASXL1) gene were identified in patients with myelodysplastic syndrome (MDS), but the interaction of this mutation with other genetic alterations and its dynamic changes during disease progression remain to be determined.
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While the increase in kcat is temperature-independent, the increase in stability shows that the resultant interactions of this mutation have a strong enthalpic component.
Kinase-impaired BRAF mutants showed a significant association with concomitant activating KRAS or NRAS mutations, but not PIK3CA mutations, supporting the reported interaction of these mutations.
Transcription factors act on target genes in concert and as more becomes known about TBX1 protein interactions the effect of this mutation on protein interactions should be investigated.
The report concerning interaction of ASXL1 mutation with other genetic alterations in the pathogenesis of MDS and its progression is very limited.
We examined the interaction of germline mutation status and exposure to radiotherapy in the pathogenesis of CBC in a case-only design.
Furthermore, interactions of the mutations within these interfaces were identified [ 53].
We therefore tested the effect of this mutation on the interaction between Fab1 and Vac14.
We further investigated the effects of this mutation on the binding interactions of the mutant enzyme with the substrates.
Given that previous studies show that mutation status (carrier versus non-carrier) is an important factor affecting adjustment [ 7, 8], the interaction of hope and mutation status and the interaction of T1 depression or anxiety and mutation status were also entered into the regression equations.
The majority of these 18 mutations distort the interaction of this domain with other CPS1 domains, in many cases by causing improper folding of structural elements of the Integrating Domain that play key roles in these interactions.
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