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Although, from available data, a defect in mitotic divisions cannot be ruled out, the degeneration of the cellular structures observed in pollen grains of p5cs1 p5cs2 genotype, may be caused by the irreversible damages on cellular membranes caused by the process of dehydration in absence of the protective action of proline.
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In view of this information and our current data revealing a defect in CREB-CRE binding activity and a reduction in VEGF expression in diabetic SIECs, we examined in these cells HIF-1α dynamics under basal conditions and in response to the PKA activator MB-cAMP.
Our data uncover a defect in B cell selection in ALPS patients and indicate a role for B cell dysregulation in the pathogenesis of autoimmunity and B-cell lymphoma in ALPS patients.
These data suggest a defect in the acquisition of NKP as a cause for reduced NK cells in EL4 bearing mice.
Together, these data suggest a defect in retrograde IFT.
Taken together, these data suggest a defect in proximal signalling underlies the age-related decline in NET and ROS generation.
Altogether, these data suggest a defect in the proteolytic activation of CTSB in TM cells under chronic oxidative stress.
Taken together, our data suggest a defect in autophagy flux in cardiomyocytes subjected to human AL-LC protein, with a corresponding inhibition of mitochondrial clearance.
The authors also subjected the larvae to ultrastructural analysis, which, combined with the functional data, indicated a defect in excitation-contraction coupling.
Our live imaging data revealed a defect in the expansion of the PrE when embryos were treated with Gö6983, but did not show whether this was the result of a general increase in cell death throughout the embryo.
Taken together, these data suggest a defect in endosomal trafficking upon PI3K-C2β inactivation in hepatocytes, starting at the level of the very early APPL1 compartment, which could affect its maturation into EEA1-positive endosomes.
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