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Importantly, overexpression of wild-type p16 in these variants can induce a senescent-like phenotype, and 'knocking down' p16 expression with siRNA (small interfering RNA) in normal cells leads to abnormal centrosome numbers through a failure to couple centrosome duplication with the cell cycle.
Indeed biased gene conversion can be dynamic as seen in hybrid arthropod scallops where experimental hybridisation between closely related scallop species carrying different rDNA ITS variants can induce rapid early development biased gene conversion (to the maternal type) that is almost complete 14 days after fertilization [ 39].
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Beyond baseline nephron number and aging, certain gene variants impose specific risks for premature nephron loss and CKD such as uromodulin gene variants that can induce sodium-sensitive hypertension [ 16– 19], or possibly genes that affect podocyte survival.
In addition, compared with gene delivery approaches, which often involve the expression of only one cDNA variant, ATFs can induce all splice variants in their natural ratios.
The observation that tau and axotrophin RING-variant domain interact led us ask, whether the E3 ubiquitin ligase activity of the axotrophin RING-variant domain can induce ubiquitination of tau.
Much like histone variants, histone PTMs can induce structural changes in the solvent accessible nucleosome surface and interactions with nucleosomal DNA.
Different kinds of antigens can induce variant immune response, and also for different types of Th cells.
We previously showed that an UNC-40 variant, UNC-40 (A1056V) can induce the asymmetrical localization of UNC-40 in HSN even in the absence of UNC-6 and that the direction of the asymmetric localization in this case is indeterminate (Xu et al., 2009).
The A30P and E46K pathological variants, on the other hand, can induce strong pro-inflammatory and immunoregulatory responses, together with marked increases in chemokine release levels, both in total glia and microglia.
In nature, environmental changes can induce morphological variants due to the susceptibility of organisms to stress.
Complicating the study of laminopathies, over-expression of mutated lamin A variants is problematic as it can induce cell senescence [ 9], and the existing animal models do not reproduce the clinical complexity observed in humans [ 10].
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