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The introduction of passive Bending-Twisting coupling at the wing-box level has been previously demonstrated through laminate level tailoring with Extension-Shearing coupling only, but the limited design space and the possibility for ply terminations (to produce tapered thickness) effectively rule out this special class of laminate for practical construction.
Both Bax [ 67, 68] and Cycs [ 42, 69] have been previously shown to be putative direct MYC targets due to the presence of non-canonical E-box MYC-Max binding sites, and association of MYC with the Bax promoter has been previously demonstrated through ChIP [ 68].
Using MB cell line models, we were able to demonstrate that TMZ is most effective when the MB cells have a functioning MMR, in addition to low level of MGMT expression (whose correlation to TMZ sensitivity in MB has been previously demonstrated through in vitro viability assays (Daniel et al, 2010; Faoro et al, 2011) and xenograft studies (Daniel et al, 2010)).
While it has been previously demonstrated through analysis of a positive autoregulatory motif model with explicit mRNA concentration that dimerization is necessary for bistability [ 52], it is significant that modeling transcription and translation as a single operation leads to similar results.
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Nonetheless, this transcription factor was previously demonstrated, through genome-wide screenings [ 25, 26], to bind to the PDR18 promoter region.
This phenomenon was previously demonstrated through biochemical assays without a full understanding of the process because of the lack of structural information concerning heparin binding.
Similar relationships were previously demonstrated through various studies (see [ 47] and as shown for the effect of several anticancer agents [ 48- 50]).
A role for RSC at maintaining proper chromatin structure was previously demonstrated through the use of the strong Sth1 degron allele (Parnell et al., 2008; Hartley and Madhani, 2009) and other RSC alleles (Badis et al., 2008; Ganguli et al., 2014).
In this regard it has been previously demonstrated how Bcr/Abl activates p38MAPK through both upstream molecules Mkk3 and Mkk6, but c-Abl only affects Mkk6 [32, [32].
Similar phenotypes have been previously demonstrated for adipose tissue browning achievable through WAT β-adrenergic signaling or through muscle and BAT stimulation.
Although it had been previously demonstrated that transient depletion of T cells through apoptosis could lead to long-term immune tolerance, the underlying mechanism responsible for this tolerance induction and maintenance was unknown.
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