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In this study, we demonstrate that conditional deletion of Hdac3 in cells where Cre recombinase is expressed from the endogenous osterix promoter causes severe deficits in calvarial, trabecular and cortical bone volume.
It is not well understood whether NrdR interaction with the promoter causes a direct blocking of RNA polymerase by steric hindrance or if binding of NrdR dimers to both boxes (note that NrdR boxes are palindromic sequences) causes DNA to bend impairing RNA polymerase binding.
However, we found that expression of Cas9 from the eft-3 promoter causes embryonic lethality.
Lastly, transgenic expression of Ihh via a Villin promoter causes overt villus smooth muscle differentiation (Kolterud et al., 2009).
Transgenic overexpression of Angptl4 from a liver-specific promoter causes hypertriglyceridemia similar to that induced by adenoviral over-expression [ 42].
N-Myc expression driven by the TH promoter causes NB in mice (Weiss et al., 1997), suggesting that N-Myc is a critical effector of NB pathogenesis.
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In contrast, overexpression of OsDWARF4 driven by a constitutive promoter caused defects in plant growth, resulting in a decrease in grain production.
It has been shown that a recombinant TBP of rice (OsTBP2) interacts with OsTFIIB for efficient binding to the TATA-box in ZB8 promoter, causing highly efficient TATA-dependent basal transcription (Zhu et al., 2002).
Elevated expression of GL7, which might be caused by increased copy number or mutations in the promoter, caused long grains due to increased cell elongation in spikelet hulls (Wang et al., 2015b; Zhou et al., 2015), although another study showed that GL7 promotes cell proliferation in the grain-length direction (Wang et al., 2015a).
Within the same cellular context, NR2F2 binds to the rat CYP7A1 promoter causing enhanced transcription [41].
These results indicate that bacterial promoter activity, either within, or upstream of, the CMV promoter caused read-through transcription into the C-fragment gene resulting in bacterial expression.
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