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Recently, comprehensive genomic studies defined three distinct molecular subtypes (TYR, MYC and SHH) of ATRT.
Analytical solutions for the variance (σ2h), covariance (Chh), and spectrum (Shh) of h described by a linearized Boussinesq equation were derived and verified by Monte Carlo simulations.
To check whether the Hh signaling pathway is affected by CAD and DM, we compared the migratory response to Shh of monocytes isolated from CTR, CAD−DM and CAD+DM patients.
In Shh +/− placentas, Gli2-shRNA-expressing lentiviruses resulted in significant decreases in Ptc1, expected decreases in Gli2, and unexpected increases in Shh of junctional zone as compared with scribble-shRNA-expressing lentiviruses.
L. fuelleborni, M. zebra and C. afra exhibit marked variation in the field of odontogenic competence both in the epithelium (pitx2, shh) and mesenchyme (pax9), in the spacing (bmp2, bmp4, pax9, runx2, shh) and in the size (bmp4, pax9, runx2, shh) of the initial tooth germs.
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A similar situation seems to occur in the developing limbs, whereby the intermediate phenotype of double mutants suggests that, in the absence of Shh, mutation of Tulp3 is not sufficient to induce full activation of the Shh pathway.
The expression of Shh, one of the Hh ligands, was increased in the mutant cloacal epithelium.
The observation of Shh induction of Smurf expression and cytoplasmic pivoting further implicated Smurfs in Shh signaling.
Consistent with the spreading of the Shh, expression of Gli1, a target and a mediator of Shh signalling, was enhanced in the dorsal midbrain of β-cateninstab embryos (Fig. 3g,h).
We hypothesized that mutation of Tulp3 leads to loss of repression of the Shh pathway, downstream of Shh ligand.
However, upon the onset of Shh expression, control of p53 pathway appears to become dependent on Shh signaling.
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