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The specificity of decreased Gdnf expression in Ptc1−/−UB kidneys is demonstrated by normal expression of Osr1, Six2, and CITED1, each of which marks mesenchymal precursor cells [22], [23], [24], [25], [26]; Wnt4, a marker of pretubular aggregates [27]; and Wnt9b which is required for the earliest inductive response in metanephric mesenchyme and acts upstream of Wnt4 [28] (Figure S6).
In RCD type I, intraepithelial lymphocytes (IEL) are characterized by normal expression of T-cell antigens as well as polyclonal T-cell receptor gene rearrangement.
Posterior segments are unaffected, as reflected by normal expression of Nv eve posterior to stripe 5 (segment A4; Figure 2R,S).
There was disagreement between the two tests in seven cases: five cases were characterised by normal expression of the three MMR proteins but microsatellite instability after PCR.
In patients 10 and 11, with no rearrangement of the TCR genes, T-LGLs were characterized by normal expression of T-cell antigens.
Investigations on whether this could reflect partly an efficient mismatch repair (MMR) mechanism were confirmed by normal expression of hMLH1 and hMSH2, suggesting that the lack of mutations could be explained by the operation of alternative pathogenetic mechanisms modulating downstream effectors of the signaling pathways.
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Thus, promoter-hypermethylation of E-cad is significantly associated with its defective expression and tumor differentiation, and the demethylating observation proposes a therapeutic strategy to reverse the tumor's malignancy by restoring normal expression of E-cad.
Despite the AVE patterning defects caused by ablation of the Hex expressing cells, the rest of the visceral endoderm remained intact and showed no evidence of a loss of integrity, as confirmed by the normal expression of Ttr at 6.5dpc (Fig.3F).
This finding is accompanied by decreased normal expression of TDP-43 in the nucleus.
As we did not observe axons projecting to ectopic brain regions (data not shown) and the number and organisation of habenular cell subtypes appeared unaffected as revealed by the normal expression of the pou4f1-hsp70l GFP pou4f1-hsp70l GFPC,F), we intransgene the loss oFigPN connectivity as a primary defect in habenular axonal extension.
Taken together, these data suggest that the decrease of DLK not only prevents the accumulation of lipids, but also disrupts the whole differentiation program of 3T3-L1 by impairing the normal expression of C/EBPα and PPARγ2.
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Justyna Jupowicz-Kozak
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