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Histone modifications have also been discovered to play positive or negative roles in controlling miRNA expression in multiple normal cells and diseases (12, 13).
Zhao et al. [ 33] reported that trastuzumab-based 4D5 CAR T cells reacted against a panel of tumor cells of different origin that expressed even low levels of HER2, as well as multiple normal cells.
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For example, we observe a MC on chromosome 2 (HF087) in a genomic region bearing a histone modification pattern characteristic of insulators in multiple different normal cell types, but the pattern changes to that of an enhancer in hepatocellular carcinoma.
Caspase-3 dependency of PAC-1-induced cell death was supported by the data of cell death in multiple normal and cancer cell lines that strongly placed caspase-3 expression as a deciding factor for its cytotoxicity.. So, in order to further validate the caspase-3 dependency, we compared cell death in the presence (MCFC3) and absence of caspase-3 (MCF7).
In conclusion, here we present a systematic analysis based on large number of genome-wide methylation profiles across multiple normal and tumor cells demonstrating that in general, derepression of CTA and CTX genes in cancer may be largely explained by global hypomethylation mediated by disruption of laminar attachment regions.
As previously observed in multiple normal and malignant cell types [ 9, 19], T-oligo rapidly localized to the nuclei comparably well in both cell types and the majority of nuclei were positive.
Of relevance to this study, CXCR4, a seven-transmembrane span G-protein-coupled receptor expressed in multiple normal and cancer stem cells was expressed 2.63-fold higher in the cluster cells [ 42, 46].
In normal cells, multiple redundant pathways cooperate to mediate arrest, but in cancer cells the progressive loss of other checkpoints may make p27 indispensable for TGF-β-mediated arrest.
Clearly the de novo pathway is regulated by the same molecules as the canonical pathway, however it has to be very well controlled to avoid multiple centriole formation in normal cells [ 5, 6, 9].
Researchers have already identified that Malat1 RNA has multiple physiological functions in normal cells, such as regulating cell cycle [ 21], Malat1 modulates the expressions of cell cycle genes, which are required for G1/S regulation and mitotic progression with tissue-specific and developmental stage-specific patterns.
Thus, a single-cell approach can help to definitively reconstruct the cellular composition of tumours as has been effectively carried out for multiple normal tissues using single-cell transcriptomics techniques (20, 56– 61).
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