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Furthermore, mixed-lineage-leukemia (MLL) fusion genes, induce a characteristic pattern of Hox A cluster genes, including Hoxa7 and Hoxa9 in myeloid cells [52].
These data demonstrate that although restoration of either PPAR γ isoform in PPAR γ KO HGPIN cells decreases de novo lipogenesis and oxidative stress, only PPAR γ2-regulated genes induce a metabolic switch for induction of a prostatic differentiation program, potentially through disparate regulation of Scd1.
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CTCF protein is expressed in nongametogenic tissues and its binding to a promoter of CT genes induces a transcription silencing.
We observed that targeting of 23 genes resulted in significant reduction of DV1 RSPs amounts in supernatants whereas targeting of 22 other genes induced a significant increase.
The majority of optimized genes induced a clear increase in detectable protein levels throughout all protein classes, while only two membrane proteins (VKORC1 and SLC39A1) were poorly expressed in HEK293T cells compared to their wildtype counterparts.
Additionally, only specific EMT associated genes induced a CD44+/CD24- phenotype in MCF-10A cells.
These Hox genes induced a down-regulation of luciferase activity which increased in a collinear fashion (except for Hoxd10 and Hoxd11 which showed a weaker effect).
VLPs encoding the HCV core-E1E2 genes induced a large HCV-specific T-cell population in chimpanzees and all four vaccines cleared challenge with homologous strain of HCV [85].
At the same time, the expression of certain genes induced a stress response in the ER and upregulation of the UPR correlated with low plasmid copy number.
PPARα and RXRα heterodimerize and subsequently bind to PPAR response elements in the promoters of the target genes inducing a wide spectrum of metabolic effects [ 31].
Mutations in the human DAP12 gene induce a rare pathology named polycystic lipomembraneous osteodysplasia with sclerosing encephalopathy (PLOSL), also known as Nasu-Hakola disease [14].
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