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p53 has been reported to transactivate miR-200 family members by directly binding to the promoters of miR-200c and repress the expression of ZEB1 and ZEB2, leading to an inhibition of EMT [72], [73].
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MiRNAs have been reported to be directly transactivated by p53; equally, p53 and components of its pathway have been shown to be targeted by miRNA thereby affecting p53 activities [ 28].
IR has also been reported to activate NF- κB, which transactivates its target genes, including cox-2, bcl-2, bcl-xL, XIAP and survivin, and the expression of these antiapoptotic genes disrupts apoptosis signaling, thereby mediating radioresistance.
In particular, TRAIL has also been reported to activate the transcription factor NF- κB, which transactivates the genes encoding several key anti-apoptotic proteins, including cFlip, Bcl-xL, Mcl-1 and IAPs, each of which has been implicated in TRAIL resistance.
On the other hand, oncogenic Ras has been reported to differentially stabilize TAp73α [ 29], an isoform that can interact with ∆Np73α and may be blocking its capacity to transactivate BIK.
Recently, gastrin has been reported to induce EMT in colon cancer through the JAK2/STAT3 pathway (Ferrand et al, 2004), while gastrin-releasing peptides have been shown to transactivate EGFR in pancreatic cancer (Thomas et al, 2005).
Both PUMA and NOXA have been reported to be a direct transcriptional target of both wild-type p53 and the transactivating isoforms of p63 and p73 (Oda et al, 2000; Melino et al, 2004; Flinterman et al, 2005).
However, p,p´-DDE does not result in a similar delayed onset even though it is reported to weakly bind and transactivate the estrogen receptor (Andersen et al. 1999; Kelce et al. 1995; Payne et al. 2001).
Previously, PGE2, the major COX-2-derivated PG, was reported to be capable of transactivating the EGFR kinase cascade in colon cancer cells (Pai et al., 2002), whereas activation of EGFR could conversely stimulate COX-2 biosynthesis (Coffey et al., 1997).
It has been reported that oestrogen transactivates the EGFR to initiate the MAPK cascade.
It has been reported that Tax can transactivate the MDR-1 (multidrug resistance) gene promoter [ 25] and that ATLL cells very often show an enhanced MDR-1 expression [ 26].
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