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Consistently, nuclear functions of STAT3 and STAT5B were reported to be important for vSrc mediated cellular transformation [ 37- 40].
Although originally discovered as a protein involved in the pathway transducing a signal in response to interferon [ 11], STAT3 was not linked to cancer until it was shown to be essential for v-src mediated cellular transformation [ 12].
The relevance of this question is supported by experiments showing that IGF-IR is required for both JCV T-Antigen (25), and SV40 T-Antigen mediated cellular transformation (14).
Our results indicate that one of the mechanisms that could explain the necessity of IGF-IR in JCV T-Antigen mediated cellular transformation involves the reactivation of Survivin, which at least in neural progenitors, requires the presence of functional IGF-IR.
Similar(56)
Stat3 has been defined as an oncogene in light of its ability to mediate cellular transformation and block apoptosis [ 9].
MUC1 function involves mediating cellular transformation in integrating the growth factor receptor and Wnt signalling pathways (Ren et al, 2002).
In studies performed in rodent fibroblasts, STAT3 activation has been demonstrated to be both required and sufficient to mediate cellular transformation.
This is of key interest as a previous study already had demonstrated that constitutively activated STAT3 can mediate cellular transformation (Bromberg et al, 1999).
Mutated Ras can mediate cellular transformation through a network of signal-transduction pathways independent of upstream RTK activation (Malumbres and Barbacid, 2003).
Nuclear PIM1 has been proposed to be more potent in mediating cellular transformation, at least in vitro, in solid cancer cell lines (Chen et al, 2009; Peltola et al, 2009).
Other research results have reported on the significance of the viral oncoprotein E6 from HR-HPVs in mediating cellular transformation, supporting tumorigenesis, interfering with epithelial organization, and activating telomerase.
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