Author: Cooray, Samantha; Jin, Li; Best, Jennifer M
Title: The involvement of survival signaling pathways in rubella-virus induced apoptosis Document date: 2005_1_4
ID: 1i36lsj2_30
Snippet: The phosphorylation of c-myc, a downstream target of ERK1/2, did not follow the same pattern. Levels of phosphorylated c-myc decreased as infection progressed, which was probably due to its targeted degradation or the action of cellular phosphatases. RV infection has been observed to slow cell cycle progression both in vivo and in vitro [12, 34] . As c-myc is a transcription factor that stimulates cell cycle progression, its de-phosphorylation or.....
Document: The phosphorylation of c-myc, a downstream target of ERK1/2, did not follow the same pattern. Levels of phosphorylated c-myc decreased as infection progressed, which was probably due to its targeted degradation or the action of cellular phosphatases. RV infection has been observed to slow cell cycle progression both in vivo and in vitro [12, 34] . As c-myc is a transcription factor that stimulates cell cycle progression, its de-phosphorylation or degradation as RV infection progresses supports these observations. The expression and activity of c-myc and other downstream transcription factors in relation to the cell cycle during RV-infection requires further investigation. Phosphorylation of BAD, downstream of Akt, could not be detected in RV-infected cells (data not shown). However, BAD is not ubiquitously expressed and therefore may not be produced in the rabbit kidney epithelial cells (RK13) used [16] .
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