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Induction of citrullination by EGF has not previously been reported and our lab is currently working to understand the up- and downstream signaling pathways that mediate this increase in PAD2 and its catalytic activity.
How can LTP mediate this increase in the number of TC axons contacting each cell?
While the SVZ expands we do not fully understand the mechanisms that mediate this increase.
Subsequent studies therefore sought to identify the gene sequences that are required to mediate this increase in transcription rate.
Increased numbers of OCPs have been reported in the peripheral blood of mice in several animal models of arthritis [ 4, 5] and in patients with arthritis [ 3], but the mechanisms that mediate this increase have not been elucidated.
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LSCC cells harbouring wild-type p53 were significantly radiosensitised by Nutlin-3 (P<0.0001; log-rank scale), and displayed increased cell cycle arrest and significantly increased senescence (P<0.001) in the absence of increased apoptosis; thus, our data suggest that senescence may mediate this increased radiosensitivity.
Although this may not be useful as a predictor in terms of public health policy, it could have implications due to the known link between male gender and likelihood of developing conduct disorder [ 14]; it could be that parenting behaviours mediate this increased risk.
It has been unclear whether driver experience with ACC mediates this increase.
Indeed, inhibition of this response to 4-HPR by FB1 and myriocin indicates a stimulatory action on the de novo synthesis pathways of ceramide production as the mechanism mediating this increase in ceramide levels.
Although the precise mechanisms mediating this increase are still topics of active investigation, numerous studies suggest that at least some of the regulatory elements for the reactive response lie within a 2.2 kb fragment of the 5′ region of the gene.
Further, we identify a key role for Rac1 signalling in mediating this increased N-Cadherin expression.
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