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We don't even really know why the sensory conflict actually triggers vomiting; it is thought that some neural pathways activate the brain's vomiting centre, believed to be located in the medulla, part of the brain at the top of the spinal cord.
Three biochemical pathways activate the complement system: the classical complement pathway, the alternative complement pathway, and the mannose-binding lectin pathway [14].
Two signal pathways activate the TH1 transcription factor, T-bet.
These pathways activate the transcription factors NF-κB and AP-1.
Both pathways activate the caspase cascade, leading to cleavage of cellular substrates and the morphological and biochemical manifestations of apoptosis.
In particular, the JNK-dependent pathways activate the M1 phenotype transcription factors, but they can also activate the M2 genes transcription factor SMAD3.
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NF-κB is an important transcription factor linked to many signal pathways, activating the expression of various molecules that mediate many biological events including cell survival.
We will consider mutual inhibition, with each pathway inhibiting the other, or mutual activation, with each pathway activating the other.
Based on the previous reports the PI3K/Akt pro-survival pathway activates the anti-apoptotic Bcl-2, thereby preventing the caspase-3 activation [ 9].
Subsequently, the EdaA1/EdaR pathway activates the downstream NF-κB pathway [20].
First, a Ca2+-dependent signaling pathway activates the CICR pathway, which leads to neurotransmitter release in the mechanotransduction process [9], [10], [11].
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