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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.
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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.
Moreover, these pathways activate the AR through phosphorylation in the absence of the androgen ligand, thus promoting further cellular growth without androgen stimulation.
We will consider mutual inhibition, with each pathway inhibiting the other, or mutual activation, with each pathway activating the other.
Upregulation of PPARG expression is induced during mitotic arrest very early in adipose differentiation and stimulates the adipogenic pathway, activating the transcription of other adipose-specific genes [32] [34].
It ultimately activates an intracellular signal transduction pathway activating the Gli (GLIoma-associated oncogene homolog) family of transcription factors.
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