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The processes considered in the model are the activation of STAT5 by the activated receptor complex EpoR/JAK2, the translocation of cytosolic activated STAT5 to the nucleus, and the deactivation and subsequent translocation of nuclear STAT5 back to the cytoplasm.
The important signaling pathways mediating a hypertrophic phenotype in cardiomyocytes are the activation of G-proteins, phosphoinositide 3-kinase, certain protein kinase C isoforms, mitogen-activated protein kinases, and the calcium-dependent activation of calcineurin [ 5, 12, 21].
The possible mechanisms of the failure of these anti-angiogenic treatments are the activation of alternative angiogenesis pathways involved in expression of bFGF, SDF-1 and VEGF and increased invasiveness of the tumor cells [5], [16], [17].
Consequences are the activation of p53 and the release of cytochrome c from mitochondria, initiating apoptosis.
The probable reasons are the activation of osteoclast cells and the bone matrix degradation.
The interesting reactions from our point of view are the activation of MPF and the subsequent dissociation of this complex.
Similar(44)
(x_{i}(t)) and (y_{j}(t)) are the activations of the ith neuron and the jth neurons, respectively.
The key feature that is common to both types of mental activity is the activation of the medial prefrontal cortex (MPFC 41.
The mechanism appears to be the activation of signal transducer and activator of transcription 1 (STAT1) [ 3].
Another feature of checkpoint signalling is the activation of the apical kinase by activator proteins.
That is, the activation of Area 10 does not require constant, conscious rehearsing of the need to switch tasks.
More suggestions(19)
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