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Glucose deprivation induces oxidative stress and reactive oxygen species (ROS) and this may activate the MAP kinases p38 and/or JNK [ 32, 33].
This may activate a response in which the cancer cell shifts from using ER stress signaling as a survival mechanism to an apoptotic one.
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Recently, RNA sequences derived from the HIV-1 genome have been shown to induce activation via interactions with TLR 7/8 [19], [19] and this interaction may activate T cell populations indirectly [20].
This sensitivity may activate neural resources to understand the parameters of the ambiguity (OFC and insula activities) and the outcome of previous actions (OFC activity) in order to modulate value assignment so as to make a beneficial decision.
This domain may activate cell motility though its intracytoplasmic domain by associating with the cytoskeleton.
This complex may activate transcription of RANKL by binding to the C/EBPβ binding motif of the RANKL promoter.
This process may activate transcription in regions where nucleosomes are relaxed and more distant and can silence the regions where chromatin is more compact.
This feeling may activate analytical reasoning in the diagnostic process by stimulating a GP to formulate provisional hypotheses involving potentially serious outcomes.
Thus, the additional ion released from this complex may activate the cell division process in the induced or reprogrammed microspore in tetrads or the microspores.
Since this adipokine may activate chondrocytes but also osteoblasts and acts mainly by modulating NAD synthesis, targeting specifically this Nampt enzymatic activity with the oral compound APO866 may open new therapeutic perspectives in OA.
This motif may activate the AtNCED3 promoter in response to water-deficit stimuli, because base substitutions of this element had negative effects on dehydration-responsive expression (Figs 6 and 7).
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