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Another aging hallmark is deregulated nutrient sensing via the IGF-1/AKT/mTOR axis, an evolutionary conserved growth signaling pathway that integrates nutrient signals to regulate cell growth [48].
The alterations in cell morphology induced by bolA seem to be mediated by a complex pathway that integrates PBP5, PBP6, MreB, and probably other regulators of cell morphology/elongation.
Mammalian target of rapamycyin (mTOR) is a downstream serine/threonine kinase of the PI3K/AKT pathway that integrates signals from the microenvironment such as cytokines, growth factors, and nutriments to regulate multiple cellular processes, including mRNA translation, autophagy, metabolism, growth and survival.
In addition, systems pharmacology analyses of such a pathway that integrates NOTCH, WNT, AD, and apoptosis-related genes suggest magnesium (Mg2+) and rapamycin for further therapeutic exploration in the context of autism; two compounds/drugs that therapeutic use have already been discussed for different AD models.
As PHYA is the predominant phytochrome type in etiolated seedlings, and because the ASN1 misregulated molecular phenotype of cli186 is more pronounced in etiolated seedlings, CLI186 may function as a downstream component of the PHYA pathway that integrates L and C signaling pathways.
In conclusion, Noxa functions in a specific apoptotic pathway that integrates overall nutrient stress, independent from attenuated PI3K/PKB signaling and without clear involvement of autophagy.
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The mechanism that activates these dormant Müller cells is likely to involve pathways that integrate both cell-intrinsic and cell-extrinsic pathways and evidence suggests that Notch and Wnt signaling plays an important role in this regard [13].
Among the intracellular pathways that integrate mechanical and hormonal signals, MEF2 (myocyte enhancer factors-2, members A to D) transcription factors play prominent roles in the regulation of cardiac hypertrophy and remodeling[8], [9], [10].
However, little is known about the signaling pathways that integrate BCR activation with intrinsic TLR4 stimulation.
Using the two datasets, we construct "extended" pathways that integrate intracellular activity with cellular responses using a hybrid logical/data-driven computational approach.
In the present study we set out to test the hypothesis that biological pathways that mediate metal-induced birth defects could be revealed by identifying common signaling pathways that integrate both metal- and development-associated genes.
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