Nuclear regulations are a subset of social regulations (laws to control activities that may negatively impact the environment, health, and safety) that concern control of ionizing radiation from radiation-producing equipment and from radioactive materials.
The set of all candidate regulations is therefore E = (t, g ), g ∈ G, t ∈ T g, and the GRN inference problem is to identify a subset of true regulations among E. For that purpose, we assume we have gene expression measurements for all genes G in n experimental conditions.
Our observations suggest that, for a subset of genes, regulation after de novo DNA methylation in the early embryo may be sensitive to genistein.
Similarly, a network has a prohibited phenotype P with respect to a set of initial states if every subset S of regulation functions that has probability ≥α does not generate any trajectory that leads to P. A naïve way to test for a probabilistic phenotype would be to repeat the non-probabilistic algorithm for every set of regulation functions with probability >α.
Given a parameter α, 0 ≤ α ≤ 1, the definition of a phenotype can now be extended as follows: A network has a phenotype P with respect to a set of initial states if every subset S of regulation functions that has probability ≥α generates only trajectories that remain in P. Note that if the condition holds for S it will hold also for every S' ⊆ S, which can have higher probability.
Further, immunoblot analysis was employed to confirm the androgen-regulation of a subset of up-regulated proteins (Figure 3A).
The disruption of the regulation of this subset of senescence-regulated genes in the gpc mutants is likely sufficient to generate bottlenecks in the senescence process, as demonstrated by the overall delay in senescence observed in these mutant genotypes.
The mammalian target of Rapamycin (mTOR) kinase plays a key role in translational control of a subset of mRNAs through regulation of its initiation step.
From a basic research perspective, microarray expression profiles can help tease apart the complex interactions that underlie the development of a disease by implicating a subset of genes whose regulation is altered with the disease.
Taken together, these results suggest that ZBTB16 regulated Atg14L degradation is a common downstream mechanism by which multiple signaling pathways that are activated by at least a subset of GPCRs in regulation of autophagy.
