Genes induced or repressed by TGF-β in MCF-7 CN and MCF-7 H2 cells after 24 h were grouped into broad categories (cell cycle, transcription factor, cytoskeleton) by gene ontology (Table 1).
This was consistent with the observation that the number of S phase cells was reduced in c-Met mutant livers after 36 hr of liver regeneration as cells failed to transit into next S phase providing further support that c-Met deletion has a broad impact on cell cycle progression (Figure 1).
These interactions alter a broad array of cell cycle progression.
HPV16 alters a broad array of cell cycle progression by a number of PPIs.
CDKNIA's involvement further suggests that the broad category of "cell cycle" is likely to be more specifically related to cell cycle arrest, since CDKN1A is a known inhibitor of cell cycle.
These interactions, together with other proteins that bind to HPV16, alter a broad array of cell cycle progression; for example, they block cellular proliferation by causing cell cycle arrest in S-phase [ 12, 50, 51].
The analysis of protein-protein interactions indicated that HPV16 enlarged its scope of influence by interacting with human proteins as much as possible, and these interactions alter a broad array of cell cycle progression.
This broad involvement of cell cycle proteins could explain the incongruence between the large amount of neurons expressing cell cycle markers and the estimated rate of neurodegeneration in AD [ 102, 105], as not all cell cycle proteins should be interpreted as predictors of neuronal cell loss.
Simultaneously, the placement of both pro- and anti-apoptotic proteins within a broader panorama of cell cycle regulation, survival, proliferation and differentiation proteins is critical to exploring the impact of anti-apoptotic factor up-regulation or pro-apoptotic factor down-regulation in cancer.
Generally, all categories were characterized by the majority of genes forming part of the broad terms, apoptosis and cell cycle.
