Nanopublications

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_5 label "Selventa" provenance.
large_corpus.bel title "BEL Framework Large Corpus Document" provenance.
large_corpus.bel description "Approximately 61,000 statements." provenance.
large_corpus.bel version "1.4" provenance.
large_corpus.bel authoredBy _5 provenance.
assertion wasDerivedFrom large_corpus.bel provenance.
assertion wasDerivedFrom _4 provenance.
assertion hadPrimarySource 15572689 provenance.
_4 wasQuotedFrom 15572689 provenance.
_4 value "Coordinate regulation of intracellular signaling pathways is central to the ability of mitogens and oncogenes to promote cell cycle progression (24). Two pathways thought to play an important role in committing quiescent cells into S phase are the RAS-activated RAF-MEK-extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3'-kinase (PI3'- kinase)-PDK1-AKT pathways (35, 36). These pathways are reported to influence the expression, activity, or subcellular localization of key components of the cell cycle machinery such as cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors (CKIs) leading to the appropriate activation of E2F transcription factors (50, 51). In addition to sensing the activation of specific signaling pathways, cells are also able to integrate the extent and timing of signal pathway activation and convert that information into an appropriate biological response (32, 48, 64, 66). For example, depending on the level of expression or activation, activated RAS can promote either cellular immortalization, oncogenic transformation, or cell cycle arrest in the same cell type (20, 48, 64, 66). Under these circumstances, RAS (or RAF)-induced cell cycle arrest is mediated by induced expression of CKIs of the INK4 or CIP/KIP family (29, 37). Interestingly, activation of \"parallel\" signaling pathways can modify the ability of RAS to regulate the G0-G1-Sphase cell cycle transition. For example, RAS-induced cell cycle arrest in Swiss 3T3 cells is prevented by coactivation of Rho signaling pathways (9, 43)." provenance.