Cellular functions which are influenced by c Biology Diagrams A large body of physiological evidence shows that either upregulation or downregulation of intracellular c-Myc activity has profound consequences on cell cycle progression. Recent work suggests An indirect proof of the role of Myc in cell cycle progression is the fact that Mxd proteins (Mxd1, Mxi1, Mxd3, Mxd4 and Mnt), which bind to Myc-binding sites and antagonize Myc transcriptional activity, inhibit cell proliferation (reviewed in [80], [81], [82]). Cell cycle arrest is also observed upon the enforced expression of MadMyc, a Induction of cell proliferation by promoting G 1 to S-phase transition during cell cycle progression is one of Myc's best characterized functions, a feature linked to its pro‐oncogenic
Effects of c-myc expression on cell cycle progression. K D Hanson. K D Hanson. 1 Department of Molecular Biophysics, Yale University School of Medicine, New Dean M., Sonenshein G. E. Cell-cycle control of c-myc but not c-ras expression is lost following chemical transformation. Cell. 1984 Feb;36(2):241-247. doi: 10.1016/0092-8674(84)90217
Cdk6 Activity but Affects Cell Cycle ... Biology Diagrams
The timing of cyclin E induction was the earliest observable effect of reduced Myc expression. Our data indicate that Myc contributes to regulation of proliferation by a cell-autonomous mechanism that involves the modulation of cyclin E expression and, consequently, progression through the restriction point of the cell cycle. We further show that heterogeneity in c-Myc dynamics leads to variable target gene transcription and that timing of c-Myc expression predicts cell-cycle progression rates and drug sensitivities. Together, our data advocate for a model in which cancer cells increase the heterogeneity of functionally diverse transcription factors such as c-Myc to
In the present study, a c‑Myc‑knockdown model (Raji‑KD) was established using Raji cells, and it was indicated that c‑Myc regulates the expression of genes associated with cell cycle progression in G2/M‑phase, cyclin D kinase (CDK)1 and cyclin B1, by modulating 60 kDa Tat‑interactive protein (TIP60)/males absent on the first (MOF c-Myc affects cell cycle progression at multiple independent points. It is often observed that a single primary regulatory defect can elicit pleiotropic phenotypes by a cascade of downstream effects. For example, c-Myc could act primarily at the point of Cdk4 and -6 activation but cause more generalized effects by interfering with the
