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Fig. 2 | BMC Systems Biology

Fig. 2

From: Differentiation resistance through altered retinoblastoma protein function in acute lymphoblastic leukemia: in silico modeling of the deregulations in the G1/S restriction point pathway

Fig. 2

G1/S restriction point alterations and deregulations in BCP-ALL. In contrast with the normal cell cycle pathway (Fig. 1), Cyclin D:Cdk4,6 complexes except for hypo-phosphorylating pRb may also lead the protein to an intermediate phosphorylation status (termed “pseudo-hyper-phosphorylated”) which retains the ability to inhibit E2F transcription factors, although its phosphorus content is increased. This version of the protein is believed to have lost differentiation related functions [32], therefore its accumulation implies that the cell resides at or beyond the restriction point. Only when Cyclin E:Cdk2 and Cyclin A:Cdk1,2 complexes are activated, could the hypo-phosphorylated and pseudo-hyper-phosphorylated versions of the protein become hyper-phosphorylated and consequently liberate E2F transcription factors. The metabolism-mediated activation of these complexes is believed to exhibit differential time-course among patients due to differences in metabolism rates

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