High impact information on MGC76039

• In Xenopus oocytes, polyadenylation of dormant mRNAs, including cyclin B1, is controlled by the cis-acting cytoplasmic polyadenylation element (CPE) and hexanucleotide AAUAAA through associations with CPEB and CPSF, respectively [1].
• We have previously shown that Xenopus cyclin B1 has five sites of Ser phosphorylation, four of which map to a recently identified cytoplasmic retention signal (CRS) [2].
• Microtubule-associated protein (MAP) kinase from Xenopus eggs phosphorylated cyclin B1 significantly at Ser-94 or Ser-96, whereas it was largely inactive against cyclin B2 [3].
• We report here that phosphorylation of a single serine residue (Ser(113) of Xenopus cyclin B1) abrogates nuclear export of cyclin B1 [4].
• The second paradigm concerns the regulation of cyclin B1 translation in Xenopus oocytes by a protein called Maskin, which purportedly interacts with initiation factors [5].

Biological context of MGC76039

• Microinjection of Xenopus oocytes with in vitro-synthesized RNAs encoding Xenopus cyclin B1 or cyclin B2 induces the progression of meiosis, characterized by germinal vesicle breakdown (GVBD) [6].
• Degradation of cyclin B via ubiquitin-proteasome pathway seemed to be absolutely required for the M-phase exit [7].
• To test the hypothesis that the delays in mitotic entry in CSF extracts were due to increases in cyclin B thresholds, we employed interphase extracts, which are driven into mitosis by the addition of recombinant cyclin B in a nonlinear (threshold) dose-response [8].
• However, inhibition of the proteasome proteolytic activity upon the exit from the meiotic metaphase II-arrest in Xenopus cell-free extract revealed that the proteasome-dependent dissociation of cyclin B from CDK1 is sufficient to inactivate MPF without cyclin B degradation [7].

Associations of MGC76039 with chemical compounds

• Alternatively, the addition of exogenous Aurora-A or Inhibitor-2 lowered the concentration of cyclin B that triggered CDK activation [8].
• Stimulation with progesterone initiates a nontranscriptional signaling pathway that culminates in the activation of Cdc2/cyclin B and reentry into meiosis [9].

References