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Binding to receptor leads to a conformational change in capsid structure during which the VP4 is externalized.
Poliovirus translation occurs in a cap-independent manner facilitated by the Internal Ribosome Entry Site (IRES).
Poliovirus protease 2A cleaves nuclear pore proteins NUP62 and NUP214, impairing host mRNA export out of the nucleus.
Poliovirus replication proteins localize at membranous vesicles presumably originated from traffic vesicles between endoplasmic reticulum and Golgi apparatus. 3D polymerase and two 3CD subunits bind to the cre and cloverleaf sequences, inducing adi-uridylylation of VPg protein. The poliovirus capsid self assembles into a pseudo T=3 icosahedral capsid, composed of VP0, VP2 and VP3. Genome replication occurs in two phases, first the minus strand is synthesized, which is in turn used as template to produce a lot of positive strand RNA genomes. The cell cycle is an ordered set of events, culminating in cell growth and division into two daughter cells.
Cdk (cyclin dependent kinase, adds phosphate to a protein), along with cyclins, are major control switches for the cell cycle, causing the cell to move from G1 to S or G2 to M.
MPF (Maturation Promoting Factor) includes the CdK and cyclins that triggers progression through the cell cycle. I teach Business full time at the Nova Scotia Community College and part time at Dalhousie, Mount St. The hydrophobic N-termini of five VP4 penetrates into host membrane and creates a pore through which the viral genome penetrates into cell cytoplasm. The IRES is a RNA structure in the 5’UTR of the genomic RNA that promotes translation initiation by recruiting initiation factors and help to place the ribosome on the AUG. It is not clear whether the poliovirus replication complex is outside or inside the vesicle. The modified VPg is then used as primer to replicate genomic RNA, initiating on the polyA tail.

These new genomes can either be encapsidated to join in the cytoplasmic pool of translated genomes, or be encapsidated to form new virions. Upon genomic RNA encapsidation the VP0 matures and is cleaved into VP2 and VP4, maybe by self cleavage.
It would mean that for each replicated RNA, one entire polyprotein has to be synthesized, because there is only one VPg per polyprotein. That represents 60 polyproteins translated to produce a virion, and would mean also 60 polymerases created to get a single virion.
The following terms are some of the features that are important in regulation, and places where errors can lead to cancer.
An extreme case of this is Li Fraumeni syndrome, where a genetic a defect in p53 leads to a high frequency of cancer in affected individuals. Recent research (Nature Medicine 3, 152 (1997)) suggests that breast cancer prognosis is determined by p27 levels. The G1 phase is a critical stage, allowing responses to extracellular cues that induce either commitment to a further round of cell division or withdrawal from the cell cycle (G0) to embark on a differentiation pathway162. It is represented inside here, because this configuration may help to hide the dsRNA replication intermediate. The first round of replication creates a dsRNA which is in turn used for (+) RNA synthesis. This maturation step presumably assures that the membrane pore formation of VP4 is only potentially active within the mature virion, and could prevent early activation in the host cell. The genomes that are encapsidated directly after synthesis keep the VPg in 5’, which may be part of the encapsidation signal. This is a bit unusual in virology, with most viruses over-expressing their structural proteins, but express often few polymerases.
Cancer is a disease where regulation of the cell cycle goes awry and normal cell growth and behavior is lost. Called nuclear division environment suitable may confer substrate specificity upon the instituto.

The G1 phase is also involved in the control of DNA integrity before the onset of DNA replication.
It is possible that the minus strand is separated from the positive strand, but it would require some kind of nucleoprotein to avoid annealing of complementary strand.
Some cardioviruses have been shown to use a ribosomal frameshift to translate only the P1 part of their genome . Between S and M phases is the G2 phase during which the cell checks the completion of DNA replication and the genomic integrity before cell division starts.
It is possible that such a mechanism exist in enterovirus for efficient structural proteins translation.
The transition from one phase of the cell cycle to the next is controlled by cyclin–CDK (cyclin-dependent kinase) complexes which ensure that all phases of the cell cycle are executed in the correct order. The M stage stands for "mitosis", and is when nuclear (chromosomes separate) and cytoplasmic (cytokinesis) division occur. Beyond this point, precursors will invariably complete the cell cycle.Progression through the mitotic cycle is driven by the actions of CDKs and their activating cyclin subunits. The rate of cell-cycle progression is determined by the relative abundance of positive and negative regulators. Work on mutant mice has shown that the overall size of the brain is governed by the molecular machinery of the cell cycle169, 170. Replicationreproduction process of caulobacter crescentus is highly similar to short telomeres. Characterized using cdna microarrays elaborate gene-protein regulatory proteins involved in prokaryotic organisms. Cell-division cycle mutants altered in plants was characterized using cdna microarrays checkpoints.

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