Polyomaviridae: Diferenzas entre revisións

Describíronse varios mecanismos para regular a transición desde a expresión de xenes temperáns á dos tardíos, como a implicación da proteína LT na represión do [[promotor (xenética)|promotor]] temperán,<ref name=gjoerup_2010 /> a expresión duns ARNm tardíos non terminados con extensións complementarias aos ARNm temperáns,<ref name=iarc /> e a expresión de [[microARN]]s regulatorios.<ref name=iarc />

A expresión de xenes tardíos ten como resultado a acumulación de proteínas da cápside viral no citoplasma da célula hóspede. Os compoñentes da cápside entran no núcleo para encapsidar novo ARN xenómico viral. Os novos virións poden ensamblarse en [[factoría viral|factorías virais]].<ref name=ICTVReport /><ref name=viralzone /> O mecanismo da liberación viral da célula hóspede varías segundo o poliomavirus; algúns expresan proteínas que facilitan a saída da célula, como a [[agnoproteína]] ou a [[VP4]].<ref name=gjoerup_2010 /> Nalgúns casos, os altos niveis de virus encapsulados causan a [[lise]] da célula, liberándose os virións.<ref name=iarc />

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The [[large tumor antigen]] plays a key role in regulating the viral life cycle by binding to the viral origin of DNA replication where it promotes DNA synthesis. Also as the polyomavirus relies on the host cell machinery to replicate the host cell needs to be in s-phase for this to begin. Due to this, large T-antigen also modulates cellular signaling pathways to stimulate progression of the cell cycle by binding to a number of cellular control proteins.<ref>{{cite journal | vauthors = White MK, Gordon J, Reiss K, Del Valle L, Croul S, Giordano A, Darbinyan A, Khalili K | title = Human polyomaviruses and brain tumors | journal = Brain Research. Brain Research Reviews | volume = 50 | issue = 1 | pages = 69–85 | date = December 2005 | pmid = 15982744 | doi = 10.1016/j.brainresrev.2005.04.007 }}</ref> This is achieved by a two prong attack of inhibiting tumor suppressing genes p53 and members of the [[retinoblastoma protein|retinoblastoma]] (pRB) family,<ref>{{cite journal | vauthors = Kazem S, van der Meijden E, Wang RC, Rosenberg AS, Pope E, Benoit T, Fleckman P, Feltkamp MC | title = Polyomavirus-associated Trichodysplasia spinulosa involves hyperproliferation, pRB phosphorylation and upregulation of p16 and p21 | journal = PLOS One | volume = 9 | issue = 10 | pages = e108947 | year = 2014 | pmid = 25291363 | pmc = 4188587 | doi = 10.1371/journal.pone.0108947 | bibcode = 2014PLoSO...9j8947K }}</ref> and stimulating cell growth pathways by binding cellular DNA, ATPase-helicase, DNA polymerase α association, and binding of transcription preinitiation complex factors.<ref>{{cite journal | vauthors = Kelley WL, Georgopoulos C | title = The T/t common exon of simian virus 40, JC, and BK polyomavirus T antigens can functionally replace the J-domain of the Escherichia coli DnaJ molecular chaperone | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 94 | issue = 8 | pages = 3679–84 | date = April 1997 | pmid = 9108037 | pmc = 20500 | doi = 10.1073/pnas.94.8.3679 | bibcode = 1997PNAS...94.3679K }}</ref> This abnormal stimulation of the cell cycle is a powerful force for oncogenic transformation.