Rabring7 Degrades c-Myc through Complex Formation with MM-1 英文参考文献.docVIP

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Rabring7 Degrades c-Myc through Complex Formation with MM-1 英文参考文献.doc

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Rabring7 Degrades c-Myc through Complex Formation with MM-1 英文参考文献

Rabring7Degradesc-MycthroughComplexFormation withMM-1 RinaNarita1.,HirotakeKitaura2.,AyakoTorii2,ErikaTashiro2,MakotoMiyazawa2,HiroyoshiAriga2*, SanaeM.M.Iguchi-Ariga1* 1GraduateSchoolofAgriculture,HokkaidoUniversity,Sapporo,Japan,2GraduateSchoolofPharmaceuticalSciences,HokkaidoUniversity,Sapporo,Japan Abstract Wehavereportedthat anovel c-Myc-bindingprotein,MM-1,repressed E-box-dependenttranscriptionandtransforming activitiesofc-MycandthatamutationofA157RinMM-1,whichisoftenobservedinpatientswithleukemiaorlymphoma, abrogatedalloftherepressiveactivitiesofMM-1towardc-Myc,indicatingthatMM-1isanoveltumorsuppressor.MM-1 also binds totheubiquitin-proteasome system, leadingtodegradation of c-Myc.Inthis study, weidentified Rabring7, a Rab7-binding and RING finger-containing protein, as an MM-1-binding protein, and we found that Rabring7 mono- ubiquitinated MM-1 in the cytoplasm without degradation of MM-1. Rabring7 was also found to bind to c-Myc and to ubiquitinatec-Mycinathreonine58-dependentmanner.Whenc-Mycwasco-transfectedwithMM-1andRabring7,c-Myc was degraded. Furthermore, it was found that c-Myc was stabilized in MM-1-knockdown cells even when Rabring7 was transfected andthat Rabring7wasboundtoandco-localizedwithMM-1andc-MycafterMM-1andRabring7hadbeen translocated from the cytoplasm to the nucleus. These results suggest that Rabring7 stimulates c-Myc degradation via mono-ubiquitinationofMM-1. Citation: Narita R, Kitaura H, Torii A, Tashiro E, MiyazawaM, et al. (2012) Rabring7 Degrades c-Myc through Complex Formation with MM-1. PLoS ONE 7(7): e41891.doi:10.1371/journal.pone.0041891 Editor:ArunRishi,WayneStateUniversity,UnitedStatesofAmerica ReceivedFebruary21,2012;AcceptedJune29,2012;PublishedJuly23,2012 Copyright: ? 2012 Narita et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited. Funding: Th