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首页> 外文期刊>Developmental biology >Involvement of cAMP-dependent protein kinase and protein phosphorylation in regulation of mouse oocyte maturation☆
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Involvement of cAMP-dependent protein kinase and protein phosphorylation in regulation of mouse oocyte maturation☆

机译:cAMP依赖性蛋白激酶和蛋白磷酸化参与小鼠卵母细胞成熟的调控☆

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Wereporttheresultsofexperimentswhichsupportthehypothesisthat,inmouseoocytes,adecreaseinintraoocytecyclicAMP(cAMP)initiatesmeioticmaturation;oocytesmicroinjectedwithcyclicnucleotidephosphodiesterase(PDE)underwentgerminalvesiclebreakdown(GVBD)inthepresenceof3-isobutyl-1-methylxanthine(IBMX),whichinhibitedGVBDbothinoocytesnotinjectedwithPDEandinoocytesinjectedwithheat-inactivatedPDE.CyclicAMP-dependentproteinkinase(PK)hasbeenproposedtomediatemaintenanceofmeioticarrestbycAMP.Insupportofthishypothesisistheobservationthat2a€2-deoxycAMP,whichdoesnotactivatePK,didnotmaintainmeioticarrestasdidcAMP;thisresultwasobtainedbothbymicroinjectionofthesecompoundsandbyincubatingoocytesinthepresenceoftheirmembrane-permeableN6-monobutyrylderivatives.Furthermore,microinjectionintooocytesoftheheat-stableinhibitorofPK,PKI,inducedGVBDinthepresenceofeitherdibutyrylcAMP(dbcAMP)orIBMX.MeioticarrestwasmaintainedintheabsenceofdbcAMPorIBMX,however,bymicroinjectedcatalyticsubunitofPK,butnotbycatalyticsubunitcoinjectedwithPKI.Inaddition,specificchangesinoocytephosphoproteinsthatprecededresumptionofmeiosiswereinduced,inthepresenceofdbcAMP,bymicroinjectedPKI;thesechangeswerealsotightlycoupledwithcommitmentofoocytestoresumemeiosis.Theseresultsarediscussedintermsofourmodelforregulationofmeioticarrestandmaturation.
机译:Wereporttheresultsofexperimentswhichsupportthehypothesisthat,inmouseoocytes,adecreaseinintraoocytecyclicAMP(cAMP)的initiatesmeioticmaturation; oocytesmicroinjectedwithcyclicnucleotidephosphodiesterase(PDE)underwentgerminalvesiclebreakdown(GVBD)inthepresenceof3异丁基-1-甲基黄嘌呤(IBMX),whichinhibitedGVBDbothinoocytesnotinjectedwithPDEandinoocytesinjectedwithheat-inactivatedPDE.CyclicAMP-dependentproteinkinase(PK)hasbeenproposedtomediatemaintenanceofmeioticarrestbycAMP.Insupportofthishypothesisistheobservationthat2a€2- deoxycAMP,whichdoesnotactivatePK,didnotmaintainmeioticarrestasdidcAMP ; thisresultwasobtainedbothbymicroinjectionofthesecompoundsandbyincubatingoocytesinthepresenceoftheirmembrane-permeableN6-monobutyrylderivatives.Furthermore,microinjectionintooocytesoftheheat-stableinhibitorofPK,PKI,inducedGVBDinthepresenceofeitherdibutyrylcAMP(dbcAMP)orIBMX.MeioticarrestwasmaintainedintheabsenceofdbcAMPorIBMX然而,bymicroinjectedcatalyticsubunitofPK,butnotbycatalyticsubunitcoinjecte此外,在微束注射的PKI的存在下,在dbcAMP的存在下,诱导了减数分裂恢复之前的特定的细胞变体磷酸化蛋白的改变;这些变化实际上紧密地结合了卵母细胞存储减数分裂的承诺。讨论了如何调整减数分裂的方法。

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