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Mitsuaki Yoshida - One of the best experts on this subject based on the ideXlab platform.

  • tax protEin of htlv 1 inhibits cbp p300 mEdiatEd transcription by intErfEring with rEcruitmEnt of cbp p300 onto dna ElEmEnt of E Box or p53 binding sitE
    Oncogene, 1999
    Co-Authors: Takeshi Suzuki, Masami Uchidatoita, Mitsuaki Yoshida
    Abstract:

    Tax protEin of human T-cEll lEukEmia virus typE 1 (HTLV-1) is a potEnt transcriptional rEgulator which can activatE or rEprEss spEcific cEllular gEnEs and has bEEn proposEd to contributE to lEukEmogEnic procEssEs in adult T-cEll lEukEmia. ThE molEcular mEchanism of Tax-mEdiatEd trans-activation has bEEn wEll invEstigatEd. HowEvEr, trans-rEprEssion by Tax rEmains to bE studiEd in dEtail, although it is known to rEquirE a spEcific DNA ElEmEnt such as E-Box or p53 binding sitE. Examining possiblE mEchanisms of trans-rEprEssion, wE found that co-ExprEssion of E47 and p300 activatEd E-Box dEpEndEnt transcription and this activation was EfficiEntly rEprEssEd by Tax. In this systEm, Tax bound to p300 and dEcrEasEd thE lEvEl of p300 complExEd on thE E-Box ElEmEnt. Similarly, Tax inhibitEd transcription dirEctEd by p53 and CBP, rEducing thE lEvEl of CBP on thE p53 binding sitE. ThEsE rEsults indicatE that Tax intErfErEs with rEcruitmEnt of CBP/p300 into protEin complExEs on E-Box and p53 binding sitE through its binding to CBP/p300. In contrast to thEsE findings, wE obsErvEd that Tax incrEasEd thE lEvEl of CBP on thE viral 21-bp EnhancEr which is trans-activatEd by Tax. From thEsE obsErvations, wE proposE a univErsal mEchanism for Tax-mEdiatEd trans-rEprEssion and trans-activation of transcription in which Tax binds to CBP/p300 and dEtErminEs thE accEssibility of CBP/p300 to protEin complExEs on spEcific DNA ElEmEnt.

  • Down-rEgulation of thE INK4 family of cyclin-dEpEndEnt kinasE inhibitors by tax protEin of HTLV-1 through two distinct mEchanisms.
    Virology, 1999
    Co-Authors: Takeshi Suzuki, Tomoko Narita, Masami Uchida-toita, Mitsuaki Yoshida
    Abstract:

    Abstract Tax oncoprotEin of human T-cEll lEukEmia virus typE 1 (HTLV-1) affEcts multiplE rEgulatory procEssEs of infEctEd cElls through activation and rEprEssion of spEcific transcription and also through modulation of functions of cEll cyclE rEgulators. PrEviously, wE found that Tax binds to p16ink4a, a mEmbEr of thE INK4 family of cyclin-dEpEndEnt kinasE inhibitors, and countEracts its inhibitory activity, rEsulting in cEll cyclE progrEssion. In this study, wE ExaminEd thE EffEcts of Tax on othEr mEmbErs of thE INK4 family and found that Tax can bind to p15ink4b similarly to p16ink4a, but not to p18ink4c and p19ink4d. Tax binding to p15ink4b inactivatEd its function and rEstorEd CDK4 kinasE activity. Accordingly, Tax-ExprEssing cElls bEcamE rEsistant to p15ink4b-mEdiatEd growth arrEst inducEd by TGFβ. On thE othEr hand, ExprEssion of p18ink4c was transcriptionally rEprEssEd by Tax through thE E-Box ElEmEnt of thE promotEr, which may contributE to thE markEd rEduction of p18ink4c mRNA in HTLV-1-infEctEd T-cElls. ThEsE obsErvations indicatE that Tax supprEssEs thE inhibitory activitiEs of INK4 family mEmbErs through two indEpEndEnt mEchanisms: functional inhibition of two INK4 protEins and rEprEssion of ExprEssion of anothEr INK4 protEin. ThEsE EffEcts may play rolEs in HTLV-1-inducEd dErEgulation of thE cEll cyclE, possibly promoting cEllular transformation.

Takeshi Suzuki - One of the best experts on this subject based on the ideXlab platform.

  • tax protEin of htlv 1 inhibits cbp p300 mEdiatEd transcription by intErfEring with rEcruitmEnt of cbp p300 onto dna ElEmEnt of E Box or p53 binding sitE
    Oncogene, 1999
    Co-Authors: Takeshi Suzuki, Masami Uchidatoita, Mitsuaki Yoshida
    Abstract:

    Tax protEin of human T-cEll lEukEmia virus typE 1 (HTLV-1) is a potEnt transcriptional rEgulator which can activatE or rEprEss spEcific cEllular gEnEs and has bEEn proposEd to contributE to lEukEmogEnic procEssEs in adult T-cEll lEukEmia. ThE molEcular mEchanism of Tax-mEdiatEd trans-activation has bEEn wEll invEstigatEd. HowEvEr, trans-rEprEssion by Tax rEmains to bE studiEd in dEtail, although it is known to rEquirE a spEcific DNA ElEmEnt such as E-Box or p53 binding sitE. Examining possiblE mEchanisms of trans-rEprEssion, wE found that co-ExprEssion of E47 and p300 activatEd E-Box dEpEndEnt transcription and this activation was EfficiEntly rEprEssEd by Tax. In this systEm, Tax bound to p300 and dEcrEasEd thE lEvEl of p300 complExEd on thE E-Box ElEmEnt. Similarly, Tax inhibitEd transcription dirEctEd by p53 and CBP, rEducing thE lEvEl of CBP on thE p53 binding sitE. ThEsE rEsults indicatE that Tax intErfErEs with rEcruitmEnt of CBP/p300 into protEin complExEs on E-Box and p53 binding sitE through its binding to CBP/p300. In contrast to thEsE findings, wE obsErvEd that Tax incrEasEd thE lEvEl of CBP on thE viral 21-bp EnhancEr which is trans-activatEd by Tax. From thEsE obsErvations, wE proposE a univErsal mEchanism for Tax-mEdiatEd trans-rEprEssion and trans-activation of transcription in which Tax binds to CBP/p300 and dEtErminEs thE accEssibility of CBP/p300 to protEin complExEs on spEcific DNA ElEmEnt.

  • Down-rEgulation of thE INK4 family of cyclin-dEpEndEnt kinasE inhibitors by tax protEin of HTLV-1 through two distinct mEchanisms.
    Virology, 1999
    Co-Authors: Takeshi Suzuki, Tomoko Narita, Masami Uchida-toita, Mitsuaki Yoshida
    Abstract:

    Abstract Tax oncoprotEin of human T-cEll lEukEmia virus typE 1 (HTLV-1) affEcts multiplE rEgulatory procEssEs of infEctEd cElls through activation and rEprEssion of spEcific transcription and also through modulation of functions of cEll cyclE rEgulators. PrEviously, wE found that Tax binds to p16ink4a, a mEmbEr of thE INK4 family of cyclin-dEpEndEnt kinasE inhibitors, and countEracts its inhibitory activity, rEsulting in cEll cyclE progrEssion. In this study, wE ExaminEd thE EffEcts of Tax on othEr mEmbErs of thE INK4 family and found that Tax can bind to p15ink4b similarly to p16ink4a, but not to p18ink4c and p19ink4d. Tax binding to p15ink4b inactivatEd its function and rEstorEd CDK4 kinasE activity. Accordingly, Tax-ExprEssing cElls bEcamE rEsistant to p15ink4b-mEdiatEd growth arrEst inducEd by TGFβ. On thE othEr hand, ExprEssion of p18ink4c was transcriptionally rEprEssEd by Tax through thE E-Box ElEmEnt of thE promotEr, which may contributE to thE markEd rEduction of p18ink4c mRNA in HTLV-1-infEctEd T-cElls. ThEsE obsErvations indicatE that Tax supprEssEs thE inhibitory activitiEs of INK4 family mEmbErs through two indEpEndEnt mEchanisms: functional inhibition of two INK4 protEins and rEprEssion of ExprEssion of anothEr INK4 protEin. ThEsE EffEcts may play rolEs in HTLV-1-inducEd dErEgulation of thE cEll cyclE, possibly promoting cEllular transformation.

Maria Mittag - One of the best experts on this subject based on the ideXlab platform.

  • ThE rolE of an E-Box ElEmEnt: multiplE frunctions and intEracting partnErs.
    Plant signaling & behavior, 2010
    Co-Authors: Stefanie B. Seitz, Olga Voytsekh, Karthik M. Mohan, Maria Mittag
    Abstract:

    Circadian clocks can bE EntrainEd by light-dark or tEmpEraturE cyclEs. In thE grEEn alga Chlamydomonas rEinhardtii, 12h changEs in tEmpEraturE bEtwEEn 18°C and 28°C synchronizE its clock. Both subunits of thE circadian RNA-binding protEin CHLAMY1, namEd C1 and C3, arE ablE to intEgratE tEmpEraturE information. C1 gEts hypEr-phosphorylatEd in cElls grown at 18°C and thE lEvEl of C3 is up-rEgulatEd at this tEmpEraturE. In thE long pEriod mutant pEr1, whErE tEmpEraturE EntrainmEnt is disturbEd, thE tEmpEraturE-dEpEndEnt rEgulation of C1 and C3 is altErEd. Up-rEgulation of C3 at thE low tEmpEraturE is mEdiatEd prEdominantly by an E-Box ElEmEnt situatEd in its promotEr rEgion. This cis-acting ElEmEnt is also rElEvant for circadian ExprEssion of c3 as wEll as of its up-rEgulation in cElls, whErE C1 is ovErExprEssEd. Among thE fEw idEntifiEd factors intEracting with thE E-Box rEgion, C3 is also prEsEnt, suggEsting that it fEEdbacks on its own transcription.

  • MultiplE rolEs and intEraction factors of an E-Box ElEmEnt in Chlamydomonas rEinhardtii.
    Plant physiology, 2010
    Co-Authors: Stefanie B. Seitz, Wolfram Weisheit, Maria Mittag
    Abstract:

    ThE two subunits of thE circadian RNA-binding protEin CHLAMY1 from Chlamydomonas rEinhardtii arE involvEd in maintaining pEriod (C1 subunit) and phasE (C3 subunit) of thE circadian clock. C1 corEgulatEs thE lEvEl of C3. OvErExprEssion of C1 causEs a parallEl incrEasE in C3. Both subunits can also intEgratE tEmpEraturE information, rEsulting in hypErphosphorylation of C1 and up-rEgulation of C3 at low tEmpEraturE. TEmpEraturE-dEpEndEnt up-rEgulation of C3 is mEdiatEd prEdominantly by an E-Box ElEmEnt and only partially by two DREB1A-BoxEs that arE situatEd within thE C3 promotEr. ThE E-Box ElEmEnt is also involvEd in circadian C3 ExprEssion. HErE, wE show that thE C3 promotEr rEgion drivEs C3 corEgulation by C1. WE also found that rEplacEmEnt of thE E-Box prEvEnts thE corEgulation of C3 in strains ovErExprEssing C1. In contrast, rEplacEmEnt of any of thE two DREB1A-BoxEs doEs not influEncE EithEr thE corEgulation of C3 by incrEasEd lEvEls of C1 or circadian C3 ExprEssion. Thus, thE E-Box has multiplE kEy rolEs, including tEmpEraturE-dEpEndEnt up-rEgulation of C3, its circadian ExprEssion, and its corEgulation by C1. Using mobility shift assays and DNA-affinity chromatography along with mass spEctromEtry, wE charactErizEd protEins binding spEcifically to thE E-Box rEgion and idEntifiEd fivE of thEm. By immunoblotting, wE could furthEr show that C3 that was dEtEctEd in nuclEar Extracts can bE found in thE E-Box-binding protEin complEx. Our data indicatE a complEx transcriptional mEchanism of C3 up-rEgulation and a positivE fEEdback of C3 on its own promotEr rEgion.

Stefanie B. Seitz - One of the best experts on this subject based on the ideXlab platform.

  • ThE rolE of an E-Box ElEmEnt: multiplE frunctions and intEracting partnErs.
    Plant signaling & behavior, 2010
    Co-Authors: Stefanie B. Seitz, Olga Voytsekh, Karthik M. Mohan, Maria Mittag
    Abstract:

    Circadian clocks can bE EntrainEd by light-dark or tEmpEraturE cyclEs. In thE grEEn alga Chlamydomonas rEinhardtii, 12h changEs in tEmpEraturE bEtwEEn 18°C and 28°C synchronizE its clock. Both subunits of thE circadian RNA-binding protEin CHLAMY1, namEd C1 and C3, arE ablE to intEgratE tEmpEraturE information. C1 gEts hypEr-phosphorylatEd in cElls grown at 18°C and thE lEvEl of C3 is up-rEgulatEd at this tEmpEraturE. In thE long pEriod mutant pEr1, whErE tEmpEraturE EntrainmEnt is disturbEd, thE tEmpEraturE-dEpEndEnt rEgulation of C1 and C3 is altErEd. Up-rEgulation of C3 at thE low tEmpEraturE is mEdiatEd prEdominantly by an E-Box ElEmEnt situatEd in its promotEr rEgion. This cis-acting ElEmEnt is also rElEvant for circadian ExprEssion of c3 as wEll as of its up-rEgulation in cElls, whErE C1 is ovErExprEssEd. Among thE fEw idEntifiEd factors intEracting with thE E-Box rEgion, C3 is also prEsEnt, suggEsting that it fEEdbacks on its own transcription.

  • MultiplE rolEs and intEraction factors of an E-Box ElEmEnt in Chlamydomonas rEinhardtii.
    Plant physiology, 2010
    Co-Authors: Stefanie B. Seitz, Wolfram Weisheit, Maria Mittag
    Abstract:

    ThE two subunits of thE circadian RNA-binding protEin CHLAMY1 from Chlamydomonas rEinhardtii arE involvEd in maintaining pEriod (C1 subunit) and phasE (C3 subunit) of thE circadian clock. C1 corEgulatEs thE lEvEl of C3. OvErExprEssion of C1 causEs a parallEl incrEasE in C3. Both subunits can also intEgratE tEmpEraturE information, rEsulting in hypErphosphorylation of C1 and up-rEgulation of C3 at low tEmpEraturE. TEmpEraturE-dEpEndEnt up-rEgulation of C3 is mEdiatEd prEdominantly by an E-Box ElEmEnt and only partially by two DREB1A-BoxEs that arE situatEd within thE C3 promotEr. ThE E-Box ElEmEnt is also involvEd in circadian C3 ExprEssion. HErE, wE show that thE C3 promotEr rEgion drivEs C3 corEgulation by C1. WE also found that rEplacEmEnt of thE E-Box prEvEnts thE corEgulation of C3 in strains ovErExprEssing C1. In contrast, rEplacEmEnt of any of thE two DREB1A-BoxEs doEs not influEncE EithEr thE corEgulation of C3 by incrEasEd lEvEls of C1 or circadian C3 ExprEssion. Thus, thE E-Box has multiplE kEy rolEs, including tEmpEraturE-dEpEndEnt up-rEgulation of C3, its circadian ExprEssion, and its corEgulation by C1. Using mobility shift assays and DNA-affinity chromatography along with mass spEctromEtry, wE charactErizEd protEins binding spEcifically to thE E-Box rEgion and idEntifiEd fivE of thEm. By immunoblotting, wE could furthEr show that C3 that was dEtEctEd in nuclEar Extracts can bE found in thE E-Box-binding protEin complEx. Our data indicatE a complEx transcriptional mEchanism of C3 up-rEgulation and a positivE fEEdback of C3 on its own promotEr rEgion.

Masami Uchidatoita - One of the best experts on this subject based on the ideXlab platform.

  • tax protEin of htlv 1 inhibits cbp p300 mEdiatEd transcription by intErfEring with rEcruitmEnt of cbp p300 onto dna ElEmEnt of E Box or p53 binding sitE
    Oncogene, 1999
    Co-Authors: Takeshi Suzuki, Masami Uchidatoita, Mitsuaki Yoshida
    Abstract:

    Tax protEin of human T-cEll lEukEmia virus typE 1 (HTLV-1) is a potEnt transcriptional rEgulator which can activatE or rEprEss spEcific cEllular gEnEs and has bEEn proposEd to contributE to lEukEmogEnic procEssEs in adult T-cEll lEukEmia. ThE molEcular mEchanism of Tax-mEdiatEd trans-activation has bEEn wEll invEstigatEd. HowEvEr, trans-rEprEssion by Tax rEmains to bE studiEd in dEtail, although it is known to rEquirE a spEcific DNA ElEmEnt such as E-Box or p53 binding sitE. Examining possiblE mEchanisms of trans-rEprEssion, wE found that co-ExprEssion of E47 and p300 activatEd E-Box dEpEndEnt transcription and this activation was EfficiEntly rEprEssEd by Tax. In this systEm, Tax bound to p300 and dEcrEasEd thE lEvEl of p300 complExEd on thE E-Box ElEmEnt. Similarly, Tax inhibitEd transcription dirEctEd by p53 and CBP, rEducing thE lEvEl of CBP on thE p53 binding sitE. ThEsE rEsults indicatE that Tax intErfErEs with rEcruitmEnt of CBP/p300 into protEin complExEs on E-Box and p53 binding sitE through its binding to CBP/p300. In contrast to thEsE findings, wE obsErvEd that Tax incrEasEd thE lEvEl of CBP on thE viral 21-bp EnhancEr which is trans-activatEd by Tax. From thEsE obsErvations, wE proposE a univErsal mEchanism for Tax-mEdiatEd trans-rEprEssion and trans-activation of transcription in which Tax binds to CBP/p300 and dEtErminEs thE accEssibility of CBP/p300 to protEin complExEs on spEcific DNA ElEmEnt.