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Dongchon Kang - One of the best experts on this subject based on the ideXlab platform.
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RegulAtion of mitochondriAl D‐loops by trAnscription FActor A And single‐strAnded DNA‐binding protein
EMBO Reports, 2002Co-Authors: Chihiro Takamatsu, Shuyo Umeda, Takashi Ohsato, Atsushi Fukuoh, Naotaka Hamasaki, Tetsuji Ohno, Hideo Shinagawa, Dongchon KangAbstract:During replicAtion, mitochondriAl DNA (mtDNA) tAkes on A triple-strAnded structure cAlled A D-loop. Although their physiologicAl roles Are not understood, D-loops Are implicAted in replicAtion And trAnscription of mtDNA. Little is known About the turnover of D-loops. We investigAted the effects of mitochondriAl trAnscription FActor A (TFAM) And single-strAnded DNA-binding protein (mtSSB) on D-loops. In humAn HeLA cells, TFAM And mtSSB Are, respectively, 1700- And 3000-fold more AbundAnt thAn mtDNA. This level of TFAM is two orders of mAgnitude higher thAn reported previously And is sufficient to wrAp humAn mtDNA entirely. TFAM resolves D-loops in vitro if Added in similAr stoichiometries. mtSSB inhibits the resolution of mtDNA by TFAM but enhAnces resolution by RecG, A junction-specific helicAse from EscherichiA coli. Hence, mtSSB functions in both stAbilizAtion And resolution. We propose thAt TFAM And mtSSB Are cooperAtively involved in stAbilizing D-loops And in the mAintenAnce of mtDNA.
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binding of humAn mitochondriAl trAnscription FActor A An hmg box protein to A four wAy dnA junction
Biochemical and Biophysical Research Communications, 2000Co-Authors: Tetsuji Ohno, Shuyo Umeda, Naotaka Hamasaki, Dongchon KangAbstract:MitochondriAl trAnscription FActor A (mtTFA), the only known trAnscription FActor in mitochondriA, is Also implicAted in mAintenAnce of mitochondriAl genome Although little is elucidAted About its moleculAr bAsis. mtTFA is A member of HMG box proteins fAmily. Some HMG proteins bind with high Affinity to four-wAy DNA junctions thAt mimic A HollidAy structure, A putAtive intermediAte in DNA recombinAtion. To explore possible involvement of A HollidAy-like structure in the mAintenAnce of mitochondriAl genome, we exAmine the binding of recombinAnt humAn mtTFA to A synthetic four-wAy DNA junction. The humAn mtTFA binds to the four-wAy DNA junction with An ApproximAtely 10-fold higher Affinity thAn to the corresponding lineAr duplex DNA And with essentiAlly the sAme Affinity As to A 40-mer DNA contAining the humAn mitochondriAl light strAnd promoter sequence. The mtTFA binds to the four-wAy As A monomer. Both of the two HMG box domAins of humAn mtTFA Are required for the high Affinity binding to the four-wAy junction.
Hossam El Bahaie - One of the best experts on this subject based on the ideXlab platform.
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VAsculAr endotheliAl growth FActor-A mRNA gene expression in clinicAl phAses of multiple sclerosis
Annals of Clinical Biochemistry, 2016Co-Authors: Hoiyda A Abdel Rasol, Hanan Helmy, Sherine El-mously, Margeret A Aziz, Hossam El BahaieAbstract:BAckgroundVAsculAr endotheliAl growth FActor A stimulAtes Angiogenesis, but is Also pro-inflAmmAtory And plAys An importAnt role in the development of neurologicAl diseAse. This study Aimed to investigAte whether vAsculAr endotheliAl growth FActor A mRNA expression could be used As A mArker for the prediction of susceptibility to multiple sclerosis And relAte vAsculAr endotheliAl growth FActor to the clinicAl phAses of multiple sclerosis.MethodsThis wAs A cross-sectionAl study, consisting of A totAl of 60 subjects with multiple sclerosis And 20 heAlthy controls. Subjects were subjected to history tAking, neurologicAl exAminAtion And peripherAl blood sAmpling for vAsculAr endotheliAl growth FActor A mRNA gene expression. VAsculAr endotheliAl growth FActor A gene expression wAs meAsured by reAl-time polymerAse chAin reAction using the SYBR Green technique.ResultsVAsculAr endotheliAl growth FActor A mRNA gene expression level wAs significAntly lower in the multiple sclerosis group thAn in the heAlthy control...
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VAsculAr endotheliAl growth FActor-A mRNA gene expression in clinicAl phAses of multiple sclerosis.
Annals of clinical biochemistry, 2015Co-Authors: Hoiyda A Abdel Rasol, Hanan Helmy, Sherine El-mously, Margeret A Aziz, Hossam El BahaieAbstract:VAsculAr endotheliAl growth FActor A stimulAtes Angiogenesis, but is Also pro-inflAmmAtory And plAys An importAnt role in the development of neurologicAl diseAse. This study Aimed to investigAte whether vAsculAr endotheliAl growth FActor A mRNA expression could be used As A mArker for the prediction of susceptibility to multiple sclerosis And relAte vAsculAr endotheliAl growth FActor to the clinicAl phAses of multiple sclerosis. This wAs A cross-sectionAl study, consisting of A totAl of 60 subjects with multiple sclerosis And 20 heAlthy controls. Subjects were subjected to history tAking, neurologicAl exAminAtion And peripherAl blood sAmpling for vAsculAr endotheliAl growth FActor A mRNA gene expression. VAsculAr endotheliAl growth FActor A gene expression wAs meAsured by reAl-time polymerAse chAin reAction using the SYBR Green technique. VAsculAr endotheliAl growth FActor A mRNA gene expression level wAs significAntly lower in the multiple sclerosis group thAn in the heAlthy control group (P < 0.001). VAsculAr endotheliAl growth FActor A mRNA gene expression level wAs higher in relApsing remitting multiple sclerosis (RRMS) pAtients thAn in those in remission (P < 0.001) And in relApsing remitting multiple sclerosis compAred with secondAry progressive multiple sclerosis (P < 0.001). There wAs no correlAtion between vAsculAr endotheliAl growth FActor A gene expression levels And durAtion of diseAse, multiple sclerosis progression index or expAnded disAbility stAtus scAle. A lower vAsculAr endotheliAl growth FActor A mRNA gene expression level wAs independently AssociAted with A higher risk of multiple sclerosis. © The Author(s) 2015.
Tongcun Zhang - One of the best experts on this subject based on the ideXlab platform.
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vAsculAr endotheliAl growth FActor stimulAtes endotheliAl differentiAtion from mesenchymAl stem cells viA rho myocArdin relAted trAnscription FActor A signAling pAthwAy
The International Journal of Biochemistry & Cell Biology, 2013Co-Authors: Nan Wang, Tongcun Zhang, Rui Zhang, Shuijing Wang, Chunling Zhang, Chunyu Zhuang, Yanyang Tang, Hao ZhouAbstract:MesenchymAl stem cells (MSCs) Are pluripotent progenitors thAt cAn differentiAte into A vAriety of cell types. VAsculAr endotheliAl growth FActor (VEGF) is one of the mAjor FActors of initiAting And regulAting Angiogenesis. It hAs been reported thAt VEGF cAn induce MSCs differentiAted into endotheliAl cells (ECs). However, the mechAnism thAt VEGF-induced MSC differentiAtion is not completely understood. Here, we showed thAt VEGF induced humAn And rAt bone mArrow-derived MSCs differentiAtion to ECs. Rho fAmily plAys An importAnt role in VEGF-induced endotheliAl cell migrAtion And Angiogenesis. Our results indicAted thAt in MSCs, VEGF ActivAted Rho/ROCK signAling pAthwAy And promoted nucleAr trAnslocAtion of myocArdin-relAted trAnscription FActor-A (MRTF-A), which is controlled by Rho/ROCK signAling. In Addition, Rho inhibitor C3 trAnsferAse, ROCK inhibitor Y27632 or depletion of endogenous MRTF-A Abolished the VEGF-induced differentiAtion of MSCs into ECs. Furthermore, VEGF Also enhAnced the expression levels of CYR61/CCN1, As A regulAtor of vAsculAr development And Angiogenesis, And knockdown of endogenous MRTF-A reduced VEGF-induced the upregulAtion of CYR61/CCN1. Report AssAys with site-direct mutAtion AnAlysis of CYR61/CCN1 promoter demonstrAted thAt MRTF-A trAnsActivAted CYR61/CCN1 promoter mAinly depending on CArG box. In this study, we identify the Rho/MRTF-A signAling pAthwAy As A mAin Actor in controlling VEGF-induced differentiAtion of humAn And rAt bone mArrow-derived MSCs into endotheliAl cells.
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MyocArdin-relAted trAnscription FActor-A induces cArdiomyocyte hypertrophy
Iubmb Life, 2011Co-Authors: Xing-hua Liao, Nan Wang, Tongcun ZhangAbstract:MyocArdin is A remArkAbly potent trAnscriptionAl coActivAtor expressed specificAlly in cArdiAc muscle lineAges And smooth muscle cells during postnAtAl development. MyocArdin shAres homology with myocArdin-relAted trAnscription FActor-A (MRTF-A), which Are expressed in A broAd rAnge of embryonic And Adult tissues. Our previous results show thAt myocArdin induces cArdiAc hypertrophy. However, the effects of MRTF-A in cArdiAc hypertrophy remAin poorly understood. Our present work further demonstrAtes thAt myocArdin plAys An importAnt role in inducing hypertrophy. At the sAme time, we find thAt overexpression of MRTF-A in neonAtAl rAt cArdiomyocytes might induce cArdiomyocyte hypertrophy. Furthermore, MRTF-A expression is induced in phenylephrine, Angiotensin-II, And trAnsforming growth FActor-β-stimulAted cArdiAc hypertrophy, whereAs A dominAnt-negAtive form of MRTF-A or MRTF-A siRNA strongly inhibited upregulAtion of hypertrophy genes in response to hypertrophic Agonists in neonAtAl rAt cArdiomyocytes. Our studies indicAte thAt besides myocArdin, MRTF-A might plAy An importAnt role in cArdiAc hypertrophy. Our findings provide novel evidence for the future studies to explore the roles of MRTFs in cArdiAc hypertrophy. © 2011 IUBMB IUBMB Life, 63(1):54–61, 2011.
Hoiyda A Abdel Rasol - One of the best experts on this subject based on the ideXlab platform.
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VAsculAr endotheliAl growth FActor-A mRNA gene expression in clinicAl phAses of multiple sclerosis
Annals of Clinical Biochemistry, 2016Co-Authors: Hoiyda A Abdel Rasol, Hanan Helmy, Sherine El-mously, Margeret A Aziz, Hossam El BahaieAbstract:BAckgroundVAsculAr endotheliAl growth FActor A stimulAtes Angiogenesis, but is Also pro-inflAmmAtory And plAys An importAnt role in the development of neurologicAl diseAse. This study Aimed to investigAte whether vAsculAr endotheliAl growth FActor A mRNA expression could be used As A mArker for the prediction of susceptibility to multiple sclerosis And relAte vAsculAr endotheliAl growth FActor to the clinicAl phAses of multiple sclerosis.MethodsThis wAs A cross-sectionAl study, consisting of A totAl of 60 subjects with multiple sclerosis And 20 heAlthy controls. Subjects were subjected to history tAking, neurologicAl exAminAtion And peripherAl blood sAmpling for vAsculAr endotheliAl growth FActor A mRNA gene expression. VAsculAr endotheliAl growth FActor A gene expression wAs meAsured by reAl-time polymerAse chAin reAction using the SYBR Green technique.ResultsVAsculAr endotheliAl growth FActor A mRNA gene expression level wAs significAntly lower in the multiple sclerosis group thAn in the heAlthy control...
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VAsculAr endotheliAl growth FActor-A mRNA gene expression in clinicAl phAses of multiple sclerosis.
Annals of clinical biochemistry, 2015Co-Authors: Hoiyda A Abdel Rasol, Hanan Helmy, Sherine El-mously, Margeret A Aziz, Hossam El BahaieAbstract:VAsculAr endotheliAl growth FActor A stimulAtes Angiogenesis, but is Also pro-inflAmmAtory And plAys An importAnt role in the development of neurologicAl diseAse. This study Aimed to investigAte whether vAsculAr endotheliAl growth FActor A mRNA expression could be used As A mArker for the prediction of susceptibility to multiple sclerosis And relAte vAsculAr endotheliAl growth FActor to the clinicAl phAses of multiple sclerosis. This wAs A cross-sectionAl study, consisting of A totAl of 60 subjects with multiple sclerosis And 20 heAlthy controls. Subjects were subjected to history tAking, neurologicAl exAminAtion And peripherAl blood sAmpling for vAsculAr endotheliAl growth FActor A mRNA gene expression. VAsculAr endotheliAl growth FActor A gene expression wAs meAsured by reAl-time polymerAse chAin reAction using the SYBR Green technique. VAsculAr endotheliAl growth FActor A mRNA gene expression level wAs significAntly lower in the multiple sclerosis group thAn in the heAlthy control group (P < 0.001). VAsculAr endotheliAl growth FActor A mRNA gene expression level wAs higher in relApsing remitting multiple sclerosis (RRMS) pAtients thAn in those in remission (P < 0.001) And in relApsing remitting multiple sclerosis compAred with secondAry progressive multiple sclerosis (P < 0.001). There wAs no correlAtion between vAsculAr endotheliAl growth FActor A gene expression levels And durAtion of diseAse, multiple sclerosis progression index or expAnded disAbility stAtus scAle. A lower vAsculAr endotheliAl growth FActor A mRNA gene expression level wAs independently AssociAted with A higher risk of multiple sclerosis. © The Author(s) 2015.
Michael D. Cameron - One of the best experts on this subject based on the ideXlab platform.
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Design of A smAll molecule thAt stimulAtes vAsculAr endotheliAl growth FActor A enAbled by screening RNA fold–smAll molecule interActions
Nature Chemistry, 2020Co-Authors: Hafeez S. Haniff, Laurent Knerr, Gogce Crynen, Jonas Boström, Daniel Abegg, Alexander Adibekian, Elizabeth Lekah, Kye Won Wang, Michael D. Cameron, Ilyas YildirimAbstract:A selection-bAsed screen hAs now reveAled preferences in smAll-molecule chemotypes thAt bind RNA As well As preferences in the RNA motifs thAt bind smAll molecules. AnAlysis of these dAtA enAbled the design of A smAll molecule thAt selectively binds A non-coding microRNA And upregulAtes expression of vAsculAr endotheliAl growth FActor A. VAsculAr endotheliAl growth FActor A (VEGFA) stimulAtes Angiogenesis in humAn endotheliAl cells, And increAsing its expression is A potentiAl treAtment for heArt fAilure. Here, we report the design of A smAll molecule (TGP-377) thAt specificAlly And potently enhAnces VEGFA expression by the tArgeting of A non-coding microRNA thAt regulAtes its expression. A selection-bAsed screen, nAmed two-dimensionAl combinAtoriAl screening, reveAled preferences in smAll-molecule chemotypes thAt bind RNA And preferences in the RNA motifs thAt bind smAll molecules. The screening progrAm increAsed the dAtAset of known RNA motif–smAll molecule binding pArtners by 20-fold. AnAlysis of this dAtAset AgAinst the RNA-mediAted pAthwAys thAt regulAte VEGFA defined thAt the microRNA-377 precursor, which represses VegfA messenger RNA trAnslAtion, is druggAble in A selective mAnner. We designed TGP-377 to potently And specificAlly upregulAte VEGFA in humAn umbilicAl vein endotheliAl cells. These studies illustrAte the power of two-dimensionAl combinAtoriAl screening to define moleculAr recognition events between ‘undruggAble’ biomolecules And smAll molecules, And the Ability of sequence-bAsed design to deliver efficAcious structure-specific compounds.
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Design of A smAll molecule thAt stimulAtes vAsculAr endotheliAl growth FActor A enAbled by screening RNA fold–smAll molecule interActions
Nature chemistry, 2020Co-Authors: Hafeez S. Haniff, Laurent Knerr, Gogce Crynen, Jonas Boström, Daniel Abegg, Alexander Adibekian, Elizabeth Lekah, Kye Won Wang, Xiaohui Liu, Michael D. CameronAbstract:VAsculAr endotheliAl growth FActor A (VEGFA) stimulAtes Angiogenesis in humAn endotheliAl cells, And increAsing its expression is A potentiAl treAtment for heArt fAilure. Here, we report the design of A smAll molecule (TGP-377) thAt specificAlly And potently enhAnces VEGFA expression by the tArgeting of A non-coding microRNA thAt regulAtes its expression. A selection-bAsed screen, nAmed two-dimensionAl combinAtoriAl screening, reveAled preferences in smAll-molecule chemotypes thAt bind RNA And preferences in the RNA motifs thAt bind smAll molecules. The screening progrAm increAsed the dAtAset of known RNA motif-smAll molecule binding pArtners by 20-fold. AnAlysis of this dAtAset AgAinst the RNA-mediAted pAthwAys thAt regulAte VEGFA defined thAt the microRNA-377 precursor, which represses VegfA messenger RNA trAnslAtion, is druggAble in A selective mAnner. We designed TGP-377 to potently And specificAlly upregulAte VEGFA in humAn umbilicAl vein endotheliAl cells. These studies illustrAte the power of two-dimensionAl combinAtoriAl screening to define moleculAr recognition events between 'undruggAble' biomolecules And smAll molecules, And the Ability of sequence-bAsed design to deliver efficAcious structure-specific compounds.
