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Hansjoachim Schnittler - One of the best experts on this subject based on the ideXlab platform.

  • EbolA Virus Enters Host Cells by MAcropinocytosis And ClAthrin-MediAted
    2016
    Co-Authors: Thomas Hoenen, Hansjoachim Schnittler
    Abstract:

    Virus entry into host cells is the first step of infection And A cruciAl determinAnt of pAthogenicity. Here we show thAt EbolA virus-like pArticles (EBOV-VLPs) composed of the glycoprotein GP1,2 And the mAtrix protein VP40 use mAcropinocytosis And clAthrin-mediAted endocytosis to enter cells. EBOV-VLPs Applied to host cells induced Actin-driven ruffling And enhAnced FITC-dextrAn uptAke, which indicAted mAcropinocytosis As the mAin entry mechAnism. This wAs further supported by inhibition of entry through inhibitors of Actin polymerizAtion (LAtrunculin A), NA1/H1-exchAnger (EIPA), And PI3-kinAse (wortmAnnin). A frAction of EBOV-VLPs, however, colocAlized with clAthrin heAvy chAin (CHC), And VLP uptAke wAs reduced by CHC smAll interfering RNA trAnsfection And expression of the dominAnt negAtive dynAmin II–K44A mutAnt. In contrAst, we found no evidence thAt EBOV-VLPs enter cells viA cAveolAe. This work identifies mAcropinocytosis As the mAjor, And clAthrin-dependent endocytosis As An AlternAtive, entry route for EBOV pArticles. Therefore, EBOV seems to utilize different entry pAthwAys depending on both cell type And virus pArticle size. EbolA viruses (EBOVs), belonging to the fAmily FiloviridAe, Are enveloped, nonsegmented, negAtive-strAnded RNA viruses thAt cAn cAuse severe virAl hemorrhAgic fevers in humAn And nonhumAn primAte

  • ebolA virus enters host cells by mAcropinocytosis And clAthrin mediAted endocytosis
    The Journal of Infectious Diseases, 2011
    Co-Authors: Paulina Aleksandrowicz, Stephan Becker, Andrea Marzi, Nadine Biedenkopf, Nadine Beimforde, Thomas Hoenen, Hansjoachim Schnittler
    Abstract:

    Virus entry into host cells is the first step of infection And A cruciAl determinAnt of pAthogenicity. Here we show thAt EbolA virus-like pArticles (EBOV-VLPs) composed of the glycoprotein GP1,2 And the mAtrix protein VP40 use mAcropinocytosis And clAthrin-mediAted endocytosis to enter cells. EBOV-VLPs Applied to host cells induced Actin-driven ruffling And enhAnced FITC-dextrAn uptAke, which indicAted mAcropinocytosis As the mAin entry mechAnism. This wAs further supported by inhibition of entry through inhibitors of Actin polymerizAtion (LAtrunculin A), NA+/H+-exchAnger (EIPA), And PI3-kinAse (wortmAnnin). A frAction of EBOV-VLPs, however, colocAlized with clAthrin heAvy chAin (CHC), And VLP uptAke wAs reduced by CHC smAll interfering RNA trAnsfection And expression of the dominAnt negAtive dynAmin II–K44A mutAnt. In contrAst, we found no evidence thAt EBOV-VLPs enter cells viA cAveolAe. This work identifies mAcropinocytosis As the mAjor, And clAthrin-dependent endocytosis As An AlternAtive, entry route for EBOV pArticles. Therefore, EBOV seems to utilize different entry pAthwAys depending on both cell type And virus pArticle size.

Kaoru Inokuchi - One of the best experts on this subject based on the ideXlab platform.

  • hippocAmpAl ltp is AccompAnied by enhAnced f Actin content within the dendritic spine thAt is essentiAl for lAte ltp mAintenAnce in vivo
    Neuron, 2003
    Co-Authors: Yugo Fukazawa, Kensaku Mizuno, Yoshito Saitoh, Fumiko Ozawa, Yasuhiko Ohta, Kaoru Inokuchi
    Abstract:

    The dendritic spine is An importAnt site of neuronAl plAsticity And contAins extremely high levels of cytoskeletAl Actin. However, the dynAmics of the Actin cytoskeleton during synAptic plAsticity And its in vivo function remAin uncleAr. Here we used An in vivo dentAte gyrus LTP model to show thAt LTP induction is AssociAted with Actin cytoskeletAl reorgAnizAtion chArActerized by A long-lAsting increAse in F-Actin content within dendritic spines. This increAse in F-Actin content is dependent on NMDA receptor ActivAtion And involves the inActivAtion of Actin depolymerizing fActor/cofilin. Inhibition of Actin polymerizAtion with LAtrunculin A impAired lAte phAse of LTP without Affecting the initiAl Amplitude And eArly mAintenAnce of LTP. These observAtions suggest thAt mechAnisms regulAting the spine Actin cytoskeleton contribute to the persistence of LTP.

Paulina Aleksandrowicz - One of the best experts on this subject based on the ideXlab platform.

  • ebolA virus enters host cells by mAcropinocytosis And clAthrin mediAted endocytosis
    The Journal of Infectious Diseases, 2011
    Co-Authors: Paulina Aleksandrowicz, Stephan Becker, Andrea Marzi, Nadine Biedenkopf, Nadine Beimforde, Thomas Hoenen, Hansjoachim Schnittler
    Abstract:

    Virus entry into host cells is the first step of infection And A cruciAl determinAnt of pAthogenicity. Here we show thAt EbolA virus-like pArticles (EBOV-VLPs) composed of the glycoprotein GP1,2 And the mAtrix protein VP40 use mAcropinocytosis And clAthrin-mediAted endocytosis to enter cells. EBOV-VLPs Applied to host cells induced Actin-driven ruffling And enhAnced FITC-dextrAn uptAke, which indicAted mAcropinocytosis As the mAin entry mechAnism. This wAs further supported by inhibition of entry through inhibitors of Actin polymerizAtion (LAtrunculin A), NA+/H+-exchAnger (EIPA), And PI3-kinAse (wortmAnnin). A frAction of EBOV-VLPs, however, colocAlized with clAthrin heAvy chAin (CHC), And VLP uptAke wAs reduced by CHC smAll interfering RNA trAnsfection And expression of the dominAnt negAtive dynAmin II–K44A mutAnt. In contrAst, we found no evidence thAt EBOV-VLPs enter cells viA cAveolAe. This work identifies mAcropinocytosis As the mAjor, And clAthrin-dependent endocytosis As An AlternAtive, entry route for EBOV pArticles. Therefore, EBOV seems to utilize different entry pAthwAys depending on both cell type And virus pArticle size.

Dale D Tang - One of the best experts on this subject based on the ideXlab platform.

  • rAf 1 Actin dynAmics And Abelson tyrosine kinAse in humAn AirwAy smooth muscle cells
    American Journal of Respiratory Cell and Molecular Biology, 2013
    Co-Authors: Ruping Wang, Orion P Mercaitis, Li Jia, Reynold A Panettieri, Dale D Tang
    Abstract:

    RAf-1 is A serine/threonine protein kinAse thAt hAs An essentiAl role in cell proliferAtion. The mechAnisms thAt regulAte RAf-1 in AirwAy smooth muscle Are not well understood. In this study, treAtment with plAtelet-derived growth fActor (PDGF) induced spAtiAl redistribution of RAf-1 from the cytoplAsm to the periphery of humAn AirwAy smooth muscle cells. Moreover, A pool of RAf-1 wAs found in F-Actin of humAn AirwAy smooth muscle cells. ActivAtion with PDGF led to An increAse in the AssociAtion of RAf-1 with cytoskeletAl Actin. TreAtment of cells with the Actin polymerizAtion inhibitor LAtrunculin A (LAT-A), but not the microtubule depolymerizer nocodAzole, inhibited the interAction of RAf-1 with Actin in response to PDGF ActivAtion. BecAuse Abelson tyrosine kinAse (Abl) is known to specificAlly regulAte Actin dynAmics in smooth muscle, the role of Abl in modulAting the coupling of RAf-1 with Actin wAs Also evAluAted. Abl knockdown by RNA interference AttenuAted the AssociAtion of RAf-1 with Actin, which...

Thomas Hoenen - One of the best experts on this subject based on the ideXlab platform.

  • EbolA Virus Enters Host Cells by MAcropinocytosis And ClAthrin-MediAted
    2016
    Co-Authors: Thomas Hoenen, Hansjoachim Schnittler
    Abstract:

    Virus entry into host cells is the first step of infection And A cruciAl determinAnt of pAthogenicity. Here we show thAt EbolA virus-like pArticles (EBOV-VLPs) composed of the glycoprotein GP1,2 And the mAtrix protein VP40 use mAcropinocytosis And clAthrin-mediAted endocytosis to enter cells. EBOV-VLPs Applied to host cells induced Actin-driven ruffling And enhAnced FITC-dextrAn uptAke, which indicAted mAcropinocytosis As the mAin entry mechAnism. This wAs further supported by inhibition of entry through inhibitors of Actin polymerizAtion (LAtrunculin A), NA1/H1-exchAnger (EIPA), And PI3-kinAse (wortmAnnin). A frAction of EBOV-VLPs, however, colocAlized with clAthrin heAvy chAin (CHC), And VLP uptAke wAs reduced by CHC smAll interfering RNA trAnsfection And expression of the dominAnt negAtive dynAmin II–K44A mutAnt. In contrAst, we found no evidence thAt EBOV-VLPs enter cells viA cAveolAe. This work identifies mAcropinocytosis As the mAjor, And clAthrin-dependent endocytosis As An AlternAtive, entry route for EBOV pArticles. Therefore, EBOV seems to utilize different entry pAthwAys depending on both cell type And virus pArticle size. EbolA viruses (EBOVs), belonging to the fAmily FiloviridAe, Are enveloped, nonsegmented, negAtive-strAnded RNA viruses thAt cAn cAuse severe virAl hemorrhAgic fevers in humAn And nonhumAn primAte

  • ebolA virus enters host cells by mAcropinocytosis And clAthrin mediAted endocytosis
    The Journal of Infectious Diseases, 2011
    Co-Authors: Paulina Aleksandrowicz, Stephan Becker, Andrea Marzi, Nadine Biedenkopf, Nadine Beimforde, Thomas Hoenen, Hansjoachim Schnittler
    Abstract:

    Virus entry into host cells is the first step of infection And A cruciAl determinAnt of pAthogenicity. Here we show thAt EbolA virus-like pArticles (EBOV-VLPs) composed of the glycoprotein GP1,2 And the mAtrix protein VP40 use mAcropinocytosis And clAthrin-mediAted endocytosis to enter cells. EBOV-VLPs Applied to host cells induced Actin-driven ruffling And enhAnced FITC-dextrAn uptAke, which indicAted mAcropinocytosis As the mAin entry mechAnism. This wAs further supported by inhibition of entry through inhibitors of Actin polymerizAtion (LAtrunculin A), NA+/H+-exchAnger (EIPA), And PI3-kinAse (wortmAnnin). A frAction of EBOV-VLPs, however, colocAlized with clAthrin heAvy chAin (CHC), And VLP uptAke wAs reduced by CHC smAll interfering RNA trAnsfection And expression of the dominAnt negAtive dynAmin II–K44A mutAnt. In contrAst, we found no evidence thAt EBOV-VLPs enter cells viA cAveolAe. This work identifies mAcropinocytosis As the mAjor, And clAthrin-dependent endocytosis As An AlternAtive, entry route for EBOV pArticles. Therefore, EBOV seems to utilize different entry pAthwAys depending on both cell type And virus pArticle size.