Intracellular trafficking of Clostridium botulinum C2 toxin
Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Nagahama, Masahiro [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2014transfer abstract |
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| Schlagwörter: |
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| Umfang: |
7 |
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| Übergeordnetes Werk: |
Enthalten in: Hydrochlorothiazide use and risk for Merkel cell carcinoma and malignant adnexal skin tumors: A nationwide case-control study - Pedersen, Sidsel Arnspang ELSEVIER, 2018, an interdisciplinary journal on the toxins derived from animals, plants and microorganisms : official journal of The International Society on Toxinology, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:82 ; year:2014 ; pages:76-82 ; extent:7 |
| Links: |
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| DOI / URN: |
10.1016/j.toxicon.2014.02.009 |
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ELV033617651 |
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| 245 | 1 | 0 | |a Intracellular trafficking of Clostridium botulinum C2 toxin |
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| 520 | |a Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. | ||
| 520 | |a Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. | ||
| 650 | 7 | |a Endocytosis |2 Elsevier | |
| 650 | 7 | |a Late endosomes |2 Elsevier | |
| 650 | 7 | |a Clostridium botulinum C2 toxin |2 Elsevier | |
| 650 | 7 | |a Recycling endosomes |2 Elsevier | |
| 650 | 7 | |a Early endosomes |2 Elsevier | |
| 700 | 1 | |a Takahashi, Chihiro |4 oth | |
| 700 | 1 | |a Aoyanagi, Kouhei |4 oth | |
| 700 | 1 | |a Tashiro, Ryo |4 oth | |
| 700 | 1 | |a Kobayashi, Keiko |4 oth | |
| 700 | 1 | |a Sakaguchi, Yoshihiko |4 oth | |
| 700 | 1 | |a Ishidoh, Kazumi |4 oth | |
| 700 | 1 | |a Sakurai, Jun |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Pedersen, Sidsel Arnspang ELSEVIER |t Hydrochlorothiazide use and risk for Merkel cell carcinoma and malignant adnexal skin tumors: A nationwide case-control study |d 2018 |d an interdisciplinary journal on the toxins derived from animals, plants and microorganisms : official journal of The International Society on Toxinology |g Amsterdam [u.a.] |w (DE-627)ELV001406604 |
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| 856 | 4 | 0 | |u https://doi.org/10.1016/j.toxicon.2014.02.009 |3 Volltext |
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10.1016/j.toxicon.2014.02.009 doi GBVA2014001000023.pica (DE-627)ELV033617651 (ELSEVIER)S0041-0101(14)00053-1 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 44.93 bkl Nagahama, Masahiro verfasserin aut Intracellular trafficking of Clostridium botulinum C2 toxin 2014transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. Endocytosis Elsevier Late endosomes Elsevier Clostridium botulinum C2 toxin Elsevier Recycling endosomes Elsevier Early endosomes Elsevier Takahashi, Chihiro oth Aoyanagi, Kouhei oth Tashiro, Ryo oth Kobayashi, Keiko oth Sakaguchi, Yoshihiko oth Ishidoh, Kazumi oth Sakurai, Jun oth Enthalten in Elsevier Science Pedersen, Sidsel Arnspang ELSEVIER Hydrochlorothiazide use and risk for Merkel cell carcinoma and malignant adnexal skin tumors: A nationwide case-control study 2018 an interdisciplinary journal on the toxins derived from animals, plants and microorganisms : official journal of The International Society on Toxinology Amsterdam [u.a.] (DE-627)ELV001406604 volume:82 year:2014 pages:76-82 extent:7 https://doi.org/10.1016/j.toxicon.2014.02.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.93 Dermatologie VZ AR 82 2014 76-82 7 045F 570 |
| spelling |
10.1016/j.toxicon.2014.02.009 doi GBVA2014001000023.pica (DE-627)ELV033617651 (ELSEVIER)S0041-0101(14)00053-1 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 44.93 bkl Nagahama, Masahiro verfasserin aut Intracellular trafficking of Clostridium botulinum C2 toxin 2014transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. Endocytosis Elsevier Late endosomes Elsevier Clostridium botulinum C2 toxin Elsevier Recycling endosomes Elsevier Early endosomes Elsevier Takahashi, Chihiro oth Aoyanagi, Kouhei oth Tashiro, Ryo oth Kobayashi, Keiko oth Sakaguchi, Yoshihiko oth Ishidoh, Kazumi oth Sakurai, Jun oth Enthalten in Elsevier Science Pedersen, Sidsel Arnspang ELSEVIER Hydrochlorothiazide use and risk for Merkel cell carcinoma and malignant adnexal skin tumors: A nationwide case-control study 2018 an interdisciplinary journal on the toxins derived from animals, plants and microorganisms : official journal of The International Society on Toxinology Amsterdam [u.a.] (DE-627)ELV001406604 volume:82 year:2014 pages:76-82 extent:7 https://doi.org/10.1016/j.toxicon.2014.02.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.93 Dermatologie VZ AR 82 2014 76-82 7 045F 570 |
| allfields_unstemmed |
10.1016/j.toxicon.2014.02.009 doi GBVA2014001000023.pica (DE-627)ELV033617651 (ELSEVIER)S0041-0101(14)00053-1 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 44.93 bkl Nagahama, Masahiro verfasserin aut Intracellular trafficking of Clostridium botulinum C2 toxin 2014transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. Endocytosis Elsevier Late endosomes Elsevier Clostridium botulinum C2 toxin Elsevier Recycling endosomes Elsevier Early endosomes Elsevier Takahashi, Chihiro oth Aoyanagi, Kouhei oth Tashiro, Ryo oth Kobayashi, Keiko oth Sakaguchi, Yoshihiko oth Ishidoh, Kazumi oth Sakurai, Jun oth Enthalten in Elsevier Science Pedersen, Sidsel Arnspang ELSEVIER Hydrochlorothiazide use and risk for Merkel cell carcinoma and malignant adnexal skin tumors: A nationwide case-control study 2018 an interdisciplinary journal on the toxins derived from animals, plants and microorganisms : official journal of The International Society on Toxinology Amsterdam [u.a.] (DE-627)ELV001406604 volume:82 year:2014 pages:76-82 extent:7 https://doi.org/10.1016/j.toxicon.2014.02.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.93 Dermatologie VZ AR 82 2014 76-82 7 045F 570 |
| allfieldsGer |
10.1016/j.toxicon.2014.02.009 doi GBVA2014001000023.pica (DE-627)ELV033617651 (ELSEVIER)S0041-0101(14)00053-1 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 44.93 bkl Nagahama, Masahiro verfasserin aut Intracellular trafficking of Clostridium botulinum C2 toxin 2014transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. Endocytosis Elsevier Late endosomes Elsevier Clostridium botulinum C2 toxin Elsevier Recycling endosomes Elsevier Early endosomes Elsevier Takahashi, Chihiro oth Aoyanagi, Kouhei oth Tashiro, Ryo oth Kobayashi, Keiko oth Sakaguchi, Yoshihiko oth Ishidoh, Kazumi oth Sakurai, Jun oth Enthalten in Elsevier Science Pedersen, Sidsel Arnspang ELSEVIER Hydrochlorothiazide use and risk for Merkel cell carcinoma and malignant adnexal skin tumors: A nationwide case-control study 2018 an interdisciplinary journal on the toxins derived from animals, plants and microorganisms : official journal of The International Society on Toxinology Amsterdam [u.a.] (DE-627)ELV001406604 volume:82 year:2014 pages:76-82 extent:7 https://doi.org/10.1016/j.toxicon.2014.02.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.93 Dermatologie VZ AR 82 2014 76-82 7 045F 570 |
| allfieldsSound |
10.1016/j.toxicon.2014.02.009 doi GBVA2014001000023.pica (DE-627)ELV033617651 (ELSEVIER)S0041-0101(14)00053-1 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 44.93 bkl Nagahama, Masahiro verfasserin aut Intracellular trafficking of Clostridium botulinum C2 toxin 2014transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. Endocytosis Elsevier Late endosomes Elsevier Clostridium botulinum C2 toxin Elsevier Recycling endosomes Elsevier Early endosomes Elsevier Takahashi, Chihiro oth Aoyanagi, Kouhei oth Tashiro, Ryo oth Kobayashi, Keiko oth Sakaguchi, Yoshihiko oth Ishidoh, Kazumi oth Sakurai, Jun oth Enthalten in Elsevier Science Pedersen, Sidsel Arnspang ELSEVIER Hydrochlorothiazide use and risk for Merkel cell carcinoma and malignant adnexal skin tumors: A nationwide case-control study 2018 an interdisciplinary journal on the toxins derived from animals, plants and microorganisms : official journal of The International Society on Toxinology Amsterdam [u.a.] (DE-627)ELV001406604 volume:82 year:2014 pages:76-82 extent:7 https://doi.org/10.1016/j.toxicon.2014.02.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.93 Dermatologie VZ AR 82 2014 76-82 7 045F 570 |
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Enthalten in Hydrochlorothiazide use and risk for Merkel cell carcinoma and malignant adnexal skin tumors: A nationwide case-control study Amsterdam [u.a.] volume:82 year:2014 pages:76-82 extent:7 |
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Enthalten in Hydrochlorothiazide use and risk for Merkel cell carcinoma and malignant adnexal skin tumors: A nationwide case-control study Amsterdam [u.a.] volume:82 year:2014 pages:76-82 extent:7 |
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Hydrochlorothiazide use and risk for Merkel cell carcinoma and malignant adnexal skin tumors: A nationwide case-control study |
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Nagahama, Masahiro @@aut@@ Takahashi, Chihiro @@oth@@ Aoyanagi, Kouhei @@oth@@ Tashiro, Ryo @@oth@@ Kobayashi, Keiko @@oth@@ Sakaguchi, Yoshihiko @@oth@@ Ishidoh, Kazumi @@oth@@ Sakurai, Jun @@oth@@ |
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Nagahama, Masahiro |
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intracellular trafficking of clostridium botulinum c2 toxin |
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Intracellular trafficking of Clostridium botulinum C2 toxin |
| abstract |
Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. |
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Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. |
| abstract_unstemmed |
Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation. |
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These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Clostridium botulinum C2 toxin is a binary toxin composed of an enzymatic component (C2I) and binding component (C2II). The activated binding component (C2IIa) forms heptamers and the oligomer with C2I is taken up by receptor-mediated endocytosis. We investigated the intracellular trafficking of C2 toxin. When MDCK cells were incubated with C2I and C2IIa at 37 °C, C2I colocalized with C2IIa in cytoplasmic vesicles at 5 min, and C2I then disappeared (15 min incubation and later), and C2IIa was observed in the vesicles. Internalized C2I and C2IIa were transported to early endosomes. Some of both components were returned to the plasma membrane through recycling endosomes, whereas the rest of C2IIa was transported to late endosomes and lysosomes for degradation. Bafilomycin A1, an endosomal acidification inhibitor, caused the accumulation of C2IIa in endosomes, and both nocodazole and colchicine, microtubule-disrupting agents, restricted C2IIa's movement in the cytosol. These results indicated that an internalized C2I and C2IIa complex was delivered to early endosomes, and that subsequent delivery of C2I to the cytoplasm occurred in early endosomes. C2IIa was either sent back to the plasma membranes through recycling endosomes or transported to late endosomes and lysosomes for degradation.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Endocytosis</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Late endosomes</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Clostridium botulinum C2 toxin</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Recycling endosomes</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Early endosomes</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Takahashi, Chihiro</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Aoyanagi, Kouhei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tashiro, Ryo</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kobayashi, Keiko</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sakaguchi, Yoshihiko</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ishidoh, Kazumi</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sakurai, Jun</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Pedersen, Sidsel Arnspang ELSEVIER</subfield><subfield code="t">Hydrochlorothiazide use and risk for Merkel cell carcinoma and malignant adnexal skin tumors: A nationwide case-control study</subfield><subfield code="d">2018</subfield><subfield code="d">an interdisciplinary journal on the toxins derived from animals, plants and microorganisms : official journal of The International Society on Toxinology</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV001406604</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:82</subfield><subfield code="g">year:2014</subfield><subfield code="g">pages:76-82</subfield><subfield code="g">extent:7</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.toxicon.2014.02.009</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.93</subfield><subfield code="j">Dermatologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">82</subfield><subfield code="j">2014</subfield><subfield code="h">76-82</subfield><subfield code="g">7</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">570</subfield></datafield></record></collection>
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