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Angaben zur Quelle [Bearbeiten]

Autor     Laurent Castera, Anne Sophie Hatzfeld-Charbonnier, Caroline Ballot, Florence Charbonnel, Edith Dhuiege, Thierry Velu, Pierre Formstecher, Laurent Mortier, Philippe Marchettia
Titel    Apoptosis-related mitochondrial dysfunction defines human monocyte-derived dendritic cells with impaired immuno-stimulatory capacities
Zeitschrift    Journal of Cellular Molecular Medicine
Datum    July 2009
Jahrgang    13
Nummer    7
Seiten    1321–1335
URL    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4496146/

Literaturverz.   

nein
Fußnoten    nein
Fragmente    2


Fragmente der Quelle:
[1.] Ntx/Fragment 013 16 - Diskussion
Zuletzt bearbeitet: 2014-10-20 15:24:39 Graf Isolan
Castera et al 2009, Fragment, KomplettPlagiat, Ntx, SMWFragment, Schutzlevel, ZuSichten

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Quelle: Castera et al 2009
Seite(n): 1322, Zeilen: li. Sp. 16-29
Mitochondria initiate apoptosis through mitochondrial outer membrane permeabilization and the release of apoptogenic factors (e.g cytochrome c, AIF- apoptosis inducing factor) from the mitochondrial intermembrane space, leading to cell death through caspase-dependent and –independent pathways (Green and Reed 1998a; Mohamad et al 2005).

[...] Signaling cascades can also affect the inner mitochondrial membrane permeability in apoptosis and necrosis. As a consequence, cells also exhibit a loss of electrical potential across the inner membrane which is quantifiable by means of potentiometric dyes (Marchetti et al 1996).

[...] Mitochondrial dysfunction, characterized by marked reduction in mitochondrial membrane potential (Δψm), is an early step of ongoing DC death that can be triggered by many cytotoxic stimuli (McLellan et al 2000; Nencioni et al 2006b; Vassiliou et al 2004a).


Green,D.R., Reed,J.C., 1998a. Mitochondria and apoptosis. Science 281, 1309-1312.

Marchetti,P., Castedo,M., Susin,S.A., Zamzami,N., Hirsch,T., Macho,A., Haeffner,A., Hirsch,F., Geuskens,M., Kroemer,G., 1996. Mitochondrial permeability transition is a central coordinating event of apoptosis. J. Exp. Med. 184, 1155-1160.

McLellan,A.D., Terbeck,G., Mengling,T., Starling,G.C., Kiener,P.A., Gold,R., Brocker,E.B., Leverkus,M., Kampgen,E., 2000. Differential susceptibility to CD95 (Apo-1/Fas) and MHC class II-induced apoptosis during murine dendritic cell development. Cell Death. Differ. 7, 933-938.

Mohamad,N., Gutierrez,A., Nunez,M., Cocca,C., Martin,G., Cricco,G., Medina,V., Rivera,E., Bergoc,R., 2005. Mitochondrial apoptotic pathways. Biocell 29, 149-161.

Nencioni,A., Garuti,A., Schwarzenberg,K., Cirmena,G., Dal Bello,G., Rocco,I., Barbieri,E. Brossart,P., Patrone,F., Ballestrero,A., 2006a. Proteasome inhibitor-induced apoptosis in human monocyte-derived dendritic cells. Eur. J. Immunol. 36, 681-689.

Vassiliou,E., Sharma,V., Jing,H., Sheibanie,F., Ganea,D., 2004a. Prostaglandin E2 promotes the survival of bone marrow-derived dendritic cells. J. Immunol. 173, 6955-6964.

Mitochondria initiate apoptosis through mitochondrial outer membrane permeabilization and the release of apoptogenic factors (e.g. cytochrome c, AIF or Smac/Diablo) from the mitochondrial intermembrane space, leading to cell death through caspase-dependent and -independent pathways. Signalling cascades can also affect the inner mitochondrial membrane permeability in apoptosis and necrosis. As a consequence, cells also exhibit a loss of electrical potential across the inner membrane which is quantifiable by means of potentiometric dyes, a measure that precedes signs of nuclear apoptosis and cell death [6]. Mitochondrial dysfunction, characterized by marked reduction in mitochondrial membrane potential (Δψm), is an early step of ongoing DC death that can be triggered by many cytotoxic stimuli [7–13].

6. Marchetti P, Castedo M, Susin SA, et al. Mitochondrial permeability transition is a central coordinating event of apoptosis. J Exp Med. 1996; 184: 1155–60.

7. McLellan AD, Terbeck G, Mengling T, et al. Differential susceptibility to CD95 (Apo-1/Fas) and MHC class II-induced apoptosis during murine dendritic cell development. Cell Death Differ. 2000; 7: 933–8.

8. Jin H, Xiao C, Zhao G, Du X, et al. Induction of immature dendritic cell apoptosis by foot and mouth disease virus is an integrin receptor mediated event before viral infection. J Cell Biochem. 2007; 102: 980–91.

9. Nencioni A, Garuti A, Schwarzenberg K, et al. Proteasome inhibitor-induced apoptosis in human monocyte-derived dendritic cells. Eur J Immunol. 2006; 36: 681–9.

10. Vassiliou E, Sharma V, Jing H, et al. Prostaglandin E2 promotes the survival of bone marrow-derived dendritic cells. J Immunol. 2004; 173: 6955–64.

11. Sanchez-Sanchez N, Riol-Blanco L, de la Rosa G, et al. Chemokine receptor CCR7 induces intracellular signaling that inhibits apoptosis of mature dendritic cells. Blood. 2004; 104: 619–25.

12. Nicolo C, Tomassini B, Rippo MR, Testi R. UVB-induced apoptosis of human dendritic cells: contribution by caspase-dependent and caspase-independent pathways. Blood. 2001; 97: 1803–8.

13. Leverkus M, McLellan AD, Heldmann M, et al. MHC class II-mediated apoptosis in dendritic cells: a role for membrane-associated and mitochondrial signaling pathways. Int Immunol. 2003; 15: 993–1006. 2004; 104: 619–25.

Anmerkungen

Kein Hinweis auf die eigentliche Quelle. Art und Umfang der Übernahme bleiben ungekennzeichnet.

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(Graf Isolan)

[2.] Ntx/Fragment 014 01 - Diskussion
Zuletzt bearbeitet: 2014-10-21 20:12:48 Graf Isolan
Castera et al 2009, Fragment, KomplettPlagiat, Ntx, SMWFragment, Schutzlevel, ZuSichten

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[Compelling evidence] indicates that mitochondria-related proteins of the Bcl-2 family are crucial DC death sensors (Nencioni et al 2006a; Nicolo et al 2001; Vassiliou et al 2004b), substantiating the importance of mitochondria in DC apoptosis.

'1.10.2. Extrinsic apoptosis pathway

It is mediated by death receptors, such as the receptors for Fas and tumor necrosis factor (TNF)- related apoptosis-inducing ligand (TRAIL), and caspase-8, i.e. the major initiator caspase in this pathway. Several death receptors, including Fas, are expressed in DCs. However, DCs are known to be resistant to Fas-induced cell death through the constitutive expression of FLICE–like inhibitory protein (FLIP), a strong inhibitor of apoptosis initiated by death receptors (Willems et al 2000)


Nencioni,A., Garuti,A., Schwarzenberg,K., Cirmena,G., Dal Bello,G., Rocco,I., Barbieri,E., Brossart,P., Patrone,F., Ballestrero,A., 2006a. Proteasome inhibitor-induced apoptosis in human monocyte-derived dendritic cells. Eur. J. Immunol. 36, 681-689.

Nicolo,C., Tomassini,B., Rippo,M.R., Testi,R., 2001. UVB-induced apoptosis of human dendritic cells: contribution by caspase-dependent and caspase-independent pathways. Blood 97, 1803-1808.

Willems,F., Amraoui,Z., Vanderheyde,N., Verhasselt,V., Aksoy,E., Scaffidi,C., Peter,M.E., Krammer,P.H., Goldman,M., 2000. Expression of c-FLIP(L) and resistance to CD95-mediated apoptosis of monocyte-derived dendritic cells: inhibition by bisindolylmaleimide. Blood 95, 3478-3482.

The extrinsic apoptosis pathway is mediated by death receptors, such as the receptors for Fas and tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), and caspase-8, i.e. the major initiator caspase in this pathway. Several death receptors, including Fas, are expressed in monocyte-derived DCs. However, DCs are known to be resistant to Fas-induced cell death through the constitutive expression of FLICE (caspase-8)-like inhibitory protein (FLIP), a strong inhibitor of apoptosis initiated by death receptors [5].

[...]

[...] Compelling evidence indicates that mitochondria-related proteins of the Bcl-2 family are crucial DC death sensors [9, 12, 14–16], substantiating the importance of mitochondria in DC apoptosis.


5. Willems F, Amraoui Z, Vanderheyde N, et al. Expression of c-FLIP(L) and resistance to CD95-mediated apoptosis of monocyte-derived dendritic cells: inhibition by bisindolylmaleimide. Blood. 2000; 95: 3478–82.

9. Nencioni A, Garuti A, Schwarzenberg K, et al. Proteasome inhibitor-induced apoptosis in human monocyte-derived dendritic cells. Eur J Immunol. 2006; 36: 681–9.

12. Nicolo C, Tomassini B, Rippo MR, Testi R. UVB-induced apoptosis of human dendritic cells: contribution by caspase-dependent and caspase-independent pathways. Blood. 2001; 97: 1803–8.

14. Kriehuber E, Bauer W, Charbonnier AS, et al. Balance between NF-{kappa}B and JNK(AP-1 activity controls dendritic cell life and death. Blood. 2005; 106: 175–83.

15. Hou WS, Van Parijs L. A Bcl-2-dependent molecular timer regulates the lifespan and immunogenicity of dendritic cells. Nat Immunol. 2004; 5: 583–9.

16. Kim TW, Lee JH, He L, et al. Modification of professional antigen-presenting cells with small interfering RNA in vivo to enhance cancer vaccine potency. Cancer Res. 2005; 65: 309–16.

Anmerkungen

Eine Referenz für "Vassiliou et al 2004b" findet sich nicht im Literaturverzeichnis von Ntx. Kein Hinweis auf eine Übernahme.

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