Fandom

VroniPlag Wiki

Quelle:Ww/Milhavet et al 2003

< Quelle:Ww

31.377Seiten in
diesem Wiki
Seite hinzufügen
Diskussion0

Störung durch Adblocker erkannt!


Wikia ist eine gebührenfreie Seite, die sich durch Werbung finanziert. Benutzer, die Adblocker einsetzen, haben eine modifizierte Ansicht der Seite.

Wikia ist nicht verfügbar, wenn du weitere Modifikationen in dem Adblocker-Programm gemacht hast. Wenn du sie entfernst, dann wird die Seite ohne Probleme geladen.

Angaben zur Quelle [Bearbeiten]

Autor     Ollivier Milhavet, Devin S. Gary, and Mark P. Mattson
Titel    RNA Interference in Biology and Medicine
Zeitschrift    Pharmacological Reviews
Ausgabe    55
Datum    Dezember 2003
Nummer    4
Seiten    629-648
DOI    10.1124/pr.55.4.1
URL    http://pharmrev.aspetjournals.org/content/55/4/629.full

Literaturverz.   

nein
Fußnoten    nein
Fragmente    2


Fragmente der Quelle:
[1.] Ww/Fragment 013 01 - Diskussion
Zuletzt bearbeitet: 2014-10-28 02:57:19 Hindemith
Fragment, Gesichtet, KomplettPlagiat, Milhavet et al 2003, SMWFragment, Schutzlevel sysop, Ww

Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 13, Zeilen: 1-11
Quelle: Milhavet et al 2003
Seite(n): 643, Zeilen: 643:li.Sp. 21ff
1.2.2.1 Cancer

There are two general abnormalities in cancer cells that exhibit a dysregulation of the cell cycle resulting in uncontrolled growth and are resistant to death as a result of abnormalities in one or more proteins that mediate apoptosis (Nam and Parang, 2003). The goals for RNAi approaches for cancer therapy are therefore to silence the expression of a cell cycle gene and/or an anti-apoptotic gene in the cancer cells thereby stopping tumor growth and killing the cancer cells. To selectively eliminate cancer cells without damaging normal cells, the RNAi needs to be targeted to a gene specifically involved in the growth or survival of the cancer cell, or the siRNAs would be selectively delivered into the cancer cells.


Nam NH, Parang K. Current targets for anticancer drug discovery. Curr Drug Targets. 2003 Feb;4(2):159-179.

A. Cancer

There are two general abnormalities in cancer cells — they exhibit dysregulation of the cell cycle resulting in uncontrolled growth and they are resistant to death as a result of abnormalities in one or more proteins that mediate apoptosis (Nam and Parang, 2003). The goals for RNAi approaches for cancer therapy are therefore to knock out the expression of a cell cycle gene and/or an anti-apoptotic gene in the cancer cells thereby stopping tumor growth and killing the cancer cells. To selectively eliminate cancer cells without damaging normal cells, the RNAi would be targeted to a gene specifically involved in the growth or survival of the cancer cell, or the siRNAs would be selectively delivered into the cancer cells.


Nam NH and Parang K (2003) Current targets for anticancer drug discovery. Curr Drug Targets 4:159–179.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan), Hindemith

[2.] Ww/Fragment 014 01 - Diskussion
Zuletzt bearbeitet: 2014-10-28 02:53:55 Hindemith
Fragment, Gesichtet, KomplettPlagiat, Milhavet et al 2003, SMWFragment, Schutzlevel sysop, Ww

Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 14, Zeilen: 1-18
Quelle: Milhavet et al 2003
Seite(n): 643-644, Zeilen: 643:re.Sp. 51ff - 644:li.Sp. 1ff
The ability of RNAi to inhibit the replication or cellular uptake of viruses and other infectious agents has been clearly demonstrated in cell culture studies and, therefore, holds promise for the treatment of human patients. The ability of HIV-1 to infect cells and replicate can be severely compromised by targeting viral genes using siRNAs. Examples include the suppression of HIV-1 replication in human cells transfected with siRNA directed against the tat and the rev gene (Capodici et al, 2002; Jacque et al, 2002; Lee et al, 2002a; Novina et al, 2002). Transfection of human cells with siRNAs directed against different genes in the poliovirus genome resulted in resistance of the cells to infection with poliovirus (Gitlin et al., 2002). The ability of siRNAs targeting the gene encoding the death receptor Fas to protect mice from liver failure and fibrosis in two models of autoimmune hepatitis was tested by Song and colleagues (Song et al., 2003). Intravenous injection of Fas siRNA specifically reduced Fas protein levels in the livers of mice during a 10-day period. Fas siRNA treatment abrogated hepatocyte necrosis and inflammatory infiltration and markedly reduced serum concentrations of transaminases demonstrating a clear hepatoprotective effect of the siRNA therapy. [Seite 643]

The ability of RNAi to inhibit the replication or cellular uptake of viruses and other infectious agents has been clearly demonstrated in cell culture studies and, therefore, holds promise for the treatment of human patients. The ability of HIV-1 to infect cells and replicate can be severely compromised by targeting of

[Seite 644]

viral genes using siRNAs. Examples include the suppression of HIV-1 replication in human cells transfected with siRNA directed against tat and the rev gene (Capodici et al., 2002; Jacque et al., 2002; Lee et al., 2002a; Novina et al., 2002). Transfection of human cells with siRNAs directed against different genes in the poliovirus genome resulted in resistance of the cells to infection with poliovirus (Gitlin et al., 2002). The ability of siRNAs targeting the gene encoding the death receptor Fas to protect mice from liver failure and fibrosis in two models of autoimmune hepatitis was tested by Song and colleagues (Song et al., 2003). Intravenous injection of Fas siRNA specifically reduced Fas protein levels in the livers of mice during a 10-day period. Fas siRNA treatment abrogated hepatocyte necrosis and inflammatory infiltration and markedly reduced serum concentrations of transaminases demonstrating a clear hepatoprotective effect of the siRNA therapy.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan), Hindemith

Auch bei Fandom

Zufälliges Wiki