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Validation of shRNA clones for gene silencing in 293FT cells

von Dr. Wen Wang

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[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

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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 013 12 - Diskussion
Zuletzt bearbeitet: 2014-10-29 15:55:05 Hindemith
Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Stevenson 2004, Verschleierung, Ww

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SleepyHollow02
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Untersuchte Arbeit:
Seite: 13, Zeilen: 12-29
Quelle: Stevenson 2004
Seite(n): 1773, Zeilen: 1773: r.col: 19ff
The translocation of the Philadelphia chromosome (Ph) generates a fusion gene called BCR-ABL. The translation product of this gene creates a constitutively active protein tyrosine kinase that induces and maintains leukemic transformation in chronic myelogenous leukemia and Ph-positive acute lymphoblastic leukemia. The siRNAs specific for the BCR-ABL transcript have been shown to silence the oncogenic fusion transcripts without affecting expression levels of normal c-ABL and c-BCR transcripts (Scherr et al, 2003; Wohlbold et al, 2003).

Pancreatic and colon carcinomas, in which RAS genes are often mutated, provide another example for potential RNAi applications. In many cases, the RAS oncogenes contain point mutations that differ by a single-base mutation from their normal counterparts. The use of retroviral vectors to introduce interfering RNAs specific for an oncogenic variant of KRAS (called K-RASV12) reduced the level of K-RASV12 transcripts and resulted in a loss of anchorage-independent growth and tumorigenicity (Brummelkamp et al, 2002). Studies of this kind provided proof-of-concept data for RNAi-based strategies aiming to reverse tumorigenesis.

1.2.2.2 Infectious diseases

The translocation of the Philadelphia chromosome (Ph) generates a fusion gene called BCR-ABL. The translation product of this gene creates a constitutively active protein tyrosine kinase that induces and maintains leukemic transformation in chronic myelogenous leukemia and Ph-positive acute lymphoblastic leukemia. The siRNAs specific for the BCR-ABL transcript have been shown to silence the oncogenic fusion transcripts without affecting expression levels of normal c-ABL and c-BCR transcripts.20,21

Pancreatic and colon carcinomas, in which RAS

[Seite 1775]

genes are often mutated, provide another example. In many cases, the RAS oncogenes contain point mutations that differ by a single-base mutation from their normal counterparts. The use of retroviral vectors to introduce interfering RNAs specific for an oncogenic variant of K-RAS (called K-RASV12) reduces the level of K-RASV12 transcripts and effects a loss of anchorage-independent growth and tumorigenicity.22,23 Studies of this kind provide proof-of-concept for RNAi-based strategies aimed at reversing tumorigenesis. [...]

[...]

Infectious Diseases


20. Scherr M, Battmer K, Winkler T, Heidenreich O, Ganser A, Eder M. Specific inhibition of bcr-abl gene expression by small interfering RNA. Blood 2003;101: 1566-9.

21. Wohlbold L, van der Kuip H, Miething C, et al. Inhibition of bcr-abl gene expression by small interfering RNA sensitizes for imatinib mesylate (STI571). Blood 2003; 102:2236-9.

22. Brummelkamp TR, Bernards R, Agami R. Stable suppression of tumorigenicity by virus-mediated RNA interference. Cancer Cell 2002;2:243-7.

23. Wilda M, Fuchs U, Wossmann W, Borkhardt A. Killing of leukemic cells with a BCR/ABL fusion gene by RNA interference (RNAi). Oncogene 2002;21:5716-24.

Anmerkungen

Kein Hinweis auf die Quelle.

Sichter
(SleepyHollow02), Hindemith


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Letzte Bearbeitung dieser Seite: durch Benutzer:Hindemith, Zeitstempel: 20141029155559

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