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Androgen Receptor and PIN1 in Prostate Cancer

von Dott. Raffaele La Montagna

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Statistik und Sichtungsnachweis dieser Seite findet sich am Artikelende
[1.] Rlm/Fragment 021 01 - Diskussion
Zuletzt bearbeitet: 2014-12-02 08:18:35 Singulus
BauernOpfer, Fragment, Gesichtet, Narayanan et al 2010, Rlm, SMWFragment, Schutzlevel sysop

Typus
BauernOpfer
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 21, Zeilen: 1-8
Quelle: Narayanan et al 2010
Seite(n): 842, Zeilen: 15-19
SNARE-1 inhibits the androgen-sensitive growth of LNCaP cells and tumor xenografts. Quantitative subcellular localization studies suggest that SNARE-1 inhibits nuclear translocation of AR, but also facilitates export of nuclear AR that has been translocated by an agonist. Mechanistic studies indicate that SNARE-1 rapidly phosphorylates p38 mitogen-activated protein kinase (MAPK) and Ser650 of the AR facilitating the nuclear export of AR. Additionally, SNARE-1 was found to promote ubiquitination of AR in LNCaP cells (30).

30) Ramesh Narayanan, Muralimohan Yepuru, Adam T. Szafran, Maria Szwarc, Casey E. Bohl, Natalie L. Young, Duane D. Miller, Michael A. Mancini, and James T. Dalton. Selective Nuclear Androgen Receptor Exporter for the Treatment of Prostate Cancer. Cancer Research 2010 Jan 15;70(2):842-51. Epub 2010 Jan 12.

SNARE-1 inhibits the androgen-sensitive growth of LNCaP cells and tumor xenografts. Quantitative subcellular localization studies suggest that SNARE-1 inhibits nuclear translocation of AR, but also facilitates export of nuclear AR that has been translocated by an agonist. Mechanistic studies indicate that SNARE-1 rapidly phosphorylates p38 mitogen-activated protein kinase (MAPK) and Ser650 of the AR. Additionally, SNARE-1 was found to promote ubiquitination of AR in LNCaP cells.
Anmerkungen

Taken verbatim from the original source, continued from previous page. Alhough the authors are mentioned here, it has not been marked that the take-over has been word by word.

Sichter
(Graf Isolan), SleepyHollow02

[2.] Rlm/Fragment 021 09 - Diskussion
Zuletzt bearbeitet: 2014-12-01 14:01:28 Singulus
Balk and Knudsen 2008, Fragment, Gesichtet, KomplettPlagiat, Rlm, SMWFragment, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 21, Zeilen: 9-19
Quelle: Balk and Knudsen 2008
Seite(n): 2, Zeilen: right col. 46-59
Transitions into and within the mitotic cell cycle are dictated by the coordinate activation of cyclin-dependent kinase (CDK)/cyclin complexes, wherein cyclin binding induces the catalytic activity of the kinase (31,32). Mitogenic signaling pathways generally induce cell cycle progression through ordered activation of CDK-cyclin complexes, whereas anti-mitogenic signals that result from extracellular events (e.g., nutrient depletion) or intracellular insults (e.g., DNA damage) typically serve to attenuate CDK function. Although the signals that dictate commitment to the cell cycle are often cell type-specific, the core machinery that drives the cell cycle engine is well conserved.

31) Lee YM, Sicinski P Targeting cyclins and cyclin-dependent kinases in cancer: lessons from mice, hopes for therapeutic applications in human. Cell Cycle. 2006 Sep;5(18):2110-4. Epub 2006 Sep 15.

32) Malumbres M,, Barbacid M Cell cycle kinases in cancer. Curr Opin Genet Dev.2007 Feb;17(1):60-5.

Transitions into and within the mitotic cell cycle are dictated by the coordinate activation of cyclin-dependent kinase (CDK)/cyclin complexes, wherein cyclin binding

induces the catalytic activity of the kinase [Lee and Sicinski, 2006; Malumbres and Barbacid, 2007; Sherr, 1996; Sherr and Roberts, 2004]. Mitogenic signaling pathways generally induce cell cycle progression through ordered activation of CDK-cyclin complexes, whereas anti-mitogenic signals that result from extracellular events (e.g., nutrient depletion) or intracellular insults (e.g., DNA damage) typically serve to attenuate CDK function. Although the signals that dictate commitment to the cell cycle are often cell type-specific, the core machinery that drives the cell cycle engine is well conserved.


Lee, Y. M. and Sicinski, P. (2006) Targeting cyclins and cyclin-dependent kinases in cancer: lessons from mice, hopes for therapeutic applications in human Cell Cycle 5, 2110-4.

Malumbres, M. and Barbacid, M. (2007) Cell cycle kinases in cancer Curr Opin Genet Dev 17, 60-5.

Sherr, C. J. (1996) Cancer cell cycles Science 274, 1672-7.

Sherr, C. J. and Roberts, J. M. (2004) Living with or without cyclins and cyclin-dependent kinases Genes Dev 18, 2699-711.

Anmerkungen

Although identical with identical references nothing has been marked as a citation.

The source is mentioned in passing on the next page.

Sichter
(Graf Isolan), SleepyHollow02


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