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Androgen Receptor and PIN1 in Prostate Cancer

von Dott. Raffaele La Montagna

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[1.] Rlm/Fragment 022 01 - Diskussion
Zuletzt bearbeitet: 2014-12-01 14:03:26 Singulus
Balk and Knudsen 2008, BauernOpfer, Fragment, Gesichtet, Rlm, SMWFragment, Schutzlevel sysop

Typus
BauernOpfer
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 22, Zeilen: 1 ff. (entire page)
Quelle: Balk and Knudsen 2008
Seite(n): 2-3, 4, Zeilen: 2:right col. 59 - 3:left col. 1-3; 4: figure 1
Prior to mitogenic stimulation cells can exit the cell cycle and enter into a resting stage deemed “G0. At this stage, several key gatekeepers of cell cycle transitions are invoked to prevent unscheduled cell cycle progression (33).

Figure 3:(from Balk et all2008) AR-cell cycle crosstalk.

Activated AR stimulates the accumulation of cyclin D1 (D1), through mammalian Target of Rapamycin (mTOR), to activate CDK4 and promote phosphorylation of the retinoblastoma (RB) tumor suppressor. In addition, AR-induced expression of p21Cip1 and degradation of p27Kip1 further enhance cycD1/CDK4 and cycE/CDK2-dependent inactivation of RB and allow expression of E2F target genes like cyclin A (CycA). Cyclin A in turn activates CDK2 to drive G1-S phase transition. Subsequently engaged components of the cell cycle machinery then impinge on AR to regulate the androgen response. Elevated cyclin D1 acts as in a negative feedback loop to attenuate AR activity, thereby modulating androgen action. In G2-phase, CDK1 promotes the phosphorylation and activation of AR. However, AR is degraded in M-phase and is purposed to be a “licensing factor” for DNA replication. Components that suppress AR function are outlined in red, whereas positive effectors of AR activity are outlined in green.


33) Balk SP, Knudsen KE AR, the cell cycle, and prostate cancer. Nucl Recept Signal. 2008 Feb 1;6:e001.

[Page 2]

Prior to mitogenic stimulation cells can exit the cell cycle and

[Page 3]

enter into a resting stage deemed “G0”. At this stage, several key gatekeepers of cell cycle transitions are invoked to prevent unscheduled cell cycle progression.

[Page 4]

Figure 1. AR-cell cycle crosstalk. Activated AR stimulates the accumulation of cyclin D1 (D1), through mammalian Target of Rapamycin (mTOR), to activate CDK4 and promote phosphorylation of the retinoblastoma (RB) tumor suppressor. In addition, AR-induced expression of p21Cip1 and degradation of p27Kip1 further enhance cycD1/CDK4 and cycE/CDK2-dependent inactivation of RB and allow expression of E2F target genes like cyclin A (CycA). Cyclin A in turn activates CDK2 to drive G1-S phase transition. Subsequently engaged components of the cell cycle machinery then impinge on AR to regulate the androgen response. Elevated cyclin D1 acts as in a negative feedback loop to attenuate AR activity, thereby modulating androgen action. In G2-phase, CDK1 promotes the phosphorylation and activation of AR. However, AR is degraded in M-phase and is purposed to be a “licensing factor” for DNA replication. Components that suppress AR function are outlined in red, whereas positive effectors of AR activity are outlined in green.



Anmerkungen

Although the texts are identical the citations have not been marked as such.

The source is only mentioned in passing.

Sichter
(Graf Isolan), SleepyHollow02


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