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Autor     Shao-Yong Chen / Gerburg Wulf / Xiao Zhen Zhou / Mark A. Rubin / Kun Ping Lu / Steven P. Balk
Titel    Activation of β-Catenin Signaling in Prostate Cancer by Peptidyl-Prolyl Isomerase Pin1-Mediated Abrogation of the Androgen Receptor–β-Catenin Interaction
Zeitschrift    MOLECULAR AND CELLULAR BIOLOGY
Ausgabe    Volume 26(3)
Datum    Feb 2006
Seiten    929–939
DOI    0.1128/MCB.26.3.929-939.2006
URL    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1347015/pdf/0925-05.pdf

Literaturverz.   

yes
Fußnoten    yes
Fragmente    3


Fragmente der Quelle:
[1.] Rlm/Fragment 028 01 - Diskussion
Zuletzt bearbeitet: 2014-12-03 07:49:42 Singulus
BauernOpfer, Chen et al 2006, Fragment, Gesichtet, Rlm, SMWFragment, Schutzlevel sysop

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Quelle: Chen et al 2006
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Recently has been demonstrated that Androgen receptor (AR) interacts with β-catenin and can suppress its coactivation of T cell factor 4 (Tcf4) in prostate cancer (PCa) cells. Pin1 is a peptidyl-prolyl cis/trans isomerase that stabilizes β-catenin by inhibiting its binding to the adenomatous polyposis coli gene product and subsequent glycogen synthase kinase 3β (GSK-3β)-dependent degradation. Higher Pin1 expression in primary PCa is correlated with disease recurrence, and this study found that Pin1 expression was markedly increased in metastatic PCa.(48).

48) Shao-Yong Chen, Gerburg Wulf,Xiao Zhen Zhou,Mark A. Rubin, Kun Ping Lu, and Steven P. Balk .Activation of "-Catenin Signaling in Prostate Cancer by Peptidyl-Prolyl Isomerase Pin1-Mediated Abrogation of the Androgen Receptor–"-Catenin Interaction. Mol Cell Biol. 2006 Feb;26(3):929-39

Androgen receptor (AR) interacts with β-catenin and can suppress its coactivation of T cell factor 4 (Tcf4) in prostate cancer (PCa) cells. Pin1 is a peptidyl-prolyl cis/trans isomerase that stabilizes β-catenin by inhibiting its binding to the adenomatous polyposis coli gene product and subsequent glycogen synthase kinase 3β (GSK-3β)-dependent degradation. Higher Pin1 expression in primary PCa is correlated with disease recurrence, and this study found that Pin1 expression was markedly increased in metastatic PCa.
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Sichter
(Graf Isolan), SleepyHollow02

[2.] Rlm/Fragment 032 04 - Diskussion
Zuletzt bearbeitet: 2014-12-03 07:51:11 Singulus
Chen et al 2006, Fragment, Gesichtet, Rlm, SMWFragment, Schutzlevel sysop, Verschleierung

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Pin1 overexpression has been observed in a subset of primary prostate cancers, and its expression correlates with increased risk of recurrence after radical prostatectomy (60).

60) Abate-Shen, C., and Shen, M. M. Molecular genetics of PCa. Genes Dev., 14: 2410–2434, 2000.

Significantly, Pin1 overexpression has also been observed in a subset of primary prostate cancers, and its expression correlates with increased risk of recurrence after radical prostatectomy (2).

2. Ayala, G., D. Wang, G. Wulf, A. Frolov, R. Li, J. Sowadski, T. M. Wheeler, K. P. Lu, and L. Bao. 2003. The prolyl isomerase Pin1 is a novel prognostic marker in human prostate cancer. Cancer Res. 63:6244–6251.

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Sichter
(Graf Isolan), SleepyHollow02

[3.] Rlm/Fragment 032 14 - Diskussion
Zuletzt bearbeitet: 2014-12-04 21:02:28 Singulus
BauernOpfer, Chen et al 2006, Fragment, Gesichtet, Rlm, SMWFragment, Schutzlevel sysop

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Quelle: Chen et al 2006
Seite(n): 930, Zeilen: left col. 50-54.58-60
Increased expression of Pin1 in transfected LNCaP PCa cells strongly accelerated tumor growth in vivo in immunodeficient mice (48). However, the functional effects of Pin1 overexpression on β-catenin nuclear signaling in PCa cells (and in particular in PTEN-deficient cells), and how it contributes to more aggressive biological behavior have not been determined.

48) Shao-Yong Chen, Gerburg Wulf,Xiao Zhen Zhou,Mark A. Rubin, Kun Ping Lu, and Steven P. Balk .Activation of "-Catenin Signaling in Prostate Cancer by Peptidyl-Prolyl Isomerase Pin1-Mediated Abrogation of the Androgen Receptor–"-Catenin Interaction. Mol Cell Biol. 2006 Feb;26(3):929-39

However, the functional effects of Pin1 overexpression on β-catenin nuclear signaling in PCa cells (and in particular in PTEN-deficient cells), and how it contributes to more aggressive biological behavior have not been determined.

[...] Consistent with this result, increased expression of Pin1 in transfected LNCaP PCa cells strongly accelerated tumor growth in vivo in immunodeficient mice.

Anmerkungen

Nothing has been marked as a citation.

Sichter
(Graf Isolan), SleepyHollow02

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