---------- Forwarded message ----------
From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Sun, Sep 7, 2008 at 3:45 AM
Subject: Integrin-linked kinase regulates E-cadherin expression through PARP-1.
To: mesothelioma77@gmail.com
[1]Dev Dyn. 2008 Sep 4;
McPhee TR, McDonald PC, Oloumi A, Dedhar S
Repression of E-cadherin expression by the transcription factor, Snail, is implicated in epithelial to mesenchymal transition and cancer progression. We show here that Integrin-Linked Kinase (ILK) regulates E-cadherin expression through Poly(ADP-ribose) polymerase-1 (PARP-1). ILK overexpression in Scp2 cells resulted in stimulation of Snail expression and loss of E-cadherin expression. Silencing of ILK, Akt or Snail resulted in re-expression of E-cadherin in PC3 cells. To elucidate the signaling pathway downstream of ILK, we identified candidate Snail promoter ILK Responsive Element (SIRE) binding proteins. PARP-1 was identified as a SIRE-binding protein. ILK silencing inhibited binding of PARP-1 to SIRE. PARP-1 silencing resulted in inhibition of Snail and ZEB1, leading to up-regulation of E-cadherin. We suggest a model in which ILK represses E-cadherin expression by regulating PARP-1, leading to the binding of PARP-1 to SIRE and modulation of Snail expression. Developmental Dynamics, 2008. (c) 2008 Wiley-Liss, Inc.
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Source: http://www.hubmed.org/display.cgi?uids=18773488
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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Sun, Sep 7, 2008 at 3:45 AM
Subject: Integrin-linked kinase regulates E-cadherin expression through PARP-1.
To: mesothelioma77@gmail.com
[1]Dev Dyn. 2008 Sep 4;
McPhee TR, McDonald PC, Oloumi A, Dedhar S
Repression of E-cadherin expression by the transcription factor, Snail, is implicated in epithelial to mesenchymal transition and cancer progression. We show here that Integrin-Linked Kinase (ILK) regulates E-cadherin expression through Poly(ADP-ribose) polymerase-1 (PARP-1). ILK overexpression in Scp2 cells resulted in stimulation of Snail expression and loss of E-cadherin expression. Silencing of ILK, Akt or Snail resulted in re-expression of E-cadherin in PC3 cells. To elucidate the signaling pathway downstream of ILK, we identified candidate Snail promoter ILK Responsive Element (SIRE) binding proteins. PARP-1 was identified as a SIRE-binding protein. ILK silencing inhibited binding of PARP-1 to SIRE. PARP-1 silencing resulted in inhibition of Snail and ZEB1, leading to up-regulation of E-cadherin. We suggest a model in which ILK represses E-cadherin expression by regulating PARP-1, leading to the binding of PARP-1 to SIRE and modulation of Snail expression. Developmental Dynamics, 2008. (c) 2008 Wiley-Liss, Inc.
___
Source: http://www.hubmed.org/display.cgi?uids=18773488
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