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. 2006 Oct 9;26(24):9232–9243. doi: 10.1128/MCB.01312-06

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Copyright © 2006, American Society for Microbiology

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FIG. 5. — GSK-3β phosphorylation and activity are regulated by cell confluence. (A) Quiescent confluent (C) and nonconfluent (NC) mIMCD-3 cells plated for 24 h were stimulated in the presence or absence of HGF (40 ng/ml) for 10 min and immunoblotted with anti (α)-pGSK-3β (upper panel) and α-GSK-3β (lower panel). (B) Densitometric quantification of four independent experiments was performed as described for panel A. , P < 0.01 versus nonconfluent cells plus HGF. (C) Quiescent nonconfluent and confluent cells were treated with HGF for the indicated times (minutes), and lysates were immunoblotted with α-pGSK-3β (upper panel) and α-GSK-3β (lower panel). (D) Quiescent nonconfluent cells were pretreated for 20 min with either 10 μM LY294002 or 10 μM Akt IV inhibitor (AktI) and then treated in the presence or absence of HGF for 10 min, and cell lysates were immunoblotted with α-pGSK-3β (upper panel) and α-GSK-3β (lower panel). (E) Quiescent confluent and nonconfluent mIMCD-3 cells were stimulated with HGF for the indicated times and immunoblotted with α-pβ-catenin (upper panel) and α-β-catenin (lower panel). (F) Densitometric quantification of four independent experiments was performed as described for panel E. , P < 0.01 versus nonconfluent cells in the absence of HGF; , P < 0.01 versus nonconfluent cells in the presence of HGF for 360 min.

Inline graphic — GSK-3β phosphorylation and activity are regulated by cell confluence. (A) Quiescent confluent (C) and nonconfluent (NC) mIMCD-3 cells plated for 24 h were stimulated in the presence or absence of HGF (40 ng/ml) for 10 min and immunoblotted with anti (α)-pGSK-3β (upper panel) and α-GSK-3β (lower panel). (B) Densitometric quantification of four independent experiments was performed as described for panel A. , P < 0.01 versus nonconfluent cells plus HGF. (C) Quiescent nonconfluent and confluent cells were treated with HGF for the indicated times (minutes), and lysates were immunoblotted with α-pGSK-3β (upper panel) and α-GSK-3β (lower panel). (D) Quiescent nonconfluent cells were pretreated for 20 min with either 10 μM LY294002 or 10 μM Akt IV inhibitor (AktI) and then treated in the presence or absence of HGF for 10 min, and cell lysates were immunoblotted with α-pGSK-3β (upper panel) and α-GSK-3β (lower panel). (E) Quiescent confluent and nonconfluent mIMCD-3 cells were stimulated with HGF for the indicated times and immunoblotted with α-pβ-catenin (upper panel) and α-β-catenin (lower panel). (F) Densitometric quantification of four independent experiments was performed as described for panel E. , P < 0.01 versus nonconfluent cells in the absence of HGF; , P < 0.01 versus nonconfluent cells in the presence of HGF for 360 min.