In this article (Cancer Discovery 2011;1:170–85), which appeared in the July 2011 issue of Cancer Discovery (1), the labels along the vertical axes in Figure 5 were incorrectly formatted. The amended figure appears on the next page. The publisher regrets this error.

Figure 5.

A, HEC1A cells transfected with LacZ or p85α WT or E160* were treated with cycloheximide (CHX; left) for indicated duration or with MG132 (center) for 24 hours. Cells were then harvested for WB. PTEN levels were normalized to β-actin by densitometry (below). *, P < 0.05. Right, HEC1A cells were transfected with LacZ or WT or E160* in the absence or presence of ubiquitin (Ub) for 72 hours. Whole-cell lysates were collected for IP with anti-PTEN and then subjected to WB with anti-ubiquitin. PTEN protein levels were normalized prior to IP by using proportionally different amounts of lysates. B, left, HEC1A cells were transfected with LacZ or WT or its mutants for 72 hours and were collected for IP with PTEN and WB with anti-p85α. HEC1A cells were co-transfected with WT or increasing amount of E160*. Cell lysates were collected for IP (center) or WB (right top). Right bottom, transfected HEC1A cells were treated with CHX for the indicated time points and harvested for WB. C, cells were transfected with HA-tagged p85α (HA-p85α) and/or Flag-tagged p85α (Flag-p85α) in the absence (left) or presence (center) of increasing amounts of E160*. IP was performed with anti-HA and WB with anti-Flag. Right, cells were transfected with HA-p85α and increasing amounts of E160*. IP was performed with anti-HA and WB with anti-p85α. D, left, cells were transfected with WT p110α, Flag-p85α, and E160*. IP was performed with anti-Flag and WB with anti-p85α. Center, cells were transfected with WT p110α, Flag-p85α, and HA-p85α. IP was performed with anti-HA and WB with anti-Flag. Right, cells were transfected with WT p110α and HA-p85α, IP was performed with PTEN and WB with p85α. Numerical values below each lane of the immunoblots represent quantification of the relative protein level by densitometry.

Figure 5.

A, HEC1A cells transfected with LacZ or p85α WT or E160* were treated with cycloheximide (CHX; left) for indicated duration or with MG132 (center) for 24 hours. Cells were then harvested for WB. PTEN levels were normalized to β-actin by densitometry (below). *, P < 0.05. Right, HEC1A cells were transfected with LacZ or WT or E160* in the absence or presence of ubiquitin (Ub) for 72 hours. Whole-cell lysates were collected for IP with anti-PTEN and then subjected to WB with anti-ubiquitin. PTEN protein levels were normalized prior to IP by using proportionally different amounts of lysates. B, left, HEC1A cells were transfected with LacZ or WT or its mutants for 72 hours and were collected for IP with PTEN and WB with anti-p85α. HEC1A cells were co-transfected with WT or increasing amount of E160*. Cell lysates were collected for IP (center) or WB (right top). Right bottom, transfected HEC1A cells were treated with CHX for the indicated time points and harvested for WB. C, cells were transfected with HA-tagged p85α (HA-p85α) and/or Flag-tagged p85α (Flag-p85α) in the absence (left) or presence (center) of increasing amounts of E160*. IP was performed with anti-HA and WB with anti-Flag. Right, cells were transfected with HA-p85α and increasing amounts of E160*. IP was performed with anti-HA and WB with anti-p85α. D, left, cells were transfected with WT p110α, Flag-p85α, and E160*. IP was performed with anti-Flag and WB with anti-p85α. Center, cells were transfected with WT p110α, Flag-p85α, and HA-p85α. IP was performed with anti-HA and WB with anti-Flag. Right, cells were transfected with WT p110α and HA-p85α, IP was performed with PTEN and WB with p85α. Numerical values below each lane of the immunoblots represent quantification of the relative protein level by densitometry.

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1.
Cheung
LW
,
Hennessy
BT
,
Li
J
,
Yu
S
,
Myers
AP
,
Djordjevic
B
, et al
High frequency of PIK3R1 and PIK3R2 mutations in endometrial cancer elucidates a novel mechanism for regulation of PTEN protein stability
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Cancer Discovery
2011
;
1
:
170
85
.