Cdh1, a Substrate-recruiting Component of Anaphase-promoting Complex/Cyclosome (APC/C) Ubiquitin E3 Ligase, Specifically Interacts with Phosphatase and Tensin Homolog (PTEN) and Promotes Its Removal from Chromatin

Choi, Byeong Hyeok; Pagano, Michele; Huang, Chuanshu; Dai, Wei

doi:10.1074/jbc.m114.559005

Cited by 21 publications

(22 citation statements)

References 26 publications

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“…Through 62 activation of NEDD4-1, Ndfip1 and Ndfip2 associate with PTEN, and 63 promote both polyubiquitination-mediated PTEN degradation [9] 64 and monoubiquitination-facilitated PTEN nuclear trafficking [10]. 65 Nuclear PTEN contributes to genome stability [11] and cell cycle reg-66 ulation [12,13].…”

Section: Sipl1-facilitated Pten Ubiquitination Contributes To Its Assmentioning

confidence: 98%

SIPL1-facilitated PTEN ubiquitination contributes to its association with PTEN

Melo

Lin

et al. 2014

Cellular Signalling

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Section: Sipl1-facilitated Pten Ubiquitination Contributes To Its Assmentioning

confidence: 98%

SIPL1-facilitated PTEN ubiquitination contributes to its association with PTEN

Melo

Lin

et al. 2014

Cellular Signalling

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“…Nuclear PTEN interacts with anaphase-promoting complex/cyclosome (APC/C) and its substrate-specific activator, CDH1, to promote APC-CDH1-mediated degradation of cyclin B (Song et al, 2011 ). Importantly, it is nuclear localization of PTEN and not its phosphatase activity that accounts for regulation of the APC-CDH1 ubiquitination complex (Song et al, 2011 ; Choi et al, 2014 ). On the other hand, APC and CDH1 facilitate removal of chromatin-bound PTEN, an important step for mitotic exit (Choi et al, 2014 ).…”

Section: Nuclear Pi(345)p 3 Phosphatasesmentioning

confidence: 99%

Nuclear PI3K signaling in cell growth and tumorigenesis

Davis

Lehmann

Liu

2015

Front. Cell Dev. Biol.

112

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The PI3K/Akt signaling pathway is a major driving force in a variety of cellular functions. Dysregulation of this pathway has been implicated in many human diseases including cancer. While the activity of the cytoplasmic PI3K/Akt pathway has been extensively studied, the functions of these molecules and their effector proteins within the nucleus are poorly understood. Harboring key cellular processes such as DNA replication and repair as well as nascent messenger RNA transcription, the nucleus provides a unique compartmental environment for protein–protein and protein–DNA/RNA interactions required for cell survival, growth, and proliferation. Here we summarize recent advances made toward elucidating the nuclear PI3K/Akt signaling cascade and its key components within the nucleus as they pertain to cell growth and tumorigenesis. This review covers the spatial and temporal localization of the major nuclear kinases having PI3K activities and the counteracting phosphatases as well as the role of nuclear PI3K/Akt signaling in mRNA processing and exportation, DNA replication and repair, ribosome biogenesis, cell survival, and tumorigenesis.

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“…1). As reported in our early studies, PTEN undergoes cell-cycle dependent nuclear localization, peaking at mitosis [27, 28]. It is conceivable that deregulated PTEN regulation due to exposure to As(III) would exert a negative impact on mitotic progression, leading to CIN and aneuploidy.…”

Section: Discussionmentioning

confidence: 63%

PTEN is a negative regulator of mitotic checkpoint complex during the cell cycle

2017

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Nuclear PTEN plays an important role during mitosis. To understand the molecular basis by which PTEN mediates mitotic progression, we examined whether PTEN regulated the formation of mitotic checkpoint complex (MCC). We observed that arsenic trioxide, a mitotic inducer, stimulated nuclear translocation of PTEN in a time-dependent manner. PTEN physically interacted with Cdc20 and Mad2, two important components of MCC. Arsenic treatment diminished the physical association of PTEN with BubR1 and Bub3 but not with Cdc20 and Mad2. Our further studies revealed that downregulation of PTEN via RNAi enhanced formation of MCC during the cell cycle. Moreover, PTEN silencing induced chromosomal instability. Given the crucial role of PTEN in suppressing tumor development, our study strongly suggests that PTEN also functions to maintain chromosomal stability, partly through suppressing unscheduled formation of MCC.

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Cdh1, a Substrate-recruiting Component of Anaphase-promoting Complex/Cyclosome (APC/C) Ubiquitin E3 Ligase, Specifically Interacts with Phosphatase and Tensin Homolog (PTEN) and Promotes Its Removal from Chromatin

Cited by 21 publications

References 26 publications

SIPL1-facilitated PTEN ubiquitination contributes to its association with PTEN

SIPL1-facilitated PTEN ubiquitination contributes to its association with PTEN

Nuclear PI3K signaling in cell growth and tumorigenesis

PTEN is a negative regulator of mitotic checkpoint complex during the cell cycle

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