Ubiquitination regulates PTEN nuclear import and tumor suppression.
By L. Trotman, Xinjiang Wang, A. Alimonti, Zhenbang Chen, J. Teruya-Feldstein, Haijuan Yang, N. Pavletich, B. Carver, C. Cordon-Cardo, H. Erdjument‐Bromage and 6 more. Cell, 2007
759 citations recorded by the source corpus.
Subfields: Genetics, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/1022d1f25f28964b0ddb85600511ff4b5cb5b3eb
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In Genetics
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Citations in the corpus
- Physiological functions of the HECT family of ubiquitin ligases (2009, background): “It was suggested that, whereas NEDD4-mediated polyubiquitylation of PTEN in the cytosol targets it for proteasomal degradation, NEDD4-mediated monoubiquitylation of PTEN might direct it to the nucleus, where it is protected from degradation and where it regulates chromosomal integrit”
- PTEN loss in the continuum of common cancers, rare syndromes and mouse models (2011, positive): “PTEN amino acids Lys13 and Lys289 are monoubiquitylated, which leads to nuclear import in vitro , and Lys289 mutations have been observed in Cowden syndrome and associated with nuclear exclusio”
- Cellular Senescence: Aging, Cancer, and Injury. (2019, background): “Analysis of senescence markers in human cancer biopsies from patients previously exposed to neoadjuvant chemotherapy confirmed the occurrence of TIS and its association to treatment outcome (12, 293, 316, 321).”
- Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging (2011, background): “These mutations leave the phosphatase activity intact [115].”
- Synthetic lethal targeting of PTEN mutant cells with PARP inhibitors (2009, positive): “…specifically be assessed in tumourigenic conditions such as the more aggressive forms of oesophageal squamous cell carcinoma (Tachibana et al, 2002), cutaneous melanoma (Whiteman et al, 2002) and colorectal cancer (Trotman et al, 2007; Zhou et al, 2002), where nuclear PTEN expression is absent.”
- Tenets of PTEN tumor suppression. (2008, background): “What we have learned is that unlike cytoplasmic PTEN, the effects of nuclear PTEN are likely not mediated directly through AKT (Liu et al., 2005b), yet this is at odds with the finding that enforced nuclear PTEN expression can reduce cellular levels of phosphorylated AKT (Trotman et al., 2007).”
- The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “Lastly, PTEN nuclear–cytoplasmic shuttling is of great importance for the proper tumor-suppressive activity of the phosphatase (Denning et al., 2007; Trotman et al., 2007).”
- Excitotoxicity and stroke: identifying novel targets for neuroprotection. (2014, positive): “translocation (Trotman et al., 2007; Walker et al., 2004), protected neurons from GluN2BR-mediated excitotoxic neuronal death (Zhang et al.”
- Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “Analysis of such mutants has confirmed that aberrant sequestration of PTEN into either the nucleus or the cytoplasm compromises its tumor suppressor function (Denning et al. 2007; Trotman et al. 2007).”
- The role of ubiquitination in tumorigenesis and targeted drug discovery (2020, background): “However, most of these inhibitors work well in cell culture studies and not well enough in animal models and clinical trials.(164,168,506) One reason for this unsatisfactory situation is the incomplete understanding of the structural analysis of target proteins, pharmaceutical chemistry and combinat”
- Dysregulation of AKT Pathway by SMYD2-Mediated Lysine Methylation on PTEN (2015, background): “In addition, the E3 ligase neural precursor cell expressed developmentally down-regulated protein 4 monoubiquitylates and polyubiquitylates PTEN; polyubiquitylation promotes rapid degradation, whereas monoubiquitylation is important for PTEN nuclear translocation [11,12].”
- Phosphoinositides: tiny lipids with giant impact on cell regulation. (2013, background): “Monoubiquitylation of PTEN, on the other hand, was found important for nuclear localization and tumor suppression (1579), at the same time mono- or poly-ubiquitylation was shown to inhibit PTEN phosphatase activity (964).”
- Targeting the ubiquitin system in cancer therapy (2009, background): “The tumour suppressor PTEN (phosphatase and tensin homologue) is also subject to monoubiquitin- and polyubiquitin-dependent regulatio”
- PTEN and the PI3-kinase pathway in cancer. (2009, background): “These authors (85) showed that PTEN harboring a germline K289E mutation in intestinal polyps of a CS patient was excluded from the nucleus, although it retained its catalytic activity.”