NEDD4-1 is a proto-oncogenic ubiquitin ligase for PTEN.

By Xinjiang Wang, L. Trotman, T. Koppie, A. Alimonti, Zhenbang Chen, Zhonghua Gao, Junru Wang, H. Erdjument‐Bromage, Paul Tempst, C. Cordon-Cardo and 2 more. Cell, 2007

720 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b8a690d7015937fd6b4c93acaf9a1059d26721f6

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Citations in the corpus

Tenets of PTEN tumor suppression. (2008, background): “Cell 133, May 2, 2008 ©2008 Elsevier Inc. 407 and its overexpression mediates both the mono- and polyubiquitination of PTEN (Wang 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”
Ubiquitination regulates PTEN nuclear import and tumor suppression. (2007, methodology): “Because NEDD4-1 in addition to PTEN polyubiquitination also mediates its monoubiquitination in vitro and in vivo (Wang et al., 2007), we conclude that PTEN monoubiquitination at discrete lysines, including K13 and K289, directly regulates its import and shuttling.”
The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “On the other hand, ubiquitinylation-dependent proteasomal degradation of PTEN reduces its levels (Torres and Pulido, 2001; Wu et al., 2003; Wang et al., 2007).”
The age of crosstalk: phosphorylation, ubiquitination, and beyond. (2007, background): “Recent global phosphoproteomic analyses have revealed many diphosphorylated peptides corresponding to different motifs ( Villen et al., 2007 ), and it seems likely that these double phosphorylations act combinatorially.”
Physiological functions of the HECT family of ubiquitin ligases (2009, background): “An oncogenic role for NEDD4 as an E3 ligase for the tumour suppressor PTEN has been propose”
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): “The identity of the E3 ubiquitin ligase responsible for polyubiquitylation of PTEN has been controversial (458, 1674), but most recent studies suggest that WWP2 that belongs to the NEDD4-like family of E3 ligases is the elusive PTEN E3 ubiquitin ligase (967).”
PTEN and the PI3-kinase pathway in cancer. (2009, background): “(67) identified NEDD4–1 as an E3 ligase that ubiquitinates PTEN at several lysine residues including K289, a residue also targeted by mutation in a CS patient.”
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”