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The Nedd4-like ubiquitin E3 ligases target angiomotin/p130 to ubiquitin-dependent degradation.
TLDR
It is reported that AMOT undergoes proteasomal degradation, and three members of Nedd4 (neural-precursor-cell-expressed developmentally down-regulated)-like ubiquitin E3 ligases are identified as the ubiquitine ligases for the long isoform of AMOT, AMOT/p130 in vivo. Expand
Intrinsic BET inhibitor resistance in SPOP-mutated prostate cancer is mediated by BET protein stabilization and AKT–mTORC1 activation
TLDR
It is demonstrated that wild-type SPOP binds to and induces ubiquitination and proteasomal degradation of BET proteins by recognizing a degron motif common among them, and resistance to BET inhibitors in SPOP-mutant prostate cancer can be overcome by combination with AKT inhibitors. Expand
The Ubiquitin Ligase Itch Regulates Apoptosis by Targeting Thioredoxin-interacting Protein for Ubiquitin-dependent Degradation*
TLDR
It is reported that TXNIP undergoes proteasomal degradation in cells and is identified as the E3 ubiquitin ligase for Itch, which establishes a new mechanism for the negative regulation ofTXNIP by Itch and sheds new light on the regulation of cellular redox homeostasis. Expand
Front-signal-dependent accumulation of the RHOA inhibitor FAM65B at leading edges polarizes neutrophils
TLDR
FAM65B deficiency in neutrophils resulted in an increase in RHOA activity and localization of pMLC to the front of cells, as well as defects in chemotaxis directionality and adhesion to endothelial cells under flow. Expand
Destruction of DDIT3/CHOP Protein by Wild‐Type SPOP but Not Prostate Cancer‐Associated Mutants
TLDR
Novel molecular events underlying the regulation of DDIT3 protein homeostasis are revealed and insight is provided in understanding the relationship between SPOP mutations and ER stress dysregulation in prostate cancer. Expand
Endometrial cancer-associated mutants of SPOP are defective in regulating estrogen receptor-α protein turnover
TLDR
Novel molecular mechanisms underlying the regulation of ERα protein homeostasis in physiological and pathological conditions are revealed, and insights are provided in understanding the relationship between SPOP mutations and the development of endometrial cancer. Expand
Dysregulation of INF2-mediated mitochondrial fission in SPOP-mutated prostate cancer
TLDR
Novel molecular events underlying the regulation of INF2 function and localization are revealed, and insights are provided in understanding the relationship between SPOP mutations and dysregulation of mitochondrial dynamics in prostate cancer. Expand
Tumor suppressor SPOP mediates the proteasomal degradation of progesterone receptors (PRs) in breast cancer cells.
TLDR
This study revealed novel molecular mechanisms underlying the regulation of PR protein homeostasis in breast cancer cells, and provided insights in understanding the relationship between SPOP inactivation and the development of breast cancer. Expand
Stabilization of MCRS1 by BAP1 prevents chromosome instability in renal cell carcinoma.
TLDR
A novel mechanism for BAP1 involved in MCRS1 stability regulation is revealed, and insight is provided in understanding the relationship between B AP1 mutations and chromosome instability in ccRCC. Expand
SPOP promotes ATF2 ubiquitination and degradation to suppress prostate cancer progression
TLDR
SPOP promotes ATF2 ubiquitination and degradation, and ATF2 is an important mediator of SPOP inactivation-induced cell proliferation, migration and invasion, and is identified as a bona fide substrate of the SPOP-CUL3-RBX1 E3 ubiquitin ligase complex. Expand
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