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identified the RING E3 ligase complex Cullin-3-Rbx1-KCTD10 as key modulator of endothelial barrier integrity via its regulation of the ubiquitination, localization, and activity of RhoB.
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The E3 ubiquitin ligase and RNA-binding protein ZNF598 orchestrate ribosome quality control of premature polyadenylated mRNAs.
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SESN2 is critical to protect cells against detrimental effect of mitochondrial damage and RBX1 is a negative regulator of SESN2 which hampers its stabilization.
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RBX-1 overexpression in bladder UCC is associated with high tumor grade and advanced stage and represents biological potential of invasiveness and aggressive disease.
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The crystal structure of a pentameric CRL2(VHL) complex, composed of Cul2, Rbx1, Elongin B, Elongin C, and pVHL reveals how Rbx1 interacts with Cullin 2.
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Study demonstrated that ROC1 was overexpressed in esophageal squamous cell carcinomas, which was positive associated with poor prognosis of esophageal cancer patients.
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p97 negatively regulates NRF2 through the canonical pathway by extracting ubiquitylated NRF2 from the KEAP1-CUL3 E3 complex.
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Regulation of substrate ubiquitination and polyubiquitination takes place through Rbx1 rotations.
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High RBX1 expression was related to poor tumor differentiation, advanced TNM stage, and lymph node metastasis in non-small cell lung cancer.
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Data show that melanoma antigen, family C, 2 protein (MAGE-C2) binds with RING-box protein 1 (Rbx1) and Cullin 1, and regulates cyclin E stability in melanoma cells.
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ROC1 has an important role in the malignant progression of bladder transitional cell carcinoma via the mTOR/DEPTOR pathway.
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Nedd8(Q40E) cannot induce the same structural effect on Cul1-Rbx1 as wild-type Nedd8.
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RBX1 E3 ubiquitin protein expression responsible with multiple genetic mechanism in the development of head and neck cancer.
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This work sheds new light on the roles of NEDD8 lysines on neddylation cascades and provides a dominant negative mutant for the study of neddylation and its biological functions.
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These findings indicate that Rbx1 and Rbx2 can both activate Cul5-Vif E3 ligase in vitro, but they may undergo a more delicate selection mechanism in vivo.
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upregulation of miR-194 can inhibit proliferation, migration, and invasion of GC cells, possibly by targeting RBX1. Aberrant expression of miR-194 and RBX1 is correlated to GC patient survival time.
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RBX1 expression level was associated with the proliferation of gastric cancer.
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Studied the DNA-level mechanisms affecting KEAP1/CUL3/RBX1 E3-ubiquitin ligase complex as a regulator of NRF2 levels in ovarian cancer.
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eEF1A1 may mediate SAMHD1 turnover by targeting it to the proteosome for degradation through association with Cullin4A and Rbx1.
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data suggest a new paradigm for Hsp90-modulated assembly of a Cul3/DBC2 E3 ubiquitin ligase complex that may extend to other E3 ligase complexes.
