ArticleScientific reports2016
SAG/RBX2 E3 ligase complexes with UBCH10 and UBE2S E2s to ubiquitylate β-TrCP1 via K11-linkage for degradation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- TRIM25 enhances hypoxia signaling by catalyzing K11-linked polyubiquitination and stabilization of HIF-α.The Journal of biological chemistry · 2026Article
- The Crosstalk Between CRL5 and APC/C E3 Ligases Regulates Metastasis and Chemosensitivity of Cancer Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Ubiquitin Script: writing protein fates in chains.Essays in biochemistry · 2025Review
- FBXO10 Drives Hepatocellular Carcinoma Proliferation via K63-Linked Ubiquitination and Stabilization of FRMPD1.Current issues in molecular biology · 2025Article
- Review
- The UBE2C/CDH1/DEPTOR axis is an oncogene and tumor suppressor cascade in lung cancer cells.The Journal of clinical investigation · 2023Article
- The Functional Redundancy of Neddylation E2s and E3s in Modulating the Fitness of Regulatory T Cells.Research (Washington, D.C.) · 2023Article
- The Ube2m-Rbx1 neddylation-Cullin-RING-Ligase proteins are essential for the maintenance of Regulatory T cell fitness.Nature communications · 2022Article
- An integrative pan-cancer analysis revealing the difference in small ring finger family of SCF E3 ubiquitin ligases.Frontiers in immunology · 2022Article
- The Molecular Basis of Ubiquitin-Conjugating Enzymes (E2s) as a Potential Target for Cancer Therapy.International journal of molecular sciences · 2021Review
- Beyond K48 and K63: non-canonical protein ubiquitination.Cellular & molecular biology letters · 2021Review
- Mutual inactivation of two RING-finger-type E3 ubiquitin ligases during cell cycle progression.Molecular & cellular oncology · 2021Article
- The Negative Cross-Talk between SAG/RBX2/ROC2 and APC/C E3 Ligases in Regulation of Cell Cycle Progression and Drug Resistance.Cell reports · 2020Article
- Transgenic expression of Sag/Rbx2 E3 causes early stage tumor promotion, late stage cytogenesis and acinar loss in the Kras-PDAC model.Neoplasia (New York, N.Y.) · 2020Article
- SAG expression associates with COPB2-related signaling and a poorer prognosis in breast cancer.Aging · 2020Article
- Inactivation of SAG or ROC1 E3 Ligase Inhibits Growth and Survival of Renal Cell Carcinoma Cells: Effect of BIM.Translational oncology · 2019Article
- Hepatitis C Virus Downregulates Ubiquitin-Conjugating Enzyme E2S Expression To Prevent Proteasomal Degradation of NS5A, Leading to Host Cells More Sensitive to DNA Damage.Journal of virology · 2019Article
- An E2-ubiquitin thioester-driven approach to identify substrates modified with ubiquitin and ubiquitin-like molecules.Nature communications · 2018Article
- Ribosomal protein S27-like regulates autophagy via the β-TrCP-DEPTOR-mTORC1 axis.Cell death & disease · 2018Article
- Ubiquitin-conjugating enzyme UBE2J1 negatively modulates interferon pathway and promotes RNA virus infection.Virology journal · 2018Article
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
SAG/RBX2 and RBX1 are two family members of RING components of Cullin-RING ligases (CRLs), required for their enzymatic activity. Previous studies showed that SAG prefers to bind with CUL5, as well as CUL1, whereas RBX1 binds exclusively to CULs1-4. Detailed biochemical difference between SAG and RBX1, and whether SAG mediates cross-talk between CRL5 and CRL1 are previously unknown. Here we report that the levels of SAG and β-TrCP1 are inversely correlated, and SAG-CUL5-βTrCP1 forms a complex under physiological condition. SAG-CUL5, but not RBX1-CUL1, negatively modulates β-TrCP1 levels by shortening its protein half-life through promoting its ubiquitylation via atypical K11-linkage. Consistently, chemical inducers of SAG reduced β-TrCP1 level. Furthermore, SAG mainly binds to E2s UBCH10 and UBE2S known to mediate K11 linkage of ubiquitin, whereas RBX1 exclusively binds to E2s CDC34 and UBCH5C, known to mediate K48 linkage of ubiquitin. Finally, silencing of either UBCH10 or UBE2S, but not UBCH5C, caused accumulation of endogenous β-TrCP1, suggesting that β-TrCP1 is a physiological substrate of SAG-UBCH10C/UBE2S. Our study, for the first time, differentiates SAG and RBX1 biochemically via their respective binding to different E2s; and shows a negative cross-talk between CRL5 and CRL1 through SAG mediated ubiquitylation of β-TrCP1.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.