Affinage

CUL7

Cullin-7 · UniProt Q14999

Length
1698 aa
Mass
191.2 kDa
Annotated
2026-06-09
44 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CUL7 is a cullin-family scaffold that nucleates an SCF-ROC1-like E3 ubiquitin ligase governing cell growth, proliferation, and survival (PMID:12481031, PMID:16142236). It assembles a complex with SKP1, RBX1/ROC1, and the F-box protein FBXW8, recruiting the SKP1·FBXW8 heterodimer selectively rather than SKP1 alone or SKP1 bound to other F-box proteins (PMID:12481031, PMID:16142236), and in an FBXW8-dependent manner it further heterodimerizes with CUL1 (PMID:16880526). Through this ligase activity CUL7 targets a series of substrates whose turnover shapes growth-factor signaling and apoptosis: IRS-1, degraded in an mTOR/S6K-dependent fashion to restrain AKT and MEK/ERK signaling (PMID:18498745); the kinase HPK1, ubiquitinated in a phosphorylation-dependent manner that is antagonized by PP4 (PMID:24362026); serum-stimulated, phospho-dependent TBC1D3 (PMID:23029530); and additional substrates including caspase-8, which CUL7 modifies with non-degradative K215 polyubiquitin to suppress TRAIL-induced apoptosis (PMID:30807646), and AID, via a complex with FBXW11 controlling B-cell class switching (PMID:31092637). Beyond ubiquitination, CUL7 directly binds the tetramerization domain of p53 through a discrete CPH domain whose SH3/Tudor-like fold and distinct binding surface were defined by NMR (PMID:16875676, PMID:17298945), and it forms mutually exclusive complexes with either FBXW8 or the related cullin PARC (PMID:17332328, PMID:15964813). In vivo, CUL7 is essential for placental vascular morphogenesis and trophoblast differentiation (PMID:12904573) and for normal IGF1/AKT signaling (PMID:21737058, PMID:23018678), and loss-of-function mutations cause the primordial growth disorder 3-M syndrome (PMID:16142236). CUL7 binding is also required for SV40 large T antigen-mediated cellular transformation (PMID:16140746).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2002 High

    Establishing that CUL7 is a bona fide cullin defined the molecular machine: which cofactors it recruits and how it differs from canonical SCF ligases.

    Evidence Mass spectrometry identification as a ROC1-interactor, co-IP, and domain deletion mapping

    PMID:12481031

    Open questions at the time
    • No substrate identified at this stage
    • Catalytic activity inferred from complex composition rather than direct ubiquitination assay
  2. 2003 High

    Knockout of Cul7 in mice answered whether the complex matters physiologically, revealing an essential role in placental and vascular development.

    Evidence Targeted mouse gene disruption with histological analysis; co-IP defining the complex including FAP68/glomulin

    PMID:12904573

    Open questions at the time
    • Substrate driving the developmental phenotype unknown at this stage
    • Molecular basis of vascular defect not resolved
  3. 2005 High

    Linking CUL7 mutations to 3-M syndrome connected ligase assembly defects to a human growth disorder, showing disease mutations impair ROC1 recruitment.

    Evidence Disease-mutation functional assays (R1445X, H1464P) with deletion mapping and co-IP

    PMID:16142236

    Open questions at the time
    • Substrate whose stabilization causes growth failure not yet defined
    • Tissue-specific basis of growth-plate phenotype unaddressed
  4. 2005 Medium

    Identification of PARC as a CUL7 dimerization partner introduced a homolog that shares interactions but has non-overlapping function.

    Evidence Mass spectrometry, co-IP, and Parc knockout mouse (no overt phenotype)

    PMID:15964813

    Open questions at the time
    • Functional significance of PARC-CUL7 heterodimers unresolved
    • PARC does not affect p53 stability, leaving its role unclear
  5. 2005 High

    SV40 large T antigen mapping established CUL7 as a growth-control target whose inactivation enables transformation, hinting at tumor-suppressor function.

    Evidence T antigen deletion mutagenesis (delta69-83) with co-IP and MEF transformation assays

    PMID:14990695 PMID:16140746

    Open questions at the time
    • Mechanism by which T antigen neutralizes CUL7 not defined
    • Whether CUL7 acts as suppressor or oncogene context-dependent
  6. 2006 High

    Defining the CPH domain and the CUL7-CUL1 heterodimer dissected how CUL7 engages p53 and partitions FBXW8-dependent versus -independent functions.

    Evidence Domain deletion with localization imaging; FBXW8-knockout mice and genetic epistasis for CUL1 association

    PMID:16875676 PMID:16880526

    Open questions at the time
    • Functional consequence of CUL7-p53 binding not established here
    • Identity of FBXW8-independent CUL7 functions unknown
  7. 2007 High

    Structural and biochemical work resolved how CUL7 binds p53 and how PARC/FBXW8 complexes are organized and catalytically active.

    Evidence NMR structure of CPH domain mapping the p53 tetramerization-domain interface; TAP-MudPIT and in vitro ubiquitin ligase assays; functional cloning with siRNA

    PMID:17298945 PMID:17332328 PMID:17942889

    Open questions at the time
    • Whether p53 is a ubiquitination substrate of CUL7 or only a binding partner unresolved
    • Mechanism linking p53 binding to anti-apoptotic/transforming function incomplete
  8. 2008 High

    Identification of IRS-1 as a degradation substrate revealed how CUL7 ligase activity feeds back on insulin/IGF growth-factor signaling.

    Evidence Ubiquitin ligase assay and Cul7-/- MEF analysis with mTOR/S6K inhibition

    PMID:18498745

    Open questions at the time
    • How IRS-1 turnover relates to the senescence phenotype of Cul7-/- MEFs not fully resolved
    • Connection to 3-M growth phenotype indirect
  9. 2013 High

    HPK1 and TBC1D3 substrate identification established the recurring principle that CUL7/FBXW8 recognizes phosphorylated substrates, with phosphatases gating recruitment.

    Evidence In vitro ubiquitination assays, phosphosite mutagenesis, PP4/alkaline phosphatase treatment, and yeast two-hybrid

    PMID:23029530 PMID:24362026

    Open questions at the time
    • Kinases generating the priming phosphorylation not fully defined
    • Generality of phospho-degron recognition across substrates untested
  10. 2011 Medium

    Placing CCDC8 and OBSL1 in a CUL7 pathway and demonstrating impaired IGF1-AKT signaling clarified the 3-M syndrome circuitry.

    Evidence Co-IP, exome sequencing, and signaling assays in patient-derived CUL7-/- fibroblasts

    PMID:21737058 PMID:23018678

    Open questions at the time
    • CCDC8 does not bind CUL7 directly; intermediary role of OBSL1 needs biochemical detail
    • Substrate mediating the IGF1-AKT defect not identified
  11. 2019 High

    Caspase-8 and AID substrate work expanded CUL7 into apoptosis control and immune regulation, including a non-degradative ubiquitination mode.

    Evidence Co-IP, ubiquitination assays with K215 mutagenesis, conditional CUL7 knockout, apoptosis and class-switch assays

    PMID:30807646 PMID:31092637

    Open questions at the time
    • F-box adaptor for caspase-8 recognition not defined
    • Whether AID ubiquitination requires FBXW11 exclusively versus canonical FBXW8 unclear
  12. 2026 Medium

    A wave of substrate and regulatory studies (MST1, GPX4, KEAP1, HER2) and neddylation control extended CUL7 into ferroptosis, oxidative stress, and additional cancers.

    Evidence Co-IP, linkage-specific ubiquitination assays, CAND1/CCDC8 knockdown, MLN4924 neddylation inhibition, and in vivo tumor/retinal models

    PMID:32252802 PMID:39267786 PMID:41310794 PMID:41644704 PMID:42252284

    Open questions at the time
    • Several substrate claims rest on single-lab assays without reconstitution
    • How CAND1 and neddylation dynamically gate CUL7 activity across substrates not unified
    • Whether these substrates share an F-box adaptor unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how the proliferating substrate set is selected, which adaptors recruit non-FBXW8 substrates, and how CUL7 activity is dynamically regulated by neddylation and CAND1 in vivo.
  • No unified model of substrate-adaptor pairing
  • Physiological regulation of CUL7 neddylation across tissues unknown
  • Reconciliation of tumor-suppressor versus oncogenic roles incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 5 GO:0016874 ligase activity 3 GO:0060089 molecular transducer activity 2
Localization
GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-392499 Metabolism of proteins 4 R-HSA-1266738 Developmental Biology 2 R-HSA-5357801 Programmed Cell Death 2
Partners
CUL1FBXW11FBXW8OBSL1PARCRBX1SKP1TP53
Complex memberships
CUL7-CUL1 heterodimerCUL7-PARC dimerCUL7-SKP1-RBX1-FBXW8 SCF-like E3 ligase

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 CUL7 assembles an SCF-ROC1-like E3 ubiquitin ligase complex consisting of Skp1, CUL7, the Fbx29 (FBXW8) F-box protein, and ROC1. CUL7 was identified by mass spectrometry as a ROC1-interacting protein. CUL7 contains a cullin domain responsible for ROC1 binding and a DOC domain. Unlike CUL1 which binds Skp1 alone, CUL7 interacts selectively with the Skp1·Fbx29 heterodimer but not with Skp1 alone, nor with Skp1·betaTRCP2 or Skp1·Skp2. Mass spectrometry identification, co-immunoprecipitation, deletion/domain analysis Proceedings of the National Academy of Sciences of the United States of America High 12481031
2003 CUL7 (p185) forms an SCF-like complex with Skp1, Rbx1, Fbw6 (Fbx29/FBXW8), and FAP68 (glomulin). Targeted disruption of Cul7 in mice results in runted embryos that die at birth with respiratory distress, dermal hemorrhage, and placental defects including abnormal trophoblast differentiation and vascular structure, demonstrating a role for CUL7 in vascular morphogenesis and placental development. Co-immunoprecipitation, mouse knockout (targeted gene disruption), histological analysis Proceedings of the National Academy of Sciences of the United States of America High 12904573
2005 CUL7 assembles an E3 ubiquitin ligase complex with SKP1, RBX1, and the F-box protein FBXW8. CUL7 nonsense (R1445X) and missense (H1464P) mutations associated with 3-M syndrome render CUL7 deficient in recruiting ROC1, suggesting impaired ubiquitination underlies the pathogenesis. CUL7 uses its central region to interact with the Skp1-Fbx29 heterodimer. Deletion analysis, co-immunoprecipitation, mutant functional assay Nature genetics High 16142236
2004 SV40 large T antigen binds the CUL7 SCF-like complex (containing p185/CUL7, Rbx1, and Fbw6/FBXW8) via an N-terminal region. p185/CUL7-binding-deficient T antigen mutants retain binding to pRb and p53 but are unable to transform primary mouse embryo fibroblasts, indicating that CUL7 binding is required for T antigen-mediated cellular transformation and that CUL7 may regulate a growth control pathway. Co-immunoprecipitation, T antigen mutagenesis, focus formation / anchorage-independent growth assays, MEF transformation Journal of virology High 14990695
2005 SV40 T antigen residues 69–83 are required for binding to the CUL7 complex. Delta69-83 T antigen loses CUL7 binding while retaining p53 and pRB binding. Wild-type T antigen induces MEF proliferation (transformation) in the presence of CUL7, but delta69-83 T antigen does not, suggesting CUL7 is a target whose inactivation by T antigen contributes to transformation and that CUL7 may function as a tumor suppressor. Deletion mutagenesis, co-immunoprecipitation, MEF proliferation and transformation assays Journal of virology High 16140746
2006 CUL7 forms a heterodimeric complex with CUL1 in a manner dependent on FBXW8 (Fbxw8). Fbxw8-knockout mice lack CUL7–CUL1 association. Fbxw8-null mice show intrauterine growth retardation and placental defects similar to Cul7-null mice, but some abnormalities of Cul7-/- mice are absent, indicating that the CUL7–Fbxw8 complex has both Fbxw8-dependent and Fbxw8-independent functions. Co-immunoprecipitation, mouse knockout (Fbxw8 targeting), genetic epistasis Molecular and cellular biology High 16880526
2006 CUL7 directly binds p53 via a discrete, evolutionarily conserved domain (CPH domain) that is also conserved in PARC and HERC2. This p53-binding domain is necessary and sufficient for p53 interaction, p53 stabilizes expression of this domain, and the domain contributes to cytoplasmic localization of CUL7. CUL7 binding to p53 does not affect p53 expression levels. Co-immunoprecipitation, deletion analysis, subcellular localization by imaging Biochemical and biophysical research communications Medium 16875676
2007 The CPH domains of CUL7 and PARC are protein–protein interaction modules that bind the tetramerization domain of p53. NMR structure of the CUL7-CPH domain reveals a fold similar to SH3, Tudor, and KOW domains, but the p53-binding surface is distinct from the canonical peptide-binding surfaces of those domains. The p53 interaction surface on p53 resides in its tetramerization domain and involves residues from at least two subunits. NMR spectroscopy, size-exclusion chromatography, structural determination with functional validation The Journal of biological chemistry High 17298945
2007 CUL7 and PARC form homodimers and heterodimers. Tandem affinity purification–MudPIT analysis revealed that the CUL7 interaction with FBXW8 is mutually exclusive with CUL7 binding to PARC or p53. PARC binds RBX1 and is covalently modified by NEDD8, defining PARC as a cullin, but PARC fails to bind SKP1 or F-box proteins including FBXW8. All examined PARC- and CUL7-containing subcomplexes exhibit E3 ubiquitin ligase activity in vitro. Parc-/-/Fbxw8-/- double knockout does not exacerbate the Fbxw8-/- phenotype. Tandem affinity purification, MudPIT mass spectrometry, in vitro ubiquitin ligase assay, double-knockout genetic epistasis Cancer research High 17332328
2007 CUL7 binds p53 directly and its knockdown by siRNA elevates p53 protein levels. CUL7 exerts an anti-apoptotic function through p53, enabling it to inhibit Myc-induced apoptosis. CUL7 cooperates with Myc to drive cellular transformation in soft agar assays. Expression cloning screen, co-immunoprecipitation, siRNA knockdown, anchorage-independent growth assay Cancer research Medium 17942889
2005 PARC (a CUL7 homolog) was identified as a CUL7-interacting protein by mass spectrometry. CUL7 and PARC form endogenous hetero- and homodimers in vivo. Parc knockout mice are born at expected Mendelian ratios with no apparent phenotype, and Parc deletion does not affect p53 stability, localization, or function, indicating that PARC and CUL7 functions are at least partially non-overlapping. Mass spectrometry, co-immunoprecipitation, Parc knockout mouse Molecular and cellular biology Medium 15964813
2008 IRS-1 (insulin receptor substrate 1) is a proteolytic substrate of the CUL7 E3 ubiquitin ligase. IRS-1 degradation depends on mTOR and p70 S6 kinase activity. Cul7-/- mouse embryonic fibroblasts accumulate IRS-1 and show increased activation of Akt and MEK/ERK pathways, but grow poorly and display oncogene-induced senescence-like phenotypes. Ubiquitin ligase assay, Cul7-/- MEF analysis, signaling pathway analysis, mTOR/S6K inhibition Molecular cell High 18498745
2013 The CUL7/FBXW8 ubiquitin ligase targets hematopoietic progenitor kinase 1 (HPK1) for ubiquitination and proteasomal degradation. HPK1 ubiquitination requires its kinase activity and autophosphorylation (at Thr-355). Protein phosphatase 4 (PP4) dephosphorylates Thr-355 and inhibits Fbxw8–HPK1 interaction, thereby stabilizing HPK1. Knockdown of Fbxw8 restores endogenous HPK1 and inhibits pancreatic cancer cell proliferation. Co-immunoprecipitation, in vitro ubiquitination assay, phosphorylation/dephosphorylation analysis, siRNA knockdown, cell proliferation assay The Journal of biological chemistry High 24362026
2012 CUL7 E3 ligase ubiquitinates TBC1D3 in response to serum/growth factor stimulation, leading to its proteasomal degradation. TBC1D3 physically interacts with CUL7 (identified by yeast two-hybrid) and recruits FBXW8 in pulldown and in vitro assays. Phosphorylation of TBC1D3 is critical for Fbxw8 recruitment and subsequent ubiquitination; alkaline phosphatase treatment of TBC1D3 suppresses Fbxw8 recruitment. Yeast two-hybrid, co-immunoprecipitation, pulldown, in vitro ubiquitination assay, phosphatase treatment PloS one High 23029530
2011 CCDC8 co-immunoprecipitates with OBSL1 but not with CUL7, placing CCDC8 in a pathway with CUL7 and OBSL1 through OBSL1 as an intermediary. CUL7(-/-) cells show impaired IGF1-stimulated AKT activation, consistent with dysregulated IGF1 signaling downstream of CUL7. Co-immunoprecipitation, exome sequencing for pathway placement, signaling assays in patient-derived fibroblasts American journal of human genetics Medium 21737058
2012 CUL7(-/-) patient fibroblasts show impaired AKT activation in response to IGF1 stimulation at 5 min post-stimulation, while GH-induced STAT5b and MAPK activation is normal. This indicates CUL7 loss specifically impairs IGF1 signaling through the PI3K/AKT axis. Cell signaling assays (phospho-Western) in patient-derived CUL7-/- fibroblasts Journal of molecular endocrinology Medium 23018678
2019 CUL7 promotes cancer cell survival by interacting with Caspase-8 and promoting its modification with non-degradative polyubiquitin chains at K215, thereby preventing Caspase-8 activation. CUL7 knockdown sensitizes cancer cells to TRAIL-induced apoptosis in vitro and in nude mice. Co-immunoprecipitation, ubiquitination assay, site-directed mutagenesis (K215), siRNA knockdown, apoptosis assay in vitro and in vivo International journal of cancer High 30807646
2019 CUL7 E3 ubiquitin ligase mediates ubiquitination of AID (activation-induced cytidine deaminase) by forming a complex with FBXW11. CUL7 overexpression or knockdown regulates AID protein levels and IgA class switching in B cells. CUL7 conditional knockout (CUL7 fl/fl CD19-Cre) in mice increases AID protein levels in germinal center B cells and enhances IgG1 and IgA class switching. Co-immunoprecipitation, ubiquitination assay, CUL7 conditional knockout mouse, B cell class switch recombination assay Journal of immunology High 31092637
2020 CUL7 physically associates with MST1, promoting ubiquitin-mediated MST1 protein degradation, which activates the NF-κB signaling pathway to promote glioma cell growth. Co-immunoprecipitation, siRNA/shRNA knockdown, CUL7 overexpression, in vitro and in vivo tumor assays, western blot for NF-κB pathway markers Journal of experimental & clinical cancer research Medium 32252802
2024 CUL7 promotes ubiquitination and degradation of glutathione peroxidase 4 (GPX4) in photoreceptors. CUL7 knockdown prevents Cul7-mediated GPX4 ubiquitination and degradation, inhibiting photoreceptor ferroptosis and alleviating retinal degeneration in mouse models. Transcriptome sequencing to identify target, siRNA knockdown, ubiquitination assay (GPX4), in vivo mouse models (MNU-induced and Pde6βrd1/rd1 mutant) Theranostics Medium 39267786
2025 CUL7 promotes HER2 ubiquitination in HER2-positive breast cancer. CAND1 directly interacts with HER2 and stabilizes its expression; CAND1 knockdown enhances CUL7 neddylation, activating its ligase activity and leading to HER2 ubiquitination and destabilization. Co-immunoprecipitation, western blot, ubiquitination assay, CAND1 knockdown, in vivo xenograft Breast cancer research Medium 41310794
2026 CUL7 interacts with KEAP1 and catalyzes K29- and K48-linked polyubiquitination of KEAP1 to promote its proteasomal degradation, thereby activating NRF2 signaling and reducing ROS levels in colon cancer cells. The C-terminus of CUL7 is required for KEAP1 stability regulation. Co-immunoprecipitation, ubiquitination assay (linkage-specific), CUL7 knockout mouse model, CUL7 domain deletion, cancer cell KO/overexpression Cell death & disease Medium 42252284
2026 CCDC8 interacts with CUL7 to facilitate proteasome-dependent degradation of P53. Pharmacological inhibition of neddylation (MLN4924) restored P53 levels and reversed CCDC8-driven oncogenic effects, implicating neddylation-dependent CUL7 activity in CCDC8-mediated P53 degradation in bladder cancer. Co-immunoprecipitation, western blot, MLN4924 neddylation inhibition, in vitro and in vivo tumor assays Oncogene Medium 41644704

Source papers

Stage 0 corpus · 44 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 The CUL7 E3 ubiquitin ligase targets insulin receptor substrate 1 for ubiquitin-dependent degradation. Molecular cell 184 18498745
2005 Identification of mutations in CUL7 in 3-M syndrome. Nature genetics 146 16142236
2002 CUL7: A DOC domain-containing cullin selectively binds Skp1.Fbx29 to form an SCF-like complex. Proceedings of the National Academy of Sciences of the United States of America 136 12481031
2003 Targeted disruption of p185/Cul7 gene results in abnormal vascular morphogenesis. Proceedings of the National Academy of Sciences of the United States of America 122 12904573
2011 Exome sequencing identifies CCDC8 mutations in 3-M syndrome, suggesting that CCDC8 contributes in a pathway with CUL7 and OBSL1 to control human growth. American journal of human genetics 95 21737058
2007 Clinical, molecular and histopathological features of short stature syndrome with novel CUL7 mutation in Yakuts: new population isolate in Asia. Journal of medical genetics 64 17675530
2004 Cul7/p185/p193 binding to simian virus 40 large T antigen has a role in cellular transformation. Journal of virology 63 14990695
2020 Cullin-7 (CUL7) is overexpressed in glioma cells and promotes tumorigenesis via NF-κB activation. Journal of experimental & clinical cancer research : CR 58 32252802
2007 PARC and CUL7 form atypical cullin RING ligase complexes. Cancer research 57 17332328
2012 Mutations in CUL7, OBSL1 and CCDC8 in 3-M syndrome lead to disordered growth factor signalling. Journal of molecular endocrinology 50 23018678
2007 CUL7 is a novel antiapoptotic oncogene. Cancer research 50 17942889
2006 Fbxw8 is essential for Cul1-Cul7 complex formation and for placental development. Molecular and cellular biology 47 16880526
2007 The conserved CPH domains of Cul7 and PARC are protein-protein interaction modules that bind the tetramerization domain of p53. The Journal of biological chemistry 45 17298945
2005 Simian virus 40 large T antigen's association with the CUL7 SCF complex contributes to cellular transformation. Journal of virology 42 16140746
2013 The CUL7/F-box and WD repeat domain containing 8 (CUL7/Fbxw8) ubiquitin ligase promotes degradation of hematopoietic progenitor kinase 1. The Journal of biological chemistry 39 24362026
2012 Whole exome sequencing reveals a novel mutation in CUL7 in a patient with an undiagnosed growth disorder. The Journal of pediatrics 29 22974575
2005 Dimerization of CUL7 and PARC is not required for all CUL7 functions and mouse development. Molecular and cellular biology 27 15964813
2010 Maternal uniparental isodisomy and heterodisomy on chromosome 6 encompassing a CUL7 gene mutation causing 3M syndrome. Clinical genetics 24 21166787
2006 A novel p53-binding domain in CUL7. Biochemical and biophysical research communications 24 16875676
2019 CUL7 promotes cancer cell survival through promoting Caspase-8 ubiquitination. International journal of cancer 21 30807646
2012 Ubiquitination and degradation of the hominoid-specific oncoprotein TBC1D3 is mediated by CUL7 E3 ligase. PloS one 19 23029530
2015 3-M syndrome: a novel CUL7 mutation associated with respiratory distress and a good response to GH therapy. Endocrinology, diabetes & metabolism case reports 18 25945256
2019 CUL7 E3 Ubiquitin Ligase Mediates the Degradation of Activation-Induced Cytidine Deaminase and Regulates the Ig Class Switch Recombination in B Lymphocytes. Journal of immunology (Baltimore, Md. : 1950) 17 31092637
2006 Expression of a mutant p193/CUL7 molecule confers resistance to MG132- and etoposide-induced apoptosis independent of p53 or Parc binding. Biochimica et biophysica acta 12 17229476
2024 Photoreceptor-targeted extracellular vesicles-mediated delivery of Cul7 siRNA for retinal degeneration therapy. Theranostics 10 39267786
2019 Novel mutation in Cul7 gene in a family diagnosed with 3M syndrome. Journal of genetics 8 30945686
2014 Regulating microtubules and genome stability via the CUL7/3M syndrome complex and CUL9. Molecular cell 8 24905004
2020 Identification of two CUL7 variants in two Chinese families with 3-M syndrome by whole-exome sequencing. Journal of clinical laboratory analysis 7 32141654
2009 Expression of a transgene encoding mutant p193/CUL7 preserves cardiac function and limits infarct expansion after myocardial infarction. Heart (British Cardiac Society) 7 19435717
2018 A novel CUL7 mutation in a Japanese patient with 3M syndrome. Human genome variation 6 30374406
2020 Effect of recombinant human insulin-like growth factor 1 therapy in a child with 3-M syndrome-1 with CUL7 gene mutation. Journal of pediatric endocrinology & metabolism : JPEM 4 32924381
2016 Changes in facial appearance from neonate to adult in 3-M syndrome patient with novel CUL7 gene mutations. Journal of pediatric endocrinology & metabolism : JPEM 4 26488604
2023 Prenatal diagnosis and preimplantation genetics testing of 3M syndrome in a Chinese family with novel biallelic variants of CUL7. Molecular genetics & genomic medicine 3 37877343
2020 A novel mutation within intron 17 of the CUL7 gene results in appearance of premature termination codon. Clinica chimica acta; international journal of clinical chemistry 3 32278698
2026 Interstitial cystitis-related gene CCDC8 accelerates tumorigenesis by participating in CUL7-mediated degradation of P53 in bladder cancer. Oncogene 2 41644704
2025 [Genetic analysis of a case of Miller-McKusick-Malvaux syndrome type 1 caused by CUL7 gene variant and a literature review]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 2 40372227
2024 Longitudinal skeletal growth and growth plate morphological characteristics of chondro-tissue specific CUL7 knockout mice. Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft 2 38367951
2016 SV40 T-Antigen Amino Acid Changes that Disrupt Cul-7 or Bub-1 Binding Do Not Globally Distort the T-Common Region. Intervirology 2 27376672
2023 Structural and functional insights into a novel homozygous missense pathogenic variant in CUL7 identified in consanguineous Pakistani family. Journal of biomolecular structure & dynamics 1 37345548
2021 3-M syndrome - a primordial short stature disorder with novel CUL7 mutation in two Indian patients. Journal of pediatric endocrinology & metabolism : JPEM 1 34674409
2026 A Novel Homozygous CUL7 Variant in an Iranian Patient Expands the Genetic Spectrum of 3 M Syndrome. Clinical case reports 0 41797740
2026 CUL7-mediated KEAP1 ubiquitination promotes the progression of colon cancer via NRF2 signaling. Cell death & disease 0 42252284
2025 3M syndrome with novel CUL7 variants in a Chinese patient: a case report. Frontiers in pediatrics 0 41234413
2025 CAND1 mediates CUL7-dependent HER2 protein stability to drive breast cancer progression. Breast cancer research : BCR 0 41310794

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