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This shows that BOP proteins act as substrate adaptors in a CUL3(BOP1/BOP2) E3 ubiquitin ligase complex, targeting PIF4 proteins for ubiquitination and subsequent degradation.
Data show that CUL3 and BPM proteins assemble in planta with WRI1.
The plasma membrane-associated phototropic receptor phot1 is ubiquitinated in response to blue light activation. Ubiquitination of phot1 is dependent upon both the phot1-interacting proteins NPH3 and CUL3.
AtCUL3a and AtCUL3b can assemble in Arabidopsis with BTB/POZ-MATH and AtRBX1 proteins to form functional E3 ligases. [AtCUL3a]
CUL3A is ubiquitously expressed in plants and is able to interact with the ring-finger protein RBX1. [CUL3A]
Arabidopsis CUL3A gene is essential for normal embryogenesis.
work highlights that CUL3 is essential for the normal division and organisation of the root stem cell niche and columella root cap cells
CUL3a and CUL3b are essential for plant development [CUL3a]
The CRL3 complexes evolved to fulfill a pivotal role in mammalian cell differentiation.
Significantly mutated gene CUL3 displayed strong antiproliferation function in Esophageal Squamous Cell Carcinoma but not in Esophageal Adenocarcinomas.
we demonstrated that cullin 3 plays a promoting role in the malignant progression of nasopharyngeal carcinoma
our study emphasizes the discovery of a gene signature regulated by the KEAP1-NRF2-CUL3 axis which is strongly associated with tumorigenesis and drug resistance in head and neck squamous cell cancer .
CUL3 rs17479770 variant could be a protective factor in the pathogenesis of essential hypertension.
Cullin 3 regulates ADAM17-mediated ectodomain shedding of AREG.
CUL3 mutation is associated with Pseudohypoaldosteronism types II
a loss of CULLIN3 represents a common signaling node for controlling the activity of intracellular WNT and SHH signaling pathways mediated by ID1
The roles of cullin 3-based ubiquitin E3 ligases as key players in the process of various signals in endothelial cell function and angiogenesis.
Downregulation of Cul3 led to a marked increase in RhoA protein expression after 6 days of adipocytes differentiation, suggesting that Cul3 is involved in the regulation of RhoA stability.
p97 negatively regulates NRF2 through the canonical pathway by extracting ubiquitylated NRF2 from the KEAP1-CUL3 E3 complex.
CUL3 interacts with ACLY through its adaptor protein, KLHL25 (Kelch-like family member 25), to ubiquitinate and degrade ACLY in cells
this work identifies both calcium and CUL3 co-adaptors as important regulators of ubiquitylation events that control human development.
Together, the data indicate that a CUL3-SPOPL E3 ubiquitin ligase complex regulates endocytic trafficking and formation of multivesicular bodies by ubiquitinating and degrading EPS15 at endosomes.
Data show that Cullin3 exerts its function through promoting breast-cancer metastasis suppressor 1 (BRMS1) protein degradation, which was associated with epithelial-mesenchymal transition (EMT), migration and invasion.
CUL3 acts as a tumor suppressor by regulating oxidative stress
The authors find that the KCTD proteins 5, 6, 9 and 17 bind to Cul3 with high affinity, while the KCTD proteins 1 and 16 do not have detectable binding.
Study identifies a key role of Cul3-KLHL20 in autophagy termination by controlling autophagy-dependent turnover of ULK1 and VPS34 complex subunits and reveals the pathophysiological functions of this autophagy termination mechanism.
Data show that the differentiation of LiSa-2 preadipocytes is associated with an increase of cullin-associated and neddylation-dissociated 1 (CAND1), COP9 signalosome (CSN), neddylated cullin 3 (Cul3) and the BTB protein Keap1.
Heterodimeric CUL3 proteinubiquitylates TIAM1.CUL3 regulates TIAM1 abundance and subsequent RAC1 signaling.
Data (including data from studies using cells cultured from knockout mice) suggest that Sccro neddylates Cul3 with Nedd8, promoting Cul3/Klhl21 complex formation and localization of Cul3 during telophase. (Sccro = squamous cell carcinoma-related oncogene; Cul3 = cullin 3; Nedd8 = neural precursor cell expressed, developmentally down-regulated protein 8; Klhl21 = kelch-like protein 21)
Myeloid deletion of Cul3 led to defective STAT3 phosphorylation in colon macrophages, which was accompanied by exacerbated colonic inflammation and inflammation-driven tumorigenesis.
Results showed that in the basal state, the amount of Keap1 and Cul3 proteins were maintained at higher levels than that of Nrf2, and remained the same even under oxidative and electrophilic stimuli.
Suggest that the hyperkalemia in knock-in mouse with the CUL3(Delta403-459) mutation is not caused by reduced ROMK expression in the distal nephron.
These results suggest that KLHL2 likely plays a role in the pathogenesis of FHHt, and aggravates the phenotype caused by mutations in CUL3 and WNK4.
Hypoxia-responsive miR-101 stimulates angiogenesis by activating the HO-1/VEGF/eNOS axis via Cul3 targeting
Mutation of cul3 protein is involved in the development of renal hypertension and chronic kidney diseases.
Data show that Bcl6 (B cell lymphoma 6)-cullin 3 complexes provide essential negative feedback regulation during both thymocyte development and T cell activation to restrain excessive T follicular helper (Tfh) responses.
Knockdown of Cullin-3 or inhibition of cullin-RING ligase activity in aortic smooth muscle cells increased RhoA.
CUL3 deletion in mice demonstrated an essential role for CUL3 in the development of PLZF- and BCL6-dependent lineages; distinct lineage-specific BTB-ZF transcription factors recruit CUL3 to alter the ubiquitination pattern of their associated chromatin-modifying complex
The authors identified MUF1 as the first substrate for RhoBTB-Cul3 ubiquitin ligase complexes.
Data show that liver-specific ablation of the cyclin E regulator Cullin 3 in mice results in the persistence and massive expansion of hepatic progenitor cells.
Nrf2 regulates Cul3-Rbx1 by controlling regulation of expression and induction of Cul3-Rbx1
Results show negative regulation of HDAC1 by a Cul3-REN E3 ubiquitin ligase complex.
Data show that the constitutive degradation pathway for cyclin E that is regulated by the Cullin3-based E3 ligase is essential to maintain quiescence in mammalian cells.
KLHL12 specifically interacts with the D4 polymorphism, thereby building up a Cul3-E3 ligase complex with substrate specificity toward the D4 receptor
Cul3-deficient cells or Ctb9/KLHDC5-deficient cells show an increase in p60/katanin levels, indicating that Cul3/Ctb9/KLHDC5 is required for efficient p60/katanin removal
KEL-8 is a substrate receptor for Cullin 3 ubiquitin ligases that is required for the proteolysis of GLR-1 receptors and suggest a novel postmitotic role in neurons for Kelch/CUL3 ubiquitin ligases.
The BTB-containing protein MEL-26 is a component required for degradation of MEI-1 in vivo; importantly, MEL-26 specifically interacts with CUL-3 and MEI-1 in vivo and in vitro, and displays properties of a substrate-specific adaptor
the identification of a large family of BTB-domain proteins as substrate-specific adaptors for C. elegans CUL-3
FIGL-1 by the CUL-3MEL-26 E3 ligase spatially restricts FIGL-1 function to mitotic cells, where it is required for correct progression through mitosis.
cullin (CUL)-3 as a component of E3 ligase and KEL-8 as the substrate adaptor of RPY-1.
This gene encodes a member of the cullin protein family. The encoded protein plays a critical role in the polyubiquitination and subsequent degradation of specific protein substrates as the core component and scaffold protein of an E3 ubiquitin ligase complex. Complexes including the encoded protein may also play a role in late endosome maturation. Mutations in this gene are a cause of type 2E pseudohypoaldosteronism. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
, Cullin-3 (CUL-3)
, cullin 3