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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 (show TRIM31 ELISA Kits) RBX1 (show RBX1 ELISA Kits). [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 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 (show RHOA ELISA Kits) protein expression after 6 days of adipocytes differentiation, suggesting that Cul3 is involved in the regulation of RhoA (show RHOA ELISA Kits) stability.
p97 (show EIF4G2 ELISA Kits) negatively regulates NRF2 (show GABPA ELISA Kits) through the canonical pathway by extracting ubiquitylated NRF2 (show GABPA ELISA Kits) from the KEAP1 (show KEAP1 ELISA Kits)-CUL3 E3 complex.
CUL3 interacts with ACLY (show ACLY ELISA Kits) through its adaptor protein, KLHL25 (Kelch-like family member 25), to ubiquitinate and degrade ACLY (show ACLY ELISA Kits) 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 (show EPS15 ELISA Kits) at endosomes.
Data show that Cullin3 exerts its function through promoting breast-cancer metastasis suppressor 1 (BRMS1 (show BRMS1 ELISA Kits)) protein degradation, which was associated with epithelial-mesenchymal transition (EMT (show ITK ELISA Kits)), 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 (show KLHL20 ELISA Kits) in autophagy termination by controlling autophagy-dependent turnover of ULK1 (show ULK1 ELISA Kits) and VPS34 (show PIK3C3 ELISA Kits) complex subunits and reveals the pathophysiological functions of this autophagy termination mechanism.
Data (including data from studies using cells cultured from knockout mice) suggest that Sccro (show DCUN1D1 ELISA Kits) neddylates Cul3 with Nedd8 (show NEDD8 ELISA Kits), promoting Cul3/Klhl21 (show KLHL21 ELISA Kits) complex formation and localization of Cul3 during telophase. (Sccro (show DCUN1D1 ELISA Kits) = squamous cell carcinoma-related oncogene; Cul3 = cullin 3; Nedd8 (show NEDD8 ELISA Kits) = neural precursor cell expressed, developmentally down-regulated protein 8; Klhl21 (show KLHL21 ELISA Kits) = kelch-like protein 21 (show KLHL21 ELISA Kits))
Myeloid deletion of Cul3 led to defective STAT3 (show STAT3 ELISA Kits) 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 (show KEAP1 ELISA Kits) and Cul3 proteins were maintained at higher levels than that of Nrf2 (show NFE2L2 ELISA Kits), 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 (show KCNJ1 ELISA Kits) 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 (show WNK4 ELISA Kits).
Hypoxia-responsive miR (show MLXIP ELISA Kits)-101 stimulates angiogenesis by activating the HO-1 (show HMOX1 ELISA Kits)/VEGF (show VEGFA ELISA Kits)/eNOS (show NOS3 ELISA Kits) axis via Cul3 targeting
Mutation of cul3 protein is involved in the development of renal hypertension and chronic kidney diseases.
Data show that Bcl6 (show BCL6 ELISA Kits) (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.
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