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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]
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 show that the differentiation of LiSa-2 preadipocytes is associated with an increase of cullin-associated and neddylation-dissociated 1 (CAND1 (show CAND1 ELISA Kits)), COP9 (show COPS8 ELISA Kits) signalosome (CSN), neddylated cullin 3 (Cul3) and the BTB protein Keap1 (show KEAP1 ELISA Kits).
Heterodimeric CUL3 proteinubiquitylates TIAM1.CUL3 regulates TIAM1 abundance and subsequent RAC1 signaling.
these findings indicate that the designed stapled peptides can efficiently mimic protein-protein interactions and are potentially able to modulate fundamental biological processes involving Cul3.
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.
Knockdown of Cullin-3 or inhibition of cullin-RING ligase activity in aortic smooth muscle cells increased RhoA (show RHOA ELISA Kits).
CUL3 deletion in mice demonstrated an essential role for CUL3 in the development of PLZF- and BCL6 (show BCL6 ELISA Kits)-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.
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