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anti-Human Cullin 3 Antibodies:
anti-Mouse (Murine) Cullin 3 Antibodies:
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Human Polyclonal Cullin 3 Primary Antibody for IP, WB - ABIN233772
Shiraishi, Zhou, Aoki, Sato, Chiba, Tanaka, Yoshida, Nabeshima, Nabeshima, Tamura: TBP-interacting protein 120B (TIP120B)/cullin-associated and neddylation-dissociated 2 (CAND2) inhibits SCF-dependent ubiquitination of myogenin and accelerates myogenic differentiation. in The Journal of biological chemistry 2007
Show all 4 Pubmed References
Human Polyclonal Cullin 3 Primary Antibody for ICC, IF - ABIN188779
Li, Ao, Fu, Lee, Xu, Lonard, OMalley: Tumor-suppressor role for the SPOP ubiquitin ligase in signal-dependent proteolysis of the oncogenic co-activator SRC-3/AIB1. in Oncogene 2011
Show all 2 Pubmed References
Human Polyclonal Cullin 3 Primary Antibody for ICC, IF - ABIN188778
White, Sowa, Tan, Jeudy, Hayes, Santha, Münger, Harper, Howley: Systematic identification of interactions between host cell proteins and E7 oncoproteins from diverse human papillomaviruses. in Proceedings of the National Academy of Sciences of the United States of America 2012
Human Polyclonal Cullin 3 Primary Antibody for IF (p), IHC (p) - ABIN705296
Su, Zhang, Song, Shi, Fu, Xia, Bai, Hu, Xu, Song, Song: Tetrachlorobenzoquinone activates nrf2 signaling by keap1 cross-linking and ubiquitin translocation but not keap1-cullin3 complex dissociation. in Chemical research in toxicology 2015
LFY activity is fully dependent on BOP2 as well as on CUL3A and B to regulate target genes such as APETALA1 and to induce ectopic flower formation.
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]
results suggest that CEP97 degradation by the cullin-3-RBX1-KCTD10 complex plays a crucial role in serum-starvation-induced CP110 removal and ciliogenesis
The high-affinity interaction between A55BB and Cul3-NTD suggests that, in addition to directing the Cul3-RING E3 ligase complex to degrade cellular/viral target proteins that are normally unaffected, A55 may also sequester Cul3 from cellular adaptor proteins, thereby protecting substrates of these cellular adaptors from ubiquitylation and degradation.
The authors found that CUL3 complexed with KBTBD8 monoubiquitylates its essential targets only after these have been phosphorylated in multiple motifs by CK2, a kinase whose levels gradually increase during embryogenesis.
identified the RING E3 ligase complex Cullin-3-Rbx1-KCTD10 as key modulator of endothelial barrier integrity via its regulation of the ubiquitination, localization, and activity of RhoB.
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
deletion of exon 9 from Cul3 generates a protein that is itself ubiquitin-ligase defective but also capable of enhanced autophagocytic KLHL3 degradation
These results indicate that Cul3 haploinsufficiency does not cause FHHt, but dominant effects of mutant CUL3 are required.
Kelch-like ECH-associated protein 1 (Keap1) is a cullin-3 (Cul3)-RING ubiquitin ligase (CRL) adaptor/scaffold protein.
decreased abundance of KLHL3 is a specific phenomenon caused by mutant CUL3 (Deltaexon9).
High Cullin 3 expression is associated with atherogenesis.
Cul3 was specifically deleted in either skeletal muscle (SkM-Cul3 KO) or cardiomyocytes (CM-Cul3 KO) of mice. The loss of Cul3 caused neonatal lethality and dramatic alterations in the proteome, which were unique to each striated muscle type.
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.
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.
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.
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