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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 (Montrer TRIM31 Protéines) RBX1 (Montrer RBX1 Protéines). [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 (Montrer IL31RA Protéines) 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 (Montrer KEAP1 Protéines)-NRF2 (Montrer GABPA Protéines)-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 (Montrer ADAM17 Protéines)-mediated ectodomain shedding of AREG (Montrer AREG Protéines).
CUL3 mutation is associated with Pseudohypoaldosteronism types II
a loss of CULLIN3 represents a common signaling node for controlling the activity of intracellular WNT (Montrer WNT2 Protéines) and SHH (Montrer SHH Protéines) signaling pathways mediated by ID1 (Montrer ID1 Protéines)
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 (Montrer RHOA Protéines) protein expression after 6 days of adipocytes differentiation, suggesting that Cul3 is involved in the regulation of RhoA (Montrer RHOA Protéines) stability.
Data (including data from studies using cells cultured from knockout mice) suggest that Sccro (Montrer DCUN1D1 Protéines) neddylates Cul3 with Nedd8 (Montrer NEDD8 Protéines), promoting Cul3/Klhl21 (Montrer KLHL21 Protéines) complex formation and localization of Cul3 during telophase. (Sccro (Montrer DCUN1D1 Protéines) = squamous cell carcinoma-related oncogene (Montrer DCUN1D2 Protéines); Cul3 = cullin 3; Nedd8 (Montrer NEDD8 Protéines) = neural precursor cell expressed, developmentally down-regulated protein 8; Klhl21 (Montrer KLHL21 Protéines) = kelch-like protein 21 (Montrer KLHL21 Protéines))
Myeloid deletion of Cul3 led to defective STAT3 (Montrer STAT3 Protéines) 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 (Montrer KEAP1 Protéines) and Cul3 proteins were maintained at higher levels than that of Nrf2 (Montrer NFE2L2 Protéines), 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 (Montrer KCNJ1 Protéines) expression in the distal nephron.
Study identifies a key role of Cul3-KLHL20 (Montrer KLHL20 Protéines) in autophagy termination by controlling autophagy-dependent turnover of ULK1 (Montrer ULK1 Protéines) and VPS34 (Montrer PIK3C3 Protéines) complex subunits and reveals the pathophysiological functions of this autophagy termination mechanism.
These results suggest that KLHL2 (Montrer KLHL2 Protéines) likely plays a role in the pathogenesis of FHHt, and aggravates the phenotype caused by mutations in CUL3 and WNK4 (Montrer WNK4 Protéines).
Hypoxia-responsive miR (Montrer MLXIP Protéines)-101 stimulates angiogenesis by activating the HO-1 (Montrer HMOX1 Protéines)/VEGF (Montrer VEGFA Protéines)/eNOS (Montrer NOS3 Protéines) axis via Cul3 targeting
Mutation of cul3 protein is involved in the development of renal hypertension and chronic kidney diseases.
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 (Montrer MEI1 Protéines) in vivo; importantly, MEL-26 specifically interacts with CUL-3 and MEI-1 (Montrer MEI1 Protéines) 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