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cullin-5 and cullin-2 play a role in the development of neuromuscular junction and the female germ line of Drosophila
Data show that the follicular epithelium that normally encapsulates single germ line cysts develops aberrantly in cul-5 mutant.
cul-5 plays multiple roles in cell fate specification and synapse formation during Drosophila development.
CUL5 may be an important part of the mechanism for thalidomide-dependent inhibition.
These findings report genetic variants possibly associated with susceptibility to HIV-1 infection (CUL5 rs11212495, rs7103534, rs7117111) and partial viral load control (APOBEC3G rs2294367).
structural model suggests that the diverse FIV and HIV-1 Vifs use conserved residues for Cullin 5 binding, FIV Vif binds Cullin 5 independently of zinc, in contrast to HIV-1 Vif.
these findings identify Cul-5 as a signaling component that connects an LPS-activated TLR4-MyD88 complex to TRAF6 for efficient activation of NF-kappaB
CUL5 neddylation may allosterically tune polyubiquitin chain length and topology.
Study found that CUL5 expression was significantly decreased in both endometrioid adenocarcinomas with the more aggressive serous type displaying a higher reduction. Its mRNA and protein overexpression in endometrial cancer cells resulted in decreased cell proliferation.
Studies indicate that Cullin-RING E3 ubiquitin ligases (CRL) are key players of the ubiquitylation pathway.
These results provide important information on the assembly of the Vif-CUL5-E3 ubiquitin ligase and identify a new viV binding interface with CBF-beta at the C-terminus of HIV-1 Vif.
Data indicate that cell surface adhesion molecules VCAM-1 and P-selectin play some roles in mechanical stretch-induced HL-60 cell adhesion to mouse common carotid arteries.
N-terminal mutants of HIV-1 vif that demonstrated reduced Cul5 binding were also unable to degrade APOBEC3G as well as APOBEC3F.
A tumor suppressor gene, CUL5, is identified as a direct target of miR-7 in hepatocellular carcinoma.
Silencing CUL5 reduced cellular sensitivity to three distinct HSP90 inhibitors, across four cancer types driven by different protein kinases.
In the absence of CBFbeta, Vif does not bind Cul5, thus preventing the assembly of the E3 ligase complex.
CBF-beta is critical for the formation of the Vif-ElonginB/ElonginC-Cul5 core E3 ubiquitin ligase complex.
data reveal the structural basis for Vif hijacking of the CBF-beta and CUL5 E3 ligase complex, laying a foundation for rational design of novel anti-HIV drugs
ASB9 is unstable alone but forms a stable ternary complex with EloBC that binds with high affinity to the Cullin 5 N-terminal domain.
crystal structure shows interaction between SOCS2-elongin BC and Cullin-5
Data indicate tht n the Biaka, strong signal of selection was detected at CUL5 and at TSG101.
comparison of heat capacity changes supports a model in which CBFbeta prestabilizes Vif((1-192)) relative to Vif((95-192)), consistent with a stronger interaction of Cul5 with Vif's C-terminal Zn(2+)-binding motif.
detected a reduced editing associated with the CUL5 SNP6 minor allele and also with certain Vif variants (mutations at sites 46, 122, and 160).
neural precursor cell expressed developmentally downregulated protein 8 (Nedd8) modification of Cul-5 is required for its interaction with TRAF6.
Our results show that endogenous Cul5 suppresses epithelial cell transformation by several pathways, including inhibition of Src-Cas-induced ruffling through SOCS6
The expression of cullin5 on retinal cells and reduction in the percentage of dead retinal cells induced by L-glutamate suggest that cullin5 has neuroprotective properties in retinal cells.
SOCS box acts as an independent binding domain capable of recruiting elonginBC and cullin5 to promote E3 ligase formation.
The role of Cul5 is to degrade disabled homolog 1 (Dab1) and thus control neuron migration speed and neuron insertion at the top of the cortical plate.
These results suggest that, when Src is activated by mutation or physiological mechanisms, its effects are limited by Culllin 5, which downregulates active Src and its phosphorylated substrates.
data imply the existence of two distinct subclasses of SOCS proteins with a high affinity for Cullin5, the E3 ligase scaffold, possibly reflecting complete dependence upon ubiquitination for suppression of cytokine signalling
The study results suggest that VACM-1 may regulate endothelial AQP1 concentration both in vivo and in vitro.
oocyte maturation from pachytene exit and MPK-1 activation are redundantly controlled by the RBX-2-CUL-5- and RBX-1-CUL-2-based complexes.
neuropeptide arginine vasopressin receptor\; may have a role in the central nervous system
Vasopressin-activated calcium-mobilizing receptor (VACM-1)
, cullin 5
, Vasopressin-activated calcium-mobilizing receptor-1
, Cullin-5 (vasopressin-activated calcium-mobilizing receptor-1)
, vasopressin-activated calcium-mobilizing receptor 1
, vasopressin-activated calcium-mobilizing receptor protein
, vasopressin-activated calcium-mobilizing protein