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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Cullin 5

Cul5, VACM-1, Cullin5
neuropeptide arginine vasopressin receptor; may have a role in the central nervous system [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: Ubiquitin, Cullin, CAN, V1a, APOBEC3G
Papers using Cul5 antibodies
Ubiquitination differentially regulates clathrin-dependent internalization of protease-activated receptor-1
Maris John M et al., In Molecular Cancer, 2006
... Cul-5 cDNA was gel-purified by band excision and extraction using a QIAquick gel extraction kit (Qiagen) followed by sequencing to ...
Isolation of Epstein-Barr virus (EBV)-negative cell clones from the EBV-positive Burkitt's lymphoma (BL) line Akata: malignant phenotypes of BL cells are dependent on EBV.
Sugden Bill, In PLoS Pathogens, 1993
... Anti-p53 (FL-393) and anti-Cul5 (H-300) rabbit polyclonal antibodies, anti-Rbx2 (N-15) goat polyclonal antibodies and normal mouse IgG2a were purchased from Santa Cruz Biotechnology.
Papers on Cul5
The role of cullin proteins in gastric cancer.
Yao et al., Hohhot, China. In Tumour Biol, Nov 2015
There are seven cullin proteins that have been identified in eukaryotes: CUL1, CUL2, CUL3, CUL4A, CUL4B, CUL5, and CUL7/p53-associated parkin-like cytoplasmic protein.
PAR-4 and anillin regulate myosin to coordinate spindle and furrow position during asymmetric division.
Michaux et al., Rennes, France. In J Cell Biol, Oct 2015
We find that PAR-4/LKB1 impinges on myosin via two pathways, an anillin-dependent pathway that also responds to the cullin CUL-5 and an anillin-independent pathway involving the kinase PIG-1/MELK.
Cullin 5-RING E3 ubiquitin ligases, new therapeutic targets?
Lutz et al., Toulouse, France. In Biochimie, Sep 2015
This review is dedicated to the largest family of multimeric E3s, the Cullin-RING E3 (CRL) family and more specifically to cullin 5 based CRLs that remains poorly characterized.
Molecular signatures of sanguinarine in human pancreatic cancer cells: A large scale label-free comparative proteomics approach.
Ahmad et al., Madison, United States. In Oncotarget, May 2015
Four of these proteins (IL33, CUL5, GPS1 and DUSP4) appear to occupy regulatory nodes in key pathways.
The assembly of Vif ubiquitin E3 ligase for APOBEC3 degradation.
Kim, Kyŏngsan, South Korea. In Arch Pharm Res, Apr 2015
To counteract the antiviral activity of APOBEC3G, an accessory protein of HIV-1, Vif, forms ubiquitin E3 ligase through assembly with CUL5-RBX2, ELOB-ELOC and CBFβ.
Biophysical studies on interactions and assembly of full-size E3 ubiquitin ligase: suppressor of cytokine signaling 2 (SOCS2)-elongin BC-cullin 5-ring box protein 2 (RBX2).
Ciulli et al., Cambridge, United Kingdom. In J Biol Chem, Mar 2015
A member of the CRL family, SOCS2-EloBC-Cul5-Rbx2 (CRL5(SOCS2)), binds phosphorylated growth hormone receptor as its main substrate.
Downregulation of MicroRNA-145 Caused by Hepatitis B Virus X Protein Promotes Expression of CUL5 and Contributes to Pathogenesis of Hepatitis B Virus-Associated Hepatocellular Carcinoma.
Yan et al., In Cell Physiol Biochem, 2014
The following computational analysis identified CUL5 and RAB5C as virtual targets of miR-145, whereas only CUL5 was verified as a validated target gene of miR-145 in liver cells via luciferase reporter assay.
Increased CSF E-Selectin in Clinical Alzheimer's Disease without Altered CSF Aβ42 and Tau.
Zhang et al., Seattle, United States. In J Alzheimers Dis, 2014
In this multicenter cohort of 215 clinically diagnosed AD patients and 249 controls, E-selectin and vascular cell adhesion molecule 1 (VACM-1) were measured along with amyloid-β peptide 1-42 (Aβ42) and tau.
Cellular requirements for bovine immunodeficiency virus Vif-mediated inactivation of bovine APOBEC3 proteins.
Yu et al., Baltimore, United States. In J Virol, 2014
The primate lentiviral Vif complex is composed of the unique cofactor core binding factor β (CBF-β) and canonical ligase components Cullin 5 (CUL5), Elongin B/C (ELOB/C), and RBX2.
SAG/RBX2 is a novel substrate of NEDD4-1 E3 ubiquitin ligase and mediates NEDD4-1 induced chemosensitization.
Sun et al., Hangzhou, China. In Oncotarget, 2014
We also found that SAG bridges NEDD4-1 via its C-terminus and CUL-5 via its N-terminus to form a NEDD4-1/SAG/CUL-5 tri-complex.
Structural basis for hijacking CBF-β and CUL5 E3 ligase complex by HIV-1 Vif.
Huang et al., Harbin, China. In Nature, 2014
Here we report a crystal structure of the Vif-CBF-β-CUL5-ELOB-ELOC complex.
New insights into the mechanism for VACM-1/cul5 expression in vascular tissue in vivo.
Barney et al., Holland, United States. In Int Rev Cell Mol Biol, 2013
Vasopressin-activated calcium-mobilizing (VACM-1)/cul5 is the least conserved member of a cullin protein family involved in the formation of E3-specific ligase complexes that are responsible for delivering the ubiquitin protein to their target substrate proteins selected for ubiquitin-dependent degradation.
Requirement of HIV-1 Vif C-terminus for Vif-CBF-β interaction and assembly of CUL5-containing E3 ligase.
Zhang et al., Changchun, China. In Bmc Microbiol, 2013
Moreover, by determining that the BC box also is necessary for CBF-β interaction in vivo, we speculate that binding to ELOB/C induces conformational changes in Vif, facilitating its interaction with CBF-β and consequent interaction with CUL5.
APOBEC3-mediated editing in HIV type 1 from pediatric patients and its association with APOBEC3G/CUL5 polymorphisms and Vif variability.
Sen et al., Buenos Aires, Argentina. In Aids Res Hum Retroviruses, 2012
detected a reduced editing associated with the CUL5 SNP6 minor allele and also with certain Vif variants (mutations at sites 46, 122, and 160).
Vif hijacks CBF-β to degrade APOBEC3G and promote HIV-1 infection.
Krogan et al., San Francisco, United States. In Nature, 2012
The AIDS virus, human immunodeficiency virus type 1 (HIV-1), produces the accessory factor Vif, which counteracts the host's antiviral defence by hijacking a ubiquitin ligase complex, containing CUL5, ELOC, ELOB and a RING-box protein, and targeting APOBEC3G for degradation.
T-cell differentiation factor CBF-β regulates HIV-1 Vif-mediated evasion of host restriction.
Yu et al., Changchun, China. In Nature, 2012
HIV-1 Vif forms an E3 ubiquitin ligase complex with cullin 5 (CUL5), elongin B and elongin C , which promotes the polyubiquitination and degradation of APOBEC3 substrates.
Effect of HIV-1 Vif variability on progression to pediatric AIDS and its association with APOBEC3G and CUL5 polymorphisms.
Sen et al., Buenos Aires, Argentina. In Infect Genet Evol, 2011
Vif alterations may contribute to a rapid AIDS onset and Vif variability could be influenced by APOBEC3G and CUL5 polymorphisms in children
Mutational analysis of VACM-1/cul5 exons in cancer cell lines.
Burnatowska-Hledin et al., Holland, United States. In Apmis, 2011
study showed VACM-1 DNA in T47D cancer cells is not mutated; SNP found in U138MG, OVCAR-3 and ACHN cell lines results in silent mutation; results suggest in T47D cancer cells, VACM-1 activity may controlled by epigenetic or posttranslational modification
Cullin5 reduces retinal cell death induced by glutamate toxicity.
Kiuchi et al., Hiroshima, Japan. In Curr Eye Res, 2011
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.
Cullin 5 regulates cortical layering by modulating the speed and duration of Dab1-dependent neuronal migration.
Cooper et al., Seattle, United States. In J Neurosci, 2010
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.
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