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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Cullin 3

Cul3, Cullin3
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. [provided by RefSeq, Mar 2012] (from NCBI)
Top mentioned proteins: Ubiquitin, Cullin, CAN, Rbx1, Keap1
Papers using Cul3 antibodies
Dimerization of substrate adaptors can facilitate cullin-mediated ubiquitylation of proteins by a “tethering” mechanism: a two-site interaction model for the Nrf2-Keap1 complex.
Supplier
Zi Xiaolin, In PLoS ONE, 2005
... Other antibodies including anti-NQO1 (3187), anti-p-Nrf2 (2073-1; specifically recognizing phosphorylation at serine 40) and anti-Cul3 (611848) were purchased from Cell Signaling (Beverly, MA), Epitomics (Burlingame, ...
Papers on Cul3
Degradation by Cullin 3 and effect on WNK kinases suggest a role of KLHL2 in the pathogenesis of Familial Hyperkalemic Hypertension.
New
Yang et al., Shanghai, China. In Biochem Biophys Res Commun, Feb 2016
Mutations in WNK1 and WNK4, and in components of the Cullin-Ring Ligase system, kelch-like 3 (KLHL3) and Cullin 3 (CUL3), can cause the rare hereditary disease, Familial Hyperkalemic Hypertension (FHHt).
A mechanism for the suppression of homologous recombination in G1 cells.
New
Impact
Durocher et al., Toronto, Canada. In Nature, Jan 2016
We found that the BRCA1-interaction site on PALB2 is targeted by an E3 ubiquitin ligase composed of KEAP1, a PALB2-interacting protein, in complex with cullin-3 (CUL3)-RBX1 (ref.
Mechanisms of activation of the transcription factor Nrf2 by redox stressors, nutrient cues, and energy status and the pathways through which it attenuates degenerative disease.
Review
New
Hayes et al., Philadelphia, United States. In Free Radic Biol Med, Nov 2015
Its ability to orchestrate adaptation to oxidants and electrophiles is due principally to stress-stimulated modification of thiols within one of its repressors, the Kelch-like ECH-associated protein 1 (Keap1), which is present in the cullin-3 RING ubiquitin ligase (CRL) complex CRL(Keap1).
The role of cullin proteins in gastric cancer.
Review
New
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.
Cell-fate determination by ubiquitin-dependent regulation of translation.
New
Impact
Rape et al., Berkeley, United States. In Nature, Oct 2015
Here we identify the ubiquitin ligase CUL3 in complex with its vertebrate-specific substrate adaptor KBTBD8 (CUL3(KBTBD8)) as an essential regulator of human and Xenopus tropicalis neural crest specification.
Deletion of a C-terminal intrinsically disordered region of WRINKLED1 affects its stability and enhances oil accumulation in Arabidopsis.
New
Ohlrogge et al., East Lansing, United States. In Plant J, Sep 2015
Analysis by bimolecular fluorescence complementation and yeast-two-hybrid assays indicated that the IDR3 domain does not determine WRI1 stability by interacting with BTB/POZ-MATH proteins connecting AtWRI1 with CULLIN3-based E3 ligases.
Dual regulation of transcription factor Nrf2 by Keap1 and by the combined actions of β-TrCP and GSK-3.
Review
New
Sutherland et al., Dundee, United Kingdom. In Biochem Soc Trans, Sep 2015
In the former case, oxidants/electrophiles increase the stability of Nrf2 by antagonizing the ability of Kelch-like ECH-associated protein 1 (Keap1) to target the transcription factor for proteasomal degradation via the cullin-3 (Cul3)-RING ubiquitin ligase CRL(Keap1).
Molecular mechanisms of Nrf2 regulation and how these influence chemical modulation for disease intervention.
Review
New
Zhang et al., Tucson, United States. In Biochem Soc Trans, Sep 2015
Detailed mechanistic investigations have shown the Kelch-like ECH-associated protein 1 (Keap1)-cullin3 (Cul3)-ring-box1 (Rbx1) E3-ligase to be the primary Nrf2 regulatory system.
Kelch-like 3/Cullin 3 ubiquitin ligase complex and WNK signaling in salt-sensitive hypertension and electrolyte disorder.
Review
New
Uchida et al., Tokyo, Japan. In Nephrol Dial Transplant, Aug 2015
Two additional genes responsible for PHAII, Kelch-like 3 (KLHL3) and Cullin 3 (CUL3), were identified in 2012.
Generation and analysis of knock-in mice carrying pseudohypoaldosteronism type II-causing mutations in the cullin 3 gene.
Uchida et al., Tokyo, Japan. In Biol Open, 2014
Pseudohypoaldosteronism type II (PHAII) is a hereditary hypertensive disease caused by mutations in four different genes: with-no-lysine kinases (WNK) 1 and 4, Kelch-like family member 3 (KLHL3), and cullin 3 (Cul3).
Tumor suppressor SPOP mediates the proteasomal degradation of progesterone receptors (PRs) in breast cancer cells.
Wang et al., Shanghai, China. In Am J Cancer Res, 2014
Speckle-type POZ protein (SPOP) is an adaptor protein of the CUL3-based E3 ubiquitin ligase complexes.
Identification of network-based biomarkers of cardioembolic stroke using a systems biology approach with time series data.
Chen et al., In Bmc Syst Biol, 2014
Genes, including UBC, CUL3, APP, NEDD8, JUP, and SIRT7, showed high associations with time after a stroke, and Ingenuity Pathway Analysis results showed that these post-stroke time series-associated genes were related to molecular and cellular functions of cell death, cell survival, the cell cycle, cellular development, cellular movement, and cell-to-cell signaling and interactions.
Genome-scale CRISPR-Cas9 knockout screening in human cells.
Impact
Zhang et al., Cambridge, United States. In Science, 2014
Our highest-ranking candidates include previously validated genes NF1 and MED12, as well as novel hits NF2, CUL3, TADA2B, and TADA1.
The integrated landscape of driver genomic alterations in glioblastoma.
Impact
Iavarone et al., New York City, United States. In Nat Genet, 2013
We found mutations with loss of heterozygosity in LZTR1, encoding an adaptor of CUL3-containing E3 ligase complexes.
Integrated molecular analysis of clear-cell renal cell carcinoma.
Impact
Ogawa et al., Tokyo, Japan. In Nat Genet, 2013
Other newly identified pathways and components recurrently mutated in ccRCC included PI3K-AKT-mTOR signaling, the KEAP1-NRF2-CUL3 apparatus, DNA methylation, p53-related pathways and mRNA processing.
MUF1/leucine-rich repeat containing 41 (LRRC41), a substrate of RhoBTB-dependent cullin 3 ubiquitin ligase complexes, is a predominantly nuclear dimeric protein.
GeneRIF
Rivero et al., Kingston upon Hull, United Kingdom. In J Mol Biol, 2012
The authors identified MUF1 as the first substrate for RhoBTB-Cul3 ubiquitin ligase complexes.
Adaptor protein self-assembly drives the control of a cullin-RING ubiquitin ligase.
GeneRIF
Privé et al., Toronto, Canada. In Structure, 2012
Adaptor protein self-assembly provides a graded level of regulation of the SPOP/Cul3 E3 ligase toward its multiple protein substrates.
KBTBD13 interacts with Cullin 3 to form a functional ubiquitin ligase.
GeneRIF
Maynard et al., Bethesda, United States. In Biochem Biophys Res Commun, 2012
these results demonstrate that KBTBD13 is a putative substrate adaptor for Cul3-RL that functions as a muscle specific ubiquitin ligase, and thereby implicate the ubiquitin proteasome pathway in the pathogenesis of KBTBD13-associated NEM.
Mutations in kelch-like 3 and cullin 3 cause hypertension and electrolyte abnormalities.
Impact
GeneRIF
Lifton et al., New Haven, United States. In Nature, 2012
fundamental role for KLHL3 and CUL3 in blood pressure, K(+) and pH homeostasis
Cullin-3 regulates late endosome maturation.
GeneRIF
Peter et al., Zürich, Switzerland. In Proc Natl Acad Sci U S A, 2012
These results suggest a crucial role of Cul3 in regulating late steps in the endolysosomal trafficking pathway.
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