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Negative regulator of ubiquitin-like proteins 1

NUB1, BS4, NUB1L, NEDD8 ultimate buster
This gene encodes a protein that functions as a negative regulator of NEDD8, a ubiquitin-like protein that conjugates with cullin family members in order to regulate vital biological events. The protein encoded by this gene regulates the NEDD8 conjugation system post-transcriptionally by recruiting NEDD8 and its conjugates to the proteasome for degradation. This protein interacts with the product of the AIPL1 gene, which is associated with Leber congenital amaurosis, an inherited retinopathy, and mutations in that gene can abolish interaction with this protein, which may contribute to the pathogenesis. This protein is also known to accumulate in Lewy bodies in Parkinson's disease and dementia with Lewy bodies, and in glial cytoplasmic inclusions in multiple system atrophy, with this abnormal accumulation being specific to alpha-synucleinopathy lesions. Alternative splicing of this gene results in multiple transcript variants. [provided by RefSeq, Aug 2011] (from NCBI)
Top mentioned proteins: Ubiquitin, NEDD8, ACID, CAN, HAD
Papers using NUB1 antibodies
The cellular level of TRIM31, an RBCC protein overexpressed in gastric cancer, is regulated by multiple mechanisms including the ubiquitin-proteasome system
Kloetzel Peter-Michael et al., In Cellular and Molecular Life Sciences, 2010
... Monoclonal anti-LMP2 (LMP2-13), anti-Ub (FK2), anti-Rpn10 (S5a-18) and polyclonal anti-NUB1 antibodies were obtained from Biomol.
Papers on NUB1
Seasonal training load distribution of professional futsal players: effects on physical fitness, muscle damage and hormonal status.
Bara-Filho et al., São Paulo, Brazil. In J Strength Cond Res, Dec 2015
An increase in C (P = 0.007) and a decrease in T:C (P = 0.003) were observed from BS4 to BS5.
NEDD8 Ultimate Buster 1 Long (NUB1L) Protein Suppresses Atypical Neddylation and Promotes the Proteasomal Degradation of Misfolded Proteins.
Su et al., Augusta, United States. In J Biol Chem, Oct 2015
Loss of NUB1L exaggerated atypical neddylation, whereas NUB1L overexpression repressed atypical neddylation through promoting the degradation of NEDD8.
Karyotype evolution in apomictic Boechera and the origin of the aberrant chromosomes.
Lysak et al., Brno, Czech Republic. In Plant J, Jun 2015
CCP analysis allowed us to reconstruct the origin of seven chromosomes in sexual B. stricta and apomictic B. divaricarpa from the ancestral karyotype (n = 8) of Brassicaceae lineage I. Whereas three chromosomes (BS4, BS6, and BS7) retained their ancestral structure, five chromosomes were reshuffled by reciprocal translocations to form chromosomes BS1-BS3 and BS5.
Quantitative candidate gene association studies of metabolic traits in Han Chinese type 2 diabetes patients.
Li et al., Tianjin, China. In Genet Mol Res, 2014
We found that CAMTA1, ABI2, VHL, KAT2B, PKHD1, ESR1, TOX, SLC30A8, SFI1, and MYH9 polymorphisms were associated with HbA1c, FPG, and/or P2PG; GCK, HHEX, TCF7L2, KCNQ1, and TBX5 polymorphisms were associated with insulin resistance-related traits; ABCG2, SLC2A9, and PKHD1 polymorphisms were associated with SUA; CAMTA1, VHL, KAT2B, PON1, NUB1, SLITRK5, SMAD3, FTO, FANCA, and PCSK2 polymorphisms were associated with blood lipid traits; CAMTA1, SPAG16, TOX, KCNQ1, ACACB, and MYH9 polymorphisms were associated with blood pressure; and UBE2E3, SPAG16, SLC2A9, CDKAL1, CDKN2A/B, TCF7L2, SMAD3, and PNPLA3 polymorphisms were associated with BMI (all P values <0.05).
FAT10ylation as a signal for proteasomal degradation.
Groettrup et al., Konstanz, Germany. In Biochim Biophys Acta, 2014
Here we review the data on ubiquitin-independent degradation by FAT10, on how FAT10 is conjugated to its substrates, how FAT10 binds to the 26S proteasome, and how the ubiquitin-like (UBL)-ubiquitin-associated (UBA) protein NUB1L accelerates FAT10 mediated proteolysis.
Halomonas sp. BS4, A biosurfactant producing halophilic bacterium isolated from solar salt works in India and their biomedical importance.
Citarasu et al., Kanniyākumāri, India. In Springerplus, 2013
After routine biosurfactant screening by various methods, the biosurfactant producing bacteria, Halomonas sp BS4 was confirmed by 16 S rRNA sequencing.
Study designs to investigate Nox1 acceleration of neoplastic progression in immortalized human epithelial cells by selection of differentiation resistant cells.
Chamulitrat et al., Nakhon Si Thammarat, Thailand. In Redox Biol, 2013
Among several cobblestone epithelial cell lines obtained, two distinctive spindle cell lines - FIB and NuB1 cells were more progressively transformed exhibiting tubulogenesis and anchorage-independent growth associated with increased invasiveness.
Labor induction using modified metreurynters plus oxytocin at an institution in Japan: a retrospective study.
Takahashi et al., In Clin Exp Obstet Gynecol, 2013
AORs for VDF were 0.04 in BS1-3 class and 0.14 in BS4-5 class.
Structural and mechanistic insights into the arginine/lysine-rich peptide motifs that interact with P97/VCP.
Hu et al., Shanghai, China. In Biochim Biophys Acta, 2013
Based on biochemical features of the VBM motifs, we also identified NUB1L (NEDD8 ultimate buster-1 long) as a novel VBM-containing protein, which is involved in proteasomal degradation of NEDD8 through the P97 pathway.
NEDD8 ultimate buster-1 long (NUB1L) protein promotes transfer of NEDD8 to proteasome for degradation through the P97UFD1/NPL4 complex.
Hu et al., Shanghai, China. In J Biol Chem, 2013
The NEDD8 protein and neddylation levels in cells are modulated by NUB1L or NUB1 through proteasomal degradation, but the underlying molecular mechanism is not well understood.
Identification of NUB1 as a suppressor of mutant Huntington toxicity via enhanced protein clearance.
Palacino et al., Shanghai, China. In Nat Neurosci, 2013
Among these, negative regulator of ubiquitin-like protein 1 (NUB1) overexpression lowered mHTT in neuronal models and rescued mHTT-induced death.
Negative regulation of NEDD8 conjugation pathway by novel molecules and agents for anticancer therapy.
Kamitani et al., Ōsaka, Japan. In Curr Pharm Des, 2012
COP9 signalosome, CAND1, inactive mutant of Ubc12 and NUB1/NUB1L) and clarifies possible strategies for targeting the NEDD8 cascade in cancer cells.
Structural studies on AIPL1 and its functional interactions with NUB1 to identify key interacting residues in LCA4.
Valliappan et al., Chennai, India. In J Ocul Biol Dis Infor, 2012
NEDD8 Ultimate Buster 1 (NUB1), a protein that regulates cell cycle progression, interacts with AIPL1 to prevent the over expression of NUB1.
Ubiquitin-related proteins in neuronal and glial intranuclear inclusions in intranuclear inclusion body disease.
Wakabayashi et al., Hirosaki, Japan. In Pathol Int, 2012
In the present study, the proportions of intranuclear inclusion positive for NEDD8, NUB1 and SUMO-1 were significantly lower in glial cells than in neurons.
Inhibition of NEDD8-conjugation pathway by novel molecules: potential approaches to anticancer therapy.
Kamitani et al., Ōsaka, Japan. In Mol Oncol, 2012
COP9 signalosome, inactive mutant of Ubc12, and NUB1/NUB1L).
FAT10 and NUB1L bind to the VWA domain of Rpn10 and Rpn1 to enable proteasome-mediated proteolysis.
Groettrup et al., Konstanz, Germany. In Nat Commun, 2011
findings show how FAT10 and NUB1L dock with the 26S proteasome to initiate proteolysis; identified the 26S proteasome subunit hRpn10/S5a as the receptor for FAT10, whereas NUB1L can bind to both Rpn10 and Rpn1/S2.
Synphilin-1-binding protein NUB1 is colocalized with nonfibrillar, proteinase K-resistant α-synuclein in presynapses in Lewy body disease.
Wakabayashi et al., Hirosaki, Japan. In J Neuropathol Exp Neurol, 2011
The finding of this study suggested that NUB1 along with abnormal alpha-synuclein is involved in the pathogenesis of Lewy body disease.
NUB1 suppresses the formation of Lewy body-like inclusions by proteasomal degradation of synphilin-1.
Kamitani et al., Houston, United States. In Am J Pathol, 2006
These results suggest that NUB1 indeed targets synphilin-1 to the proteasome for its efficient degradation, which, because of the resultant reduction in synphilin-1, suppresses the formation of synphilin-1-positive inclusions.
The UBA domains of NUB1L are required for binding but not for accelerated degradation of the ubiquitin-like modifier FAT10.
Groettrup et al., Konstanz, Germany. In J Biol Chem, 2006
NUB1L not only acts as a linker between the 26 S proteasome and ubiquitin-like proteins, but also as a facilitator of proteasomal degradation.
Specific protein-DNA interaction at four sites flanking the chicken lysozyme gene.
Sippel et al., In Cell, 1982
The analysis showed specific retention of four restriction fragments (BS1-BS4), which map approximately 6.1 and 3.9 kb upstream from the transcription start, and 2.8 and 6.2 kb downstream from the poly(A)-addition point of the lysozyme gene.
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