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A new crystallographic structure of human ubiquitin solved from crystals grown in the presence of magnesium.
Data suggest that both human ubiquitin and HFBII (hydrophobin-II from Trichoderma reesei) exhibit a critical surface hydration level (or effective hydrophobic interface at the surface) at which percolation transition of water network occurs.
UbB was significantly increased in prolonged Trichostatin A-selected HeLa cells and it played a key role in the maintenance of cervical cancer stem-like cells
downregulation of ubiquitin through Ubb-KD is a potential anti-cancer treatment by inhibiting ubiquitination at multiple sites related to oncogenic pathways and by weakening the ability of cancer cells to overcome increased stress.
A significant decrease in amyloid beta deposition and plaque formation suggests a role for the ubiquitin-proteasome system in the amyloid pathology of Alzheimer's disease.
age-dependent accumulation of Ubb(+1) , and how Ubb(+1) -mediated proteasome inhibition may contribute to Alzheimer's disease. [review]
Studies indicate that biomedical research on ubiquitin moves into translational research and drug discovery.
Studies indicate that DUBs recycle ubiquitin by processing polyubiquitin chains to generate free ubiquitin, and can be regulated by ubiquitination or phosphorylation.
analysis of orexin receptor 1 and 2 -arrestin-ubiquitin complexes
The results of this study demonstrated that the UBB mutation caused the subtle defect in spatial reference memory formation, caused by a decrease in forebrain proteasome activity.
Ubb (show UBA52 Proteins) deficiency causes dysregulation of neural stem cell differentiation with premature gliogenesis.
The lysine 6 to tryptophan ubiquitin substitution results in the cataract development in newborn mice.
upon stress induced by disruption of Ubb (show UBA52 Proteins), neuronal vulnerability may be determined based on the ability of neurons or neighboring cells to maintain free Ub levels for the protection of neuronal function and survival.
Several genes related to fertility, metabolism, transcription, and the ubiquitin-proteasome system (UPS) are misregulated in Ubb (-/-)testes at 7 and/or 14 days. In Ubb (-/-)testes ubiquitylated levels of histone H2A are significantly reduced.
Ubb knockout mice exhibit phenotypes consistent with hypothalamic dysfunction. Our data also indicate that Ubb is essential for the maintenance of the ubiquitin levels required for proper regulation of metabolic and sleep behaviours in mice.
Data show that ubiquitin B transgenic mice appear vulnerable to toxic insults due to a modest proteasome inhibition, and underscore the relevance of an efficient ubiquitin-proteasome system in Huntington disease (show HTT Proteins).
targeted disruption of Ubb (show UBA52 Proteins) results in male and female infertility due to failure of germ cells to progress through meiosis I and hypogonadism.
Loss of Ubb (show UBA52 Proteins) led to a progressive degenerative disorder affecting neurons within the arcuate nucleus of the hypothalamus.
This gene encodes ubiquitin, one of the most conserved proteins known. Ubiquitin is required for ATP-dependent, nonlysosomal intracellular protein degradation of abnormal proteins and normal proteins with a rapid turnover. Ubiquitin is covalently bound to proteins to be degraded, and presumably labels these proteins for degradation. Ubiquitin also binds to histone H2A in actively transcribed regions but does not cause histone H2A degradation, suggesting that ubiquitin is also involved in regulation of gene expression. This gene consists of three direct repeats of the ubiquitin coding sequence with no spacer sequence. Consequently, the protein is expressed as a polyubiquitin precursor with a final amino acid after the last repeat. Aberrant form of this protein has been noticed in patients with Alzheimer's and Down syndrome.
, polyubiquitin B