Examples of 'b-catenin' in a sentence
Meaning of "b-catenin"
A protein that plays a role in cell adhesion and signaling pathways. It is involved in various cellular processes, including cell growth and development
How to use "b-catenin" in a sentence
Basic
Advanced
b-catenin
B-catenin has also been shown to be of importance in cell adhesion.
Ion channel inhibitors as well as zVAD abrogated b-catenin cleavage but not leupeptin.
B-catenin is reported as being widely expressed in adult and embryo tissues.
The excess sugar in the body increases the activity of a protein called b-catenin.
B-Catenin can be stabilized in multiple different ways.
The outer layer of the organoid consists of epithelial cells with a nuclear B-Catenin staining.
The B-catenin then translocates to the nucleus.
A number of these DsiRNAs uniquely targeted human B-catenin.
Ubiquitylated B-catenin is ultimately degraded by the proteasome.
A number of these DsiRNAs uniquely targeted mouse B-catenin.
The phosphorylated B-catenin is ubiquitinated and degraded by proteasome.
The present disclosure shows the modulation of B-catenin phosphorylation.
Aberrant B-catenin signaling plays a important role in tumorigenesis.
Final results are reported as fold induction over basal B-catenin.
These results indicate that B-catenin is reduced by SAANDs treatment.
See also
Alternatively, said enhancer may be a protein that promotes B-catenin acetylation.
Restoring B-catenin phosphorylation should halt the cancerous process.
It is also known that after ubiquitination, B-catenin is degraded by the proteasomes.
The same blot was stripped and reprobed for total B-catenin.
This interaction results in phosphorylation of B-catenin thereby targeting it for degradation.
Exemplary B-catenin targeting DsiRNA agents of the invention include the following,.
The invention describes both enhancers and inhibitors of B-catenin phosphorylation.
The effects on B-catenin were explained by ion channel - and caspase dependent mechanisms.
In contrast, little nuclear localization of B-catenin is seen in the EGFP negative fraction.
Captured B-catenin is then phosphorylated, ubiquitinated and subsequently degraded by the proteasome.
Figure 1B is a western blot analysis of B-catenin levels in hyperplastic wound cell cultures.
Independent cultures were used for these experiments, and data was normalized to B-catenin.
APC also has a role in the transport of B-catenin out of the nucleus.
In these cell lines, there is an increased level of cytosolic and nuclear B-catenin.
Hyperplastic wounds are characterized by elevated B-catenin levels during the proliferative phase.
B-catenin RNA target sites can also interchangeably be referenced by corresponding cDNA sequences.
This indicates that the degradation of B-catenin is inhibited by expression of the h-BTrCPAF mutant.
The B-catenin accumulation / stability is then quantified following densitometry analysis of protein bands.
Axin expression leads concomitantly to B-catenin destruction and apoptosis in tumor cells Satoh et al.
GSK3B facilitates a number of intracellular signalling pathways including the activation of B-catenin complex.
Why is the level and timing of B-catenin accumulation so important for reprogramming efficiency?
These associations lead to a destabilisation of the destruction complex and cytosolic accumulation of B-catenin.
Chemical B-catenin inhibitors are known in the art that may be administeredas described herein.
Various literature reports have linked B-catenin to the malignant transformation of normal cells.
Mutation of these residues to alanine significantly decreased phosphorylation of several substrates, including B-catenin.
Periodic accumulation of B-catenin in ES cells enables them to reprogramme somatic cells after fusion.
When that is done, one can visualize the presence of B-catenin with an HRPO substrate.
This phosphorylated and acetylated B-catenin is resistant to degradation, and can function as a transcriptional activator.
According to a preferable embodiment, the peptide of the present invention transfers B-catenin into a nucleus.
Individual bars represent average human B-catenin levels observed in triplicate, with standard errors shown.
The peptide of the present invention significantly elevated the expression level of B-catenin in keratinocyts.
Acetylated B-catenin species concur with the phosphorylated ones, indicating a possible linkage of the two events.
The inventors ' results suggest that phosphorylated B-catenin undergoes acetylation of its Lys residues.
There are also disclosed cell cultures exhibiting increased nuclear localization of the B-catenin polypeptide.
This reduction in B-catenin is initiated by PKG itself.
