Examples of 'bcl-xl' in a sentence
Meaning of "bcl-xl"
Bcl-xl is a protein that plays a role in regulating apoptosis, or programmed cell death
How to use "bcl-xl" in a sentence
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bcl-xl
The BCL-xL encoding gene is the most preferred.
Said antibody producing cell is protected by apoptosis by Bcl-xL.
The researchers discovered that the Bcl-xL gene was particularly important.
Said antibody producing cell may be protected by apoptosis by Bcl-xL.
Therapeutic use of peptides derived from Bcl-XL protein in cancer patients.
In a preferred embodiment, said antibody producing cell is protected by apoptosis by Bcl-xL.
Also disclosed therein are BCL-Xl inhibiting compositions and methods of promoting apoptosis in a mammal.
Providing said antibody producing cell with a nucleic acid sequence encoding Bcl-xL.
The structure of Bcl-xL contains two central hydrophobic helices surrounded by amphipathic helices.
Thus, protection of mitochondrial membrane integrity through proteins like Bcl-xL is critical for cell survival.
The expression of Bcl-XL is typically correlated with a poor prognosis and shortened survival.
The invention further describes the stabilization of the growth of antibody producing cells with Bcl-xL.
Bcl-XL is mainly found in ER negative breast cancer.
The number of blue cells can be partially restored by co-transfection of Bak with Bcl-xL.
Bcl-xL overexpression is a major contributor to drug resistance in AML.
See also
These cells are resistant to Fas-mediated apoptosis and express high levels of Bcl-xL.
Cell lines expressing Bcl-XL only had intermediate VCD.
Said B cell is further provided with Bcl-xL.
Increased Bcl-xL expression is also observed in hepatoma cell lines, such as HepG2.
The pharmaceutical composition of claim 1, comprising a Bcl-XL inhibitor.
Furthermore, we find that Bcl-xL control of cell migration is independent of its anti-apoptotic activity.
A nucleic acid sequence encoding Bcl-xL.
For example, a hamster bcl-xL gene, introduced into a hamster host cell, is by definition a heterologous gene.
The method as claimed in claim 1, in which the cell overexpressed bcl-XL.
To each tube was added a solution containing 30 nM of Bcl-xL and 4 nM fluoresceinated peptide.
Furthermore, STAT5-mediated erythroblast survival is dependent upon upregulation of Bcl-xL.
In one embodiment, Bcl-XL protein was treated using the united-atom approximation in the docking studies.
Cell survival was associated with increased expression of the anti-apoptotic genes bcl-XL and bfl-l.
Western blotting of Bcl-XL by using the same tumor lysates as in ( A ).
A combination comprising a compound of formula ( I ) according to claim 1, in combination with a Bcl-XL inhibitor.
The anti-apoptotic molecule Bcl-xL also contains the four BH.
Several laboratories are interested in designing small molecule inhibitors of Bcl-2 and Bcl-XL.
The status of serine phosphorylation of Bcl-xL and Bcl-w was next analyzed.
Both Bcl-2 and Bcl-XL have been found to be overexpressed in human breast cancers.
Figure 11 illustrated the inhibition of of Bcl-xL using the Theaflavins shown.
The normal fibroblast cell line showed low level of Bcl-2 and Bcl-XL.
Genetic deletion of both Mcl-1 and Bcl-xL in megakaryocytes resulted in preweaning lethality.
Two breast cancer cell lines have medium levels of Bcl-2 or Bcl-XL expression.
Once a peptide binds to a Bcl-2 or Bcl-XL protein, the fluorescence polarization is enhanced.
More preferably, a nucleic acid of the present invention encodes polypeptides designated BCL-xL or BCL-2.
This result suggests that Bcl-xL and Bcl-w are needed for association of PP1c to Bad.
Additional compounds also inhibit Bcl-2 dependent cell lines than Bcl-xL dependent cell lines.
BCL-like proteins include BCL-xL and BAX-alpha, which appear to function upstream of caspase activation.
The significantly greater affinity for Bcl-2, as compared to Bcl-xL suggests a selective binding affinity.
In a preferred embodiment said B cell is transduced with BCL6 and Bcl-xL.
Effect of MDM2 on Bcl-XL expressing cell lines.
The pharmaceutical composition of claim 1 to 8, further comprising a Bcl-XL inhibitor.
STAT5 positively regulates the Bcl-xL expression through STAT binding elements within the Bcl-xL promoter.
The BCL-xS lacks a section of 63 amino acids found in the BCL-xL.
Bcl-2 and Bcl-XL are highly homologous proteins.
