The fused BCR -
Abl protein interacts with the interleukin - 3 receptor beta (c) subunit.
In some cases, patients» tumors develop resistance to Gleevec — either
the Abl protein mutates so that the drug can no longer bind to it, or the protein accumulates in such quantities that the drug can't keep up, even at the highest dose.
Not exact matches
In experiments on cell cultures, both of these inhibitors succeeded in breaking various forms of the TKI resistance: including forms caused by additional mutations of the gene Bcr -
Abl as well as those caused by large quantities of the
protein Gab2.
In CML cells, Gab2 amplifies the signal of the
protein Bcr -
Abl.
Gleevec blocks the ATP pocket in
Abl and in two other
proteins, but it doesn't incapacitate the hundreds of other enzymes that also rely on ATP.
By using these reagents and v -
abl - specific antisera, it was demonstrated that the P210 in CML cells is indeed the
protein product of the 8.5 - kilobase transcript.
By analogy to the gag /
abl fusion
protein of Abelson murine leukemia virus, the replacement of amino terminal c -
abl sequences by bcr sequences in P210 may create a transforming
protein involved in CML.
The symbol
ABL is derived from Abelson, the name of a leukemia virus which carries a similar
protein.
The activity of tyrosine kinases is typically regulated in an auto - inhibitory fashion, but the BCR -
Abl fusion gene codes for a
protein that is «always on» or continuously activated leading to unregulated cell division (i.e. cancer).
The
Abl gene expresses a membrane - associated
protein, a tyrosine kinase, and the BCR -
Abl transcript is also translated into a tyrosine kinase.
[11] Since
ABL activates a number of cell cycle - controlling proteins and enzymes, the result of the BCR - Abl fusion is to speed up cell divisi
ABL activates a number of cell cycle - controlling
proteins and enzymes, the result of the BCR -
Abl fusion is to speed up cell divisi
Abl fusion is to speed up cell division.
This gene encodes for a Bcr -
abl fusion
protein.
Inhibition of c -
Abl with STI571 attenuates stress - activated
protein kinase activation and apoptosis in the cellular response to 1 - β - d - arabinofuranosylcytosine.
We found that depletion of
ABL kinases in breast cancer cells decreased STAT5A mRNA expression (Fig. 6D) without decreasing total STAT5
protein abundance as measured by Western blotting with antibodies that detect both STAT5A and STAT5B (Fig. 7D and fig.
Similarly, inhibiting
ABL kinase activity with the allosteric inhibitor GNF5 decreased TAZ
protein abundance (fig.
Regardless, our data support a role for
ABL kinases in the regulation of TAZ
protein abundance and activity in breast cancer cells.
To directly evaluate the relationship between
ABL family kinases and metastasis, we analyzed
ABL1 and
ABL2
protein abundance in MDA - MB - 231 — derived breast cancer cell lines with different organ metastasis tropisms (19).
Depletion of
ABL kinases does not affect YAP1
protein abundance, localization, or tyrosine phosphorylation in breast cancer cells.
We also found that the SRC and
ABL non-receptor tyrosine kinases and the SHEP1 scaffolding
protein are binding partners of the Eph receptors, and we identified signaling connections between Eph receptors and integrins.
Initial empirical testing for c -
ABL was carried out via an in vitro kinase approach with purified recombinant kinases at the MRC
Protein Phosphorylation and Ubiquitination Unit in Dundee, Scotland.