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ABL1 — TMED7
Text-mined interactions from Literome
Gesbert et al., J Biol Chem 2000
:
We demonstrate that the decrease of
p27 ( Kip1 ) is directly
due to
BCR/ABL in hematopoietic cells by two different approaches ... The PI3K inhibitor LY-294002 blocks the ability of
BCR/ABL to
induce p27 ( Kip1 ) down-regulation and inhibits BCR/ABL induced entry into S phase ... Overall, these data are consistent with a model in which
BCR/ABL suppresses
p27 ( Kip1 ) protein levels through PI3K/AKT, leading to accelerated entry into S phase
Fan et al., Chin Med J (Engl) 2001
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive) :
In this model, we showed that the presence of
p210BCR/ABL leads to elevated levels of
p27kip in p210BCR/ABL expressing CD34+ cells
Schuster et al., Blood 2003
:
In contrast, the up-regulation of PU.1 and
p27 ( Kip1 ) by G-CSF was not
affected by
Bcr-Abl
Andreu et al., Cancer Res 2005
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive) :
We further show that
BCR-ABL also
regulates p27 ( Kip1 ) protein levels by increasing its degradation by the proteasome ... In conclusion, these results suggest that
BCR-ABL regulates cell cycle in CML cells at least in part by inducing proteasome mediated degradation of the cell cycle inhibitor
p27 ( Kip1 ) and provide a rationale for the use of inhibitors of the proteasome in patients with BCR-ABL leukemias
Rangatia et al., Leukemia 2006
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive) :
Lack of
BCR-ABL leads to cell cycle arrest in G1 phase as observed by decrease in cyclin D1 and
increase in p21 and
p27 cdk inhibitors mRNA