GRB2
GAB2
SOS1
CRKL
CBL
STAT5A
JAK2
SKP2
CDKN1B
MTOR
RPS6KB1
BAD
BCL2L1
MDM2
TP53
MYC
BCR-ABL1
CRK
PIK3R1
Bafetinib
Ras
Akt
RAF
MEK
MAPK
FOXO
Transcription
Proliferation and Survival
Survival
Proliferation
Nucleus Outer Membrane
Nucleus Inner Membrane
Protein Synthesis
PI3K/Akt Pathway
MAPK/ERK Pathway
Cytosol
JAK-STAT Pathway
Decreased signalling of the
JAK-STAT pathway decreases
the cell's likelihood for
proliferation and survival.
Both the JAK-STAT pathway
and the MAPK/ERK pathway
influence the cell's
transcription. Inhibiting
these pathways decreases
transcription so the cell
will eventually die.
The PI3K/AKT pathway is
responsible for many
regulatory functions of the
cell and it's inhibition
would affect downstream
processes of protein
synthesis and cellular
proliferation.
With decreased protein
synthesis, less cellular
functions will be able to
proceed eventually killing
the cell.
As Bafetinib is still under
clinical trials there is no
defined way in literature of
routes administration. It is
most likely administered
intravenously into the blood
so it can travel to the bone
marrow.
Bafetinib specifically binds
and inhibits the BCR/ABL1
fusion protein tyrosine
kinase. The BCR-ABL1 is an
abnormal enzyme created by
the Philadelphia chromosomal
translocation. This
chromosomal translocation is
associated with chronic
myeloid leukemia .
Inhibition of BCR/ABL1
inhibits the JAK-STAT,
MAPK/ERK, and PI3K/Akt
pathways cascade effects.
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