This transcription factor transcribes proapoptotic PUMA (s10), contributing to the permeabilization of the outer mitochondrial membrane (s11). The signaling molecule H 2O 2 either oxidized the oxidative sensor protein DJ-1-Cys106-SH into DJ-1-SO 3 (s5) or indirectly activated prodeath kinases (ASK-1 (s6) and MKK4 (s7)) and JNK (s8), which in turn activate c-JUN (s9). This compound targets mitochondrial complex I or II (s3), resulting in an over generation of ROS-H 2O 2 (s4). Once TPGS enters the cell, it is metabolically processed by cytoplasmic esterases and converted into alpha-tocopherol acetate ( α-TOS, s2). The TPGS (step 1) triggers a cell death subroutine in K562, a well-established model of CML. Proposed model of minimal completeness of cell death signaling induced by TPGS as a mechanistic explanation of CML cell demise.
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