Title : NOXA-mediated degradation of MCL1 and BCL2L1 causes apoptosis of daunorubicin-treated human acute myeloid leukemia cells.

Pub. Date : 2021 Nov

PMID : 33982799






4 Functional Relationships(s)
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1 NOXA-mediated degradation of MCL1 and BCL2L1 causes apoptosis of daunorubicin-treated human acute myeloid leukemia cells. Daunorubicin MCL1 apoptosis regulator, BCL2 family member Homo sapiens
2 DNR-induced apoptosis in U937 cells accompanied by downregulation of MCL1 and BCL2L1, upregulation of Phorbol-12-myristate-13-acetate-induced protein 1 (NOXA), and mitochondrial depolarization. Daunorubicin MCL1 apoptosis regulator, BCL2 family member Homo sapiens
3 Restoration of MCL1 or BCL2L1 expression alleviated DNR-induced mitochondrial depolarization and cell death. Daunorubicin MCL1 apoptosis regulator, BCL2 family member Homo sapiens
4 Collectively, these results indicate that the upregulation of NOXA expression through the NOX4-ROS-p38 MAPK-GSK3beta-CREB axis results in the degradation of MCL1 and BCL2L1 in DNR-treated U937 and HL-60 cells. Daunorubicin MCL1 apoptosis regulator, BCL2 family member Homo sapiens