Bcl-2 down-regulation causes autophagy in a caspase-independent manner in human leukemic HL60 cells

Cell Death and Differentiation

Volumn 7, Issue 12, 2000, Pages 1263-1269

  Saeki, K ^a   Yuo, A ^a   Okuma, E ^a   Yazaki, Y ^a   Susin, S A ^b   Kroemer, G ^b   Takaku, F ^a  

^a NATIONAL CENTER FOR GLOBAL HEALTH AND MEDICINE   (Japan)

^b CNRS   (France)

Author keywords

Antisense; Autophagy; Bcl 2; HL60; Tet ON

Indexed keywords

APOPTOSIS INDUCING FACTOR; CASPASE; CASPASE INHIBITOR; COMPLEMENTARY DNA; PROTEIN BCL 2; TETRACYCLINE;

APOPTOSIS; ARTICLE; AUTOPHAGY; CELL DEATH; CELL GROWTH; CELL NUCLEUS; CELL STRAIN HL 60; CELL SURVIVAL; CELL TRANSFORMATION; CONTROLLED STUDY; DOWN REGULATION; ELECTRON MICROSCOPY; GENE EXPRESSION SYSTEM; GENE INDUCTION; HUMAN; HUMAN CELL; INTRACELLULAR TRANSPORT; LEUKEMIA CELL; MEMBRANE POTENTIAL; MITOCHONDRIAL MEMBRANE; MITOCHONDRION; MORPHOLOGY; MYELOID LEUKEMIA; PRIORITY JOURNAL; PROTEIN TRANSPORT;

ANTI-BACTERIAL AGENTS; ANTIGENS, CD34; APOPTOSIS; AUTOPHAGY; BONE MARROW CELLS; CASPASES; DOWN-REGULATION; DOXYCYCLINE; GENE EXPRESSION REGULATION, LEUKEMIC; HL-60 CELLS; HUMANS; LEUKEMIA; PROTO-ONCOGENE PROTEINS C-BCL-2; RNA, ANTISENSE;

EID: 0034520466     PISSN: 13509047     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.cdd.4400759     Document Type: Article

References (22)

1. The morphology of various types of cell death in prenatal tissues
2. Developmental cell death: Morphological diversity and multiple mechanisms
3. Cell death: Programmed, apoptosis, necrosis or other?
4. Caspase-independent programmed cell death with necrotic morphology
5. Mitochondria as regulators of apoptosis: Doubt no more
6. Bcl-2 blocks loss of mitochondrial membrane potential while ICE inhibitors act at a different step during inhibition of death induced by respiratory chain inhibitors
7. Prevention of apoptosis by Bcl-2: Release of cytochrome c from mitochondria blocked
8. The release of cytochrome c from mitochondria: A primary site for Bcl-2 regulation of apoptosis
9. Molecular characterization of mitochondrial apoptosis-inducing factor
10. Mitochondrial release of caspase-2 and -9 during the apoptotic process
11. Investigation of the subcellular distribution of the bcl-2 oncoprotein: Residence in the nuclear envelope, endoplasmic reticulum, and outer mitochondrial membranes
12. Bcl-2 protein expression in aged brain and neurodegenerative diseases
13. Massive cell death of immature hematopoietic cells and neurons in Bcl-x-deficient mice
14. Targeted disruption of Bcl-2 alpha beta in mice: Occurrence of gray hair, polycystic kidney disease, and lymphocytopenia
15. High expression of bcl-2 protein in acute myeloid leukemia cells is associated with poor response to chemotherapy
16. Cell density-dependent apoptosis in HL-60 cells, which is mediated by an unknown soluble factor, is inhibited by transforming growth factor β1 and overexpression of Bcl-2
17. Induction of apoptosis (programmed cell death) in human leukemic HL-60 cells by inhibition of RNA or protein synthesis
18. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis
19. Induction of autophagy and inhibition of tumorgenesis by beclin 1
20. Oncogenic Ras triggers cell suicide through the activation of a caspase-independent cell death program in human cancer cells
21. bcl-2 proto-oncogene expression in normal and neoplastic human myeloid cells
22. Aberrant expression of cAMP-response-element-binding protein ('CREB') induces apoptosis