The autophagosomal–lysosomal compartment in programmed cell death

By W. Bursch. Cell Death and Differentiation, 2001

645 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Parasitology

View Paper: https://www.semanticscholar.org/paper/72f1bc6ae2b771e6c826af35b94a03a817932528

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. N. Mizushima
2. Beth Levine
3. Guido Kroemer
4. D. Klionsky
5. I. Slaninová
6. Ralph A. Nixon
7. A. Cuervo
8. M. Komatsu

In Molecular Biology

1. N. Mizushima
2. Guido Kroemer
3. Beth Levine
4. D. Klionsky
5. Ralph A. Nixon
6. T. Yoshimori
7. Y. Ohsumi
8. A. Cuervo

In Parasitology

1. N. Mizushima
2. Guido Kroemer
3. Beth Levine
4. Y. Ohsumi
5. M. Komatsu
6. T. Yoshimori
7. Ralph A. Nixon
8. P. Codogno

Citations in the corpus

• Another way to die: autophagic programmed cell death (2005, positive): “that cells with autophagic features often exist in regions where PCD is occurring seem to support the existence of autophagic cell death.(7) One question that constantly arises, however, is whether autophagic activity in dying cells is the cause of death”
• Lysosomes in cell death (2004, background): “A complete breakdown of the organelle with release of high concentrations of lysosomal enzymes into the cytosol results in unregulated necrosis, whereas partial, selective permeabilization triggers apoptosis (Bursch, 2001; Turk et al., 2002).”
• Role of Bcl-2 family proteins in a non-apoptotic programmed cell death dependent on autophagy genes (2004, methodology): “DKO MEFs were treated with 20 μM etoposide plus 10 μM 3-MA in the presence of 2 μM PI and observed from 12 hours to 48 hours under a phase-contrast (6) and fluorescence (7) microscope.”
• Macroautophagy—a novel β-amyloid peptide-generating pathway activated in Alzheimer's disease (2005, background): “…development (Clarke, 1990), response to ER stress, exposure to toxins (Kanzawa et al., 2004), or dysfunction of the autophagic pathway in pathological states mediate a caspase-independent form of cell death that shares certain features with apoptosis (Bursch, 2001; Gozuacik and Kimchi, 2004).”
• Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice (2005, background): “…J O U R N A L O F C E L L B IO L O G Y © The Rockefeller University Press $8.00 The Journal of Cell Biology, Vol. 169, No. 3, May 9, 2005 425–434 http://www.jcb.org/cgi/doi/10.1083/jcb.200412022 JCB: ARTICLE JCB 425 Impairment of starvation-induced and constitutive autophagy in Atg7 -deficient mice”
• Inhibition of Macroautophagy Triggers Apoptosis (2005, background): “Thus, HCQ acted in a fashion similar to that of other known inhibitors of autophagy, namely, Baf A1 (an inhibitor of vacuolar H ATPase) (5, 74), monensin (which mediates the exchange of protons for potassium or sodium) (2, 23), and 3-MA (4, 9, 63), all of which prevented the starvation-induced coloc”
• Autophagy: a lysosomal degradation pathway with a central role in health and disease. (2009, background): “Type II programmed cell death, or autophagic cell death, was originally described in mammary carcinoma cells [112,113].”
• LC3 conjugation system in mammalian autophagy (2004, background): “Type II autophagic cell death is frequently observed when type I apoptosis is inhibited or when a cell-death-related kinase, such as DAP kinase, is overexpressed (for review, see (Bursch, 2001) ).”