Growth factor regulation of autophagy and cell survival in the absence of apoptosis.

By J. Lum, Daniel E. Bauer, M. Kong, Marian H. Harris, Chi Li, T. Lindsten, Craig B. Thompson. Cell, 2005

1,590 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Surgery

View Paper: https://www.semanticscholar.org/paper/707e335ca64960241260ab8118af7d67c0f32b35

How researchers see this paper

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

In Epidemiology

In Immunology

In Surgery

Citations in the corpus

Self-eating and self-killing: crosstalk between autophagy and apoptosis (2007, background): “Inhibition of autophagy by knockdown of Atg5 or Atg7 or by the addition of 3-methyladenine (an inhibitor of the phosphatidylinositol 3-kinase Vps34 ) or chloroquine (an inhibitor of lysosomal acidification, which, in turn, is required for fusion between autophagosomes and lysosomes; Box 1 ) ki”
Autophagic and tumour suppressor activity of a novel Beclin1-binding protein UVRAG (2006, background): “It has been speculated that autophagy may both benefit and hinder tumour development and/or progressio”
Growth arrest and autophagy are required for salivary gland cell degradation in Drosophila. (2007, positive): “Finally, extreme levels of autophagy may be sufficient to cause a metabolic catastrophe by degrading substrates and mitochondria that are needed for energy (Lum et al., 2005).”
Autophagy Is Activated for Cell Survival after Endoplasmic ReticulumStress (2006, background): “Recently, autophagy was demonstrated to play a role in the maintenance of ATP production from catabolism of intracellular substrates for cell survival after growth factor withdrawal (18).”
Translational regulation of gene expression during conditions of cell stress. (2010, background): “It is known that under starvation conditions TORC1 promotes autophagy, which will supply starving cells essential bioenergetic components (Lum et al., 2005), and that the increased removal of damagedmolecules and organelles via this route could be beneficial for the prevention of aging (Mizushima…”
Mitochondrial outer membrane permeabilization during apoptosis: the innocent bystander scenario (2006, background): “For example, many of the proteins that have been described to regulate the mPT pore also have claims to participate additionally in MOMP.”
Toll-like receptor 4 is a sensor for autophagy associated with innate immunity. (2007, background): “In cells treated with LPS, M. tuberculosis bacilli were seen inside double membrane-bound vacuoles typical of autophagosomes (Figure 6B, 3–4) (Gutierrez et al., 2004; Ogawa et al., 2005; Lum et al., 2005).”
Lysosomes and autophagy in cell death control (2005, background): “Inhibition of autophagy also sensitizes cells to the depletion of obligatory growth (or survival) factors, resulting in a decreased import of nutrients through the plasma membran”
Calcium and apoptosis: ER-mitochondria Ca2+ transfer in the control of apoptosis (2008, background): “Indeed, in apoptosis-deficient mammalian cells, autophagy acts as an alternative death mechanism (Lum et al., 2005) and in Bax-Bak double knockout of MEF (which are unable to perform the apoptotic program), treatment with apoptotic inducers, such as etoposide, thapsigargin or SDS, enhance autophagos”
Loss of autophagy diminishes pancreatic beta cell mass and function with resultant hyperglycemia. (2008, background): “Autophagy is activated during nutrient deprivation to promote cell survival and to increase 318 Cell Metabolism 8, 318–324, October 8, 2008 ª2008 Elsevier In amino acid retrieval (Lum et al., 2005).”
Regulation of Autophagy by Reactive Oxygen Species (ROS): Implications for Cancer Progression and Treatment (2009, positive): “On growth-factor withdrawal, these cells lose their ability to take up extracellular nutrients but maintain ATP production from catabolism of intracellular substrates through autophagy (70).”
Autophagy inhibition enhances therapy-induced apoptosis in a Myc-induced model of lymphoma. (2007, methodology): “shRNA designed to silence no mouse or human genes (hairpin control, HC) and 2 distinct shRNA sequences against ATG5 (shATG5 hairpin 2 [h2], shATG5 hairpin [h7]) were cloned into the control expression vector pKD (9) and introduced into primary tumor cells harvested from a Myc/p53ERTAM B cell lymphom”