The pleiotropic role of autophagy: from protein metabolism to bactericide

Mizushima, Noboru

doi:10.1038/sj.cdd.4401728

Cited by 429 publications

(350 citation statements)

References 56 publications

(79 reference statements)

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“…CMA's intrinsic selectivity seems beneficial under particular conditions in which discrimination between different types of proteins for degradation is required. For example, although macroautophagy is induced early in starvation to generate essential amino acids (otherwise supplied in the diet) through the breakdown of existing organelles and proteins (Mizushima, 2005), this random degradation can only be maintained during a relatively short period of time (10h), beyond which it needs to be replaced by the selective degradation provided by CMA (Wing et al, 1991;Cuervo et al, 1995). Activation of CMA under these conditions favors degradation of unnecessary proteins against that of proteins essential for cell survival.…”

Section: Selective Autophagy Via Chaperone-mediated Autophagymentioning

confidence: 99%

Autophagy as a cell-repair mechanism: Activation of chaperone-mediated autophagy during oxidative stress

Kaushik

Cuervo

2006

Molecular Aspects of Medicine

129

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Proper removal of oxidized proteins is an important determinant of success when evaluating the ability of cells to handle oxidative stress. The ubiquitin/proteasome system has been considered the main responsible mechanism for the removal of oxidized proteins, as it can discriminate between normal and altered proteins, and selectively target the last ones for degradation. A possible role for lysosomes, the other major intracellular proteolytic system, in the removal of oxidized proteins has been often refused, mostly on the basis of the lack of selectivity of this system. Although most of the degradation of intracellular components in lysosomes (autophagy) takes place through "in bulk" sequestration of complete cytosolic regions, selective targeting of proteins to lysosomes for their degradation is also possible via what is known as chaperone-mediated autophagy (CMA). In this work, we review recent evidence supporting the participation of CMA in the clearance of oxidized proteins in the forefront of the cellular response to oxidative stress. The consequences of an impairment in CMA activity, observed during aging and in some age-related disorders, are also discussed.

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Section: Selective Autophagy Via Chaperone-mediated Autophagymentioning

confidence: 99%

Autophagy as a cell-repair mechanism: Activation of chaperone-mediated autophagy during oxidative stress

Kaushik

Cuervo

2006

Molecular Aspects of Medicine

129

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“…When nutrition is depleted, cell survival is attributed to autophagy by producing ATP energy from the degradation of intracellular organelles. 44 In contrast, autophagy in the absence of nutrient depletion leads to cell death. Beclin 1 is an autophagy-inducible gene in mammalian cells, which was initially discovered as a Bcl-2 interacting protein.…”

Section: Introductionmentioning

confidence: 99%

Antisense and nonantisense effects of antisense Bcl-2 on multiple roles of Bcl-2 as a chemosensitizer in cancer therapy

et al. 2006

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Bcl-2 is an oncoprotein that plays a critical role in inhibiting apoptotic cell death in the mitochondria-dependent pathway in cancer chemotherapy. As a strategy for blocking Bcl-2 for enhancement of the chemotherapeutic effect, antisense Bcl-2 (AS Bcl-2; G3139, oblimersen sodium, Genasense) has shown promise, and there are several ongoing clinical studies with hematological malignancies as well as solid tumors. Although several preclinical and clinical studies have shown the therapeutic efficacy of Bcl-2 in combination with an anticancer drug as a chemosensitizer, in clinical trials the downregulation of Bcl-2 has not been observed with a high frequency in tumor cells. Nevertheless, previous studies showed nonantisense effects such as production of reactive oxygen species and immunostimulatory action through cytosine-phosphate-guanosine-motif in the antisense oligodeoxynucleotides. Further, Bcl-2 is able to inhibit Beclin 1-dependent autophagic cell death, which is a nonapoptotic cell death. The current status and future directions of AS Bcl-2 and the potential mechanisms for multiple roles that Bcl-2 has in cancer therapy are reviewed.

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“…2,4 Both in animals [5][6][7] and yeast, 8 good ultrastructural evidence exists for the presence of autophagosomes. In root-tip meristem cells of various species, the formation of structures that are similar to autophagosomes/autolysosomes in animal cells has been documented in an excellent series of papers (reviewed in ref.…”

Section: Do Plastids In Dendrobium CV Lucky Duan Petals Function Simmentioning

confidence: 99%

Do plastids inDendrobiumcv. Lucky Duan petals function similar to autophagosomes and autolysosomes?

Doorn¹,

Kirasak²,

Sonong³

et al. 2011

Autophagy

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The pleiotropic role of autophagy: from protein metabolism to bactericide

Cited by 429 publications

References 56 publications

Autophagy as a cell-repair mechanism: Activation of chaperone-mediated autophagy during oxidative stress

Autophagy as a cell-repair mechanism: Activation of chaperone-mediated autophagy during oxidative stress

Antisense and nonantisense effects of antisense Bcl-2 on multiple roles of Bcl-2 as a chemosensitizer in cancer therapy

Do plastids inDendrobiumcv. Lucky Duan petals function similar to autophagosomes and autolysosomes?

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