Mitochondrial Protein Quality Control Systems in Aging and Disease

Luce, K. Scott; Weil, Andrea; Osiewacz, Heinz D.

doi:10.1007/978-1-4419-7002-2_9

Cited by 51 publications

(31 citation statements)

References 129 publications

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“…Autophagy in this scenario might be triggered by the cytosolic accumulation of ROS, which occurs as a consequence of mitochondrial failure (Luce et al, 2010).…”

Section: Autophagymentioning

confidence: 99%

Overcoming anoikis – pathways to anchorage-independent growth in cancer

Guadamillas

Cerezo

Pozo

2011

Journal of Cell Science

353

331

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SummaryAnoikis (or cell-detachment-induced apoptosis) is a self-defense strategy that organisms use to eliminate 'misplaced' cells, i.e. cells that are in an inappropriate location. Occasionally, detached or misplaced cells can overcome anoikis and survive for a certain period of time in the absence of the correct signals from the extracellular matrix (ECM). If cells are able to adapt to their new environment, then they have probably become anchorage-independent, which is one of the hallmarks of cancer cells. Anoikis resistance and anchorage-independency allow tumor cells to expand and invade adjacent tissues, and to disseminate through the body, giving rise to metastasis. Thus, overcoming anoikis is a crucial step in a series of changes that a tumor cell undergoes during malignant transformation.Tumor cells have developed a variety of strategies to bypass or overcome anoikis. Some strategies consist of adaptive cellular changes that allow the cells to behave as they would in the correct environment, so that induction of anoikis is aborted. Other strategies aim to counteract the negative effects of anoikis induction by hyperactivating survival and proliferative cascades. The recently discovered processes of autophagy and entosis also highlight the contribution of these mechanisms to rendering the cells in a dormant state until they receive a signal initiated at the ECM, thereby circumventing anoikis. In all situations, the final outcome is the ability of the tumor to grow and metastasize. A better understanding of the mechanisms underlying anoikis resistance could help to counteract tumor progression and prevent metastasis formation.

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“…Autophagy in this scenario might be triggered by the cytosolic accumulation of ROS, which occurs as a consequence of mitochondrial failure (Luce et al, 2010).…”

Section: Autophagymentioning

confidence: 99%

Overcoming anoikis – pathways to anchorage-independent growth in cancer

Guadamillas

Cerezo

Pozo

2011

Journal of Cell Science

353

331

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“…Fortunately, different pathways have evolved to cope with this hazardous situation and to maintain a functional population of mitochondria. [2][3][4] Important components of the mitochondrial surveillance system are pathways controlling the quality of mitochondrial proteins. These pathways rely on enzymes able to repair damaged proteins, chaperones involved in refolding of misfolded polypeptides, as well as ATP-dependent proteases that selectively degrade irreversibly damaged proteins.…”

Section: Introductionmentioning

confidence: 99%

“…These pathways rely on enzymes able to repair damaged proteins, chaperones involved in refolding of misfolded polypeptides, as well as ATP-dependent proteases that selectively degrade irreversibly damaged proteins. 2 The inner mitochondrial membrane harbors two AAA proteases, the i-AAA protease and the m-AAA protease. Both belong to the highly conserved family of AAA proteins found in all eukaryotes.…”

Section: Introductionmentioning

confidence: 99%

Unmasking a temperature-dependent effect of theP. anserinai-AAA protease on aging and development

Weil

Luce²,

Dröse³

et al. 2011

Cell Cycle

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“…Aging appears to also play a role, consistent with the late-onset of most PMD. The loss of KS might represent a hazard for the organism, especially for older individuals who have less efficient protein quality control systems (Koga, Kaushik, & Cuervo, 2010;Luce, Weil, & Osiewacz, 2010). In familial amyloid polyneuropathy it is known that missense mutations can compromise the KS of transthyretin (TTR), facilitating tetrameric TTR dissociation and subsequent aggregation into amyloid fibrils (Saraiva, 1995).…”

Section: Thermodynamics Vs Kinetic Stabilitymentioning

confidence: 99%