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Directly Quantifying Autophagy in Peripheral Blood Mononuclear Ce - Enzo Life Sciences

Directly Quantifying Autophagy in Peripheral Blood Mononuclear Ce - Enzo Life Sciences | autophagy | Scoop.it
Directly Quantifying Autophagy in Peripheral Blood Mononuclear Cells (PBMCs).
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Interesting post about autophagy.

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Classification of cell death: How do cells die?

Classification of cell death: How do cells die? | autophagy | Scoop.it
Cell death can be classified according to its morphological appearance (which may be apoptotic, necrotic, autophagic or associated with mitosis), enzymological criteria (with and without the involvement of nucleases or of distinct classes of proteases, such as caspases, calpains, cathepsins and transglutaminases), functional aspects (programmed or accidental, physiological or pathological) or immunological characteristics (immunogenic or non-immunogenic). The Nomenclature Committee on Cell Death (NCCD) has formulated a first round of recommendations in 2005, in Cell Death and Differentiation. Since then, the field of cell death research has continued its expansion, significant progress has been made and new putative cell death modalities have been described. The NCCD provides a forum in which names describing distinct modalities of cell death are critically evaluated and recommendations on their definition and use are formulated, hoping that a non-rigid, yet uniform, nomenclature will facilitate the communication among scientists and ultimately accelerate the pace of discovery. As it stands now, three distinct routes of cellular catabolism can be defined according to morphological criteria, namely apoptosis (which is a form of cell death), autophagy (which causes the destruction of a part of the cytoplasm, but mostly avoids cell death) and necrosis (which is another form of cell death). Although frequently employed in the past, the use of Roman numerals (i.e., type I, type II and type III cell death, respectively) to indicate these catabolic processes should be abandoned. Moreover, several critiques can be formulated against the clear-cut distinction of different cell types in the triad of apoptosis, autophagic cell death and necrosis. First, although this vocabulary was originally introduced based on observations of developing animals, it has rapidly been adopted to describe the results of in vitro studies performed on immortalized cell lines, which reflect very poorly the physiology of cell death in vivo. In tissues, indeed, dying cells are usually engulfed well before signs of advanced apoptosis or necrosis become detectable. Thus, it may be acceptable - if the irreversibility of these phenomena is demonstrated - to assess caspase activation and/or DNA fragmentation to diagnose apoptotic cell death in vivo. Second, there are numerous examples in which cell death displays mixed features, for instance with signs of both apoptosis and necrosis, a fact that lead to the introduction of terms like ‘necroapoptosis’ and ‘aponecrosis’ (whose use is discouraged by the NCCD to avoid further confusion). Similarly, in the involuting D. melanogaster salivary gland, autophagic vacuolization is synchronized with signs of apoptosis, and results from genetic studies indicate that caspases and autophagy act in an additive manner to ensure cell death in this setting. Altogether, these data argue against a clear-cut and absolute distinction between different forms of cell death based on morphological criteria. Third (and most important), it would be a desideratum to replace morphological aspects with biochemical/functional criteria to classify cell death modalities. Unfortunately, there is no clear equivalence between morphology and biochemistry, suggesting that the ancient morphological terms are doomed to disappear and to be replaced by truly biochemical definitions. In this context, ‘loss-of-function’ and ‘gain-of function’ genetic approaches (e.g., RNA interference, knockout models and plasmid-driven overexpression systems) represent invaluable tools to characterize cell death modes with more precision, but only if such interventions truly reduce/augment the rate of death, instead of changing its morphological appearance (as it is often the case). Present cell death classifications are reminiscent of the categorization of tumors that has been elaborated by pathologists over the last one and a half centuries. As old morphological categorizations of tumors are being more and more supported (and will presumably be replaced) by molecular diagnostics (which allows for a more sophisticated stratification of cancer subtypes based on molecular criteria), the current catalog of cell death types is destined to lose its value as compared with biochemical/functional tests. In the end, such efforts of classification are only justified when they have a prognostic and/or predictive impact, allowing the matching of each individual cancer with the appropriate therapy. Similarly, a cell death nomenclature will be considered useful only if it predicts the possibilities to pharmacologically/genetically modulate (induce or inhibit) cell death and/or if it predicts the consequences of cell death in vivo, with regard to inflammation and recognition by the immune system.
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Nature-Functional interaction between autophagy and ciliogenesis


Via PaG
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PaG's curator insight, October 3, 2013 4:45 AM

• Disruption of IFT compromises autophagy

• Ciliary Hh signalling induces autophagy

• Autophagic machinery localizes at the cilia

• IFT-dependent trafficking of ATG16L

• Autophagy activation reduces cilia growth

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Genetic and epigenetic factors in cancer, cellular senescence and the light and dark sides of exosome communications in cancer

Genetic and epigenetic factors in cancer, cellular senescence and the light and dark sides of exosome communications in cancer | autophagy | Scoop.it
By James P Watson with assistance by Vince Giuliano This blog entry looks at the genetic and epigenetic factors in cancer.  The news here is basically good – epigenetic transformations seem in many cases to be upstream of genetic mutations and...
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Autophagy Suppresses Progression of K-ras-induced Lung Tumors to Oncocytomas and Maintains Lipid Homeostasis

Macroautophagy (autophagy) degrades and recycles proteins and organelles to support metabolism and survival in starvation. Oncogenic Ras up-regulates autophagy, and Ras-transformed cell lines require autophagy for mitochondrial function, stress survival, and engrafted tumor growth. Here, the essential autophagy gene autophagy-related-7 (atg7) was deleted concurrently with K-rasG12D activation in mouse models for non-small-cell lung cancer (NSCLC). atg7 loss altered tumor fate from adenomas and carcinomas to oncocytomas—rare, predominantly benign tumors characterized by the accumulation of defective mitochondria. atg7- and p53-deficient tumor-derived cell lines (TDCLs) had compromised starvation survival and formed lipidic cysts instead of tumors, suggesting defective utilization of lipid stores. atg7 deficiency reduced fatty acid oxidation (FAO) and increased sensitivity to FAO inhibition, indicating that with p53 loss, Ras-driven tumors require autophagy for mitochondrial function and lipid catabolism.

 

 


Via Cancer Commons
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Cancer Commons's curator insight, July 4, 2013 5:26 PM

Guo JY, Karsli-Uzunbas G, Mathew R, Aisner SC, et al. Genes Dev. Jun, 2013.

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Autophagy and neurodegenerative disorders - Science Codex

Autophagy and neurodegenerative disorders - Science Codex | autophagy | Scoop.it
Science Codex
Autophagy and neurodegenerative disorders
Science Codex
Autophagy is a highly conserved process through the evolution of species, from eukaryotic microorganisms to humans.
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Twitter / ElyseIreland: Autophagy. #ChesterBMS ...

Twitter / ElyseIreland: Autophagy. #ChesterBMS ... | autophagy | Scoop.it
RT @ElyseIreland: Autophagy. #ChesterBMS http://t.co/3ff07MS0Ow
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USC Scientists ID Protein That Regulates Cellular Trafficking, See Potential ... - The Beverly Hills Courier

USC Scientists ID Protein That Regulates Cellular Trafficking, See Potential ... - The Beverly Hills Courier | autophagy | Scoop.it
USC Scientists ID Protein That Regulates Cellular Trafficking, See Potential ...
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Molecular Mechanisms Underlying the Autophagy Processing in Cell, March 2013

All Rights Are Reserved. For any use of this video, please contact me at malireza@scripps.edu Thank you Acknowledgment: Dr. Lindsay Whitton, my mentor. Dr. M...
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Key cellular auto-cleaning mechanism mediates formation of plaques in Alzheimer's brain

Key cellular auto-cleaning mechanism mediates formation of plaques in Alzheimer's brain | autophagy | Scoop.it
Autophagy, a key cellular auto-cleaning mechanism, mediates the formation of amyloid beta plaques, one of the hallmarks of Alzheimer's disease. It might be a potential drug target for the treatment of the disease, concludes new research.
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Autophagy-regulation of STAT3 phosphorylation determines subtype differences in autophagy addiction and breast cancer cell survival

Autophagy-regulation of STAT3 phosphorylation determines subtype differences in autophagy addiction and breast cancer cell survival | autophagy | Scoop.it

"Autophagy is a long-lived protein and organelle degradation
pathway in which cytoplasmic material is engulfed in a double membrane
structure known as the autophagosome and later delivered to the lysosome for its degradation."


Via Curated by A4BC.ORG
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Curated by A4BC.ORG's curator insight, April 11, 2013 9:37 AM

According to this study, autophagy blocking regulation of STST3 activation might be a potential therapy for triple negative breast cancers that are hard to treat.

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Autophagy's Role in Alzheimer's - Scientist

Autophagy's Role in Alzheimer's - Scientist | autophagy | Scoop.it
Autophagy's Role in Alzheimer's Scientist RIKEN BRAIN SCIENCE INSTITUTE, PER NILSSONPathological hallmarks of Alzheimer's disease (AD) include the aggregation of amyloid beta (Aβ) peptides inside neurons and the accumulation of extracellular Aβ...
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Role of autophagic and lysosomal pathways in ischemic brain injury - Phys.Org

Role of autophagic and lysosomal pathways in ischemic brain injury - Phys.Org | autophagy | Scoop.it
Role of autophagic and lysosomal pathways in ischemic brain injury Phys.Org After tail vein injection of rapamycin, autolysosome with bilayer structures formed in the cytoplasm of ischemic rat cerebral cortical neurons, and there are deep-dyed...
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