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【聚焦】走进细胞自噬 [精华]

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achates

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继续关注。自嗜还是肿瘤等关注的比较多。

2011-01-24 23:21

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• 丁香晚间病例-各科室医患沟通中的神比喻！90% 的医生都会遇到

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tangdl2000

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EMBO Rep. 2011 Jan 21. [Epub ahead of print]

BAG3 mediates chaperone-based aggresome-targeting and selective autophagy of misfolded proteins.
Bag3调节选择性自噬

Gamerdinger M, Kaya AM, Wolfrum U, Clement AM, Behl C.

Institute of Pathobiochemistry, University Medical Center, Johannes Gutenberg University, Duesbergweg 6, Mainz 55099, Germany.

Abstract
Increasing evidence indicates the existence of selective autophagy pathways, but the manner in which substrates are recognized and targeted to the autophagy system is poorly understood. One strategy is transport of a particular substrate to the aggresome, a perinuclear compartment with high autophagic activity. In this paper, we identify a new cellular pathway that uses the specificity of heat-shock protein 70 (Hsp70) to misfolded proteins as the basis for aggresome-targeting and autophagic degradation. This pathway is regulated by the stress-induced co-chaperone Bcl-2-associated athanogene 3 (BAG3), which interacts with the microtubule-motor dynein and selectively directs Hsp70 substrates to the motor and thereby to the aggresome. Notably, aggresome-targeting by BAG3 is distinct from previously described mechanisms, as it does not depend on substrate ubiquitination.

PMID: 21252941

embor2010203a.pdf(1468.04k)

2011-01-25 00:42

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• 忙着集各种福？这儿有医疗专属福，还有490元医院管理课程免费送

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tangdl2000

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Cell Death Differ. 2011 Jan 21. [Epub ahead of print]

Endoplasmic reticulum stress activates autophagy but not the proteasome in neuronal cells: implications for Alzheimer's disease.
ER应激活化神经元细胞中的自噬，而不是蛋白酶降解

Nijholt DA, de Graaf TR, van Haastert ES, Oliveira AO, Berkers CR, Zwart R, Ovaa H, Baas F, Hoozemans JJ, Scheper W.

Department of Genome Analysis, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

Abstract
Protein folding stress in the endoplasmic reticulum (ER) may lead to activation of the unfolded protein response (UPR), aimed to restore cellular homeostasis via transcriptional and post-transcriptional mechanisms. ER stress is also reported to activate the ER overload response (EOR), which activates transcription via NF-κB. We previously demonstrated that UPR activation is an early event in pre-tangle neurons in Alzheimer's disease (AD) brain. Misfolded and unfolded proteins are degraded via the ubiquitin proteasome system (UPS) or autophagy. UPR activation is found in AD neurons displaying both early UPS pathology and autophagic pathology. Here we investigate whether activation of the UPR and/or EOR is employed to enhance the proteolytic capacity of neuronal cells. Expression of the immunoproteasome subunits β2i and β5i is increased in AD brain. However, expression of the proteasome subunits is not increased by the UPR or EOR. UPR activation does not relocalize the proteasome or increase overall proteasome activity. Therefore proteasomal degradation is not increased by ER stress. In contrast, UPR activation enhances autophagy and LC3 levels are increased in neurons displaying UPR activation in AD brain. Our data suggest that autophagy is the major degradational pathway following UPR activation in neuronal cells and indicate a connection between UPR activation and autophagic pathology in AD brain.Cell Death and Differentiation advance online publication, 21 January 2011; doi:10.1038/cdd.2010.176.

PMID: 21252911

cdd2010176a.pdf(901.1k)

2011-01-25 00:49

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tangdl2000 编辑于 2011-01-25 00:54

• 忙着集各种福？这儿有医疗专属福，还有490元医院管理课程免费送

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tangdl2000

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Autophagy. 2011 Mar 1;7(3). [Epub ahead of print]

Mitochondria removal by autophagy.
通过自噬清除线粒体

Wang K, Klionsky DJ.

Life Sciences Institute; University of Michigan; Ann Arbor, MI USA.

Abstract
Mitochondrial dysfunction has severe cellular consequences and is linked with neurodegenerative diseases and aging. Maintaining a healthy population of mitochondria is thus essential for proper cellular homeostasis. Several strategies have evolved to prevent and limit mitochondria damage, and macroautophagy plays a role in degrading superfluous or severely damaged mitochondria. Selective removal of mitochondria by autophagy (termed mitophagy) has been extensively studied recently in both yeast and mammalian cells. In this review, we summarize our current knowledge of mitophagy. We also compare the molecular process of mitophagy with other types of specific autophagic pathways and discuss its biological importance.

PMID: 21252623

WangAUTO7-3.pdf(493.5k)

2011-01-25 00:55

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• 慢性肾脏病患者中糖尿病的管理 | KDIGO 指南 2020

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