Faculty Opinions recommendation of Mitochondria-anchored receptor Atg32 mediates degradation of mitochondria via selective autophagy.

2009 ◽  
Author(s):  
Eric Baehrecke ◽  
Christina McPhee
Keyword(s):  
Selective Autophagy

scholarly journals BAG3 mediates chaperone‐based aggresome‐targeting and selective autophagy of misfolded proteins

EMBO Reports ◽  
2011 ◽  
Vol 12 (2) ◽  
pp. 149-156 ◽  
Author(s):  
Martin Gamerdinger ◽  
A Murat Kaya ◽  
Uwe Wolfrum ◽  
Albrecht M Clement ◽  
Christian Behl
Keyword(s):  
Misfolded Proteins ◽  
Selective Autophagy

scholarly journals Annexin-A1 SUMOylation regulates microglial polarization after cerebral ischemia by modulating IKKα stability via selective autophagy

2021 ◽  
Vol 7 (4) ◽  
pp. eabc5539
Author(s):  
Xing Li ◽  
Qian Xia ◽  
Meng Mao ◽  
Huijuan Zhou ◽  
Lu Zheng ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Underlying Mechanism ◽  
Nuclear Factor Κb ◽  
Annexin A1 ◽  
Selective Autophagy ◽  
Microglial Polarization ◽  
Proinflammatory Mediators ◽  
Therapeutic Benefits ◽  
Iκb Kinase ◽  
Ikk Complex

Annexin-A1 (ANXA1) has recently been proposed to play a role in microglial activation after brain ischemia, but the underlying mechanism remains poorly understood. Here, we demonstrated that ANXA1 is modified by SUMOylation, and SUMOylated ANXA1 could promote the beneficial phenotype polarization of microglia. Mechanistically, SUMOylated ANXA1 suppressed nuclear factor κB activation and the production of proinflammatory mediators. Further study revealed that SUMOylated ANXA1 targeted the IκB kinase (IKK) complex and selectively enhanced IKKα degradation. Simultaneously, we detected that SUMOylated ANXA1 facilitated the interaction between IKKα and NBR1 to promote IKKα degradation through selective autophagy. Further work revealed that the overexpression of SUMOylated ANXA1 in microglia/macrophages resulted in marked improvement in neurological function in a mouse model of cerebral ischemia. Collectively, our study demonstrates a previously unidentified mechanism whereby SUMOylated ANXA1 regulates microglial polarization and strongly indicates that up-regulation of ANXA1 SUMOylation in microglia may provide therapeutic benefits for cerebral ischemia.

scholarly journals Autophagy Modulators in Cancer Therapy

2021 ◽  
Vol 22 (11) ◽  
pp. 5804
Author(s):  
Kamila Buzun ◽  
Agnieszka Gornowicz ◽  
Roman Lesyk ◽  
Krzysztof Bielawski ◽  
Anna Bielawska
Keyword(s):  
Cancer Research ◽  
Cancer Therapy ◽  
Adverse Effects ◽  
Nutrient Deficiency ◽  
Molecular Regulation ◽  
Regulatory Pathways ◽  
Selective Autophagy ◽  
Atg Proteins ◽  
Different Types ◽  
The Relationship

Autophagy is a process of self-degradation that plays an important role in removing damaged proteins, organelles or cellular fragments from the cell. Under stressful conditions such as hypoxia, nutrient deficiency or chemotherapy, this process can also become the strategy for cell survival. Autophagy can be nonselective or selective in removing specific organelles, ribosomes, and protein aggregates, although the complete mechanisms that regulate aspects of selective autophagy are not fully understood. This review summarizes the most recent research into understanding the different types and mechanisms of autophagy. The relationship between apoptosis and autophagy on the level of molecular regulation of the expression of selected proteins such as p53, Bcl-2/Beclin 1, p62, Atg proteins, and caspases was discussed. Intensive studies have revealed a whole range of novel compounds with an anticancer activity that inhibit or activate regulatory pathways involved in autophagy. We focused on the presentation of compounds strongly affecting the autophagy process, with particular emphasis on those that are undergoing clinical and preclinical cancer research. Moreover, the target points, adverse effects and therapeutic schemes of autophagy inhibitors and activators are presented.

scholarly journals Palmitate reduces starvation-induced ER stress by inhibiting ER-phagy in hypothalamic cells

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Yun Lim ◽  
Seolsong Kim ◽  
Eun-Kyoung Kim
Keyword(s):  
Er Stress ◽  
High Fat Diet ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
High Fat ◽  
Selective Autophagy ◽  
Induced Stress ◽  
Hypothalamic Cells ◽  
The Brain ◽  
Main Region

AbstractPalmitate is a saturated fatty acid that is well known to induce endoplasmic reticulum (ER) stress and autophagy. A high-fat diet increases the palmitate level in the hypothalamus, the main region of the brain regulating energy metabolism. Interestingly, hypothalamic palmitate level is also increased under starvation, urging the study to distinguish the effects of elevated hypothalamic palmitate level under different nutrient conditions. Herein, we show that ER-phagy (ER-targeted selective autophagy) is required for progress of ER stress and that palmitate decreases ER stress by inhibiting ER-phagy in hypothalamic cells under starvation. Palmitate inhibited starvation-induced ER-phagy by increasing the level of B-cell lymphoma 2 (Bcl-2) protein, which inhibits autophagy initiation. These findings suggest that, unlike the induction of ER stress under nutrient-rich conditions, palmitate protects hypothalamic cells from starvation-induced stress by inhibiting ER-phagy.

scholarly journals Selective autophagy receptor Joka2 co-localizes with cytoskeleton in plant cells

2014 ◽  
Vol 9 (5) ◽  
pp. e28523 ◽  
Author(s):  
Katarzyna Zientara-Rytter ◽  
Agnieszka Sirko
Keyword(s):  
Plant Cells ◽  
Selective Autophagy

scholarly journals Reconstitution of cargo-induced LC3 lipidation in mammalian selective autophagy

2021 ◽  
Vol 7 (17) ◽  
pp. eabg4922
Author(s):  
Chunmei Chang ◽  
Xiaoshan Shi ◽  
Liv E. Jensen ◽  
Adam L. Yokom ◽  
Dorotea Fracchiolla ◽  
...  
Keyword(s):  
Complex I ◽  
Kinase Activity ◽  
Protein Aggregates ◽  
Class Iii ◽  
Phosphatidylinositol 3 Kinase ◽  
Giant Unilamellar Vesicles ◽  
Core Complex ◽  
Selective Autophagy ◽  
The Core ◽  
Stimulation Of

Selective autophagy of damaged mitochondria, protein aggregates, and other cargoes is essential for health. Cargo initiates phagophore biogenesis, which entails the conjugation of LC3 to phosphatidylethanolamine. Current models suggest that clustered ubiquitin chains on a cargo trigger a cascade from autophagic cargo receptors through the core complexes ULK1 and class III phosphatidylinositol 3-kinase complex I, WIPI2, and the ATG7, ATG3, and ATG12ATG5-ATG16L1 machinery of LC3 lipidation. This was tested using giant unilamellar vesicles (GUVs), GST-Ub4 as a model cargo, the cargo receptors NDP52, TAX1BP1, and OPTN, and the autophagy core complexes. All three cargo receptors potently stimulated LC3 lipidation on GUVs. NDP52- and TAX1BP1-induced LC3 lipidation required all components, but not ULK1 kinase activity. However, OPTN bypassed the ULK1 requirement. Thus, cargo-dependent stimulation of LC3 lipidation is common to multiple autophagic cargo receptors, yet the details of core complex engagement vary between the different receptors.

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