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Article ; Online: Direct quantification of autophagic flux by a single molecule-based probe.

Geng, Jiefei / Klionsky, Daniel J

2017 Volume 13, Issue 4, Page(s) 639–641

Abstract: Macroautophagy/autophagy remains a rapidly advancing research topic, and there continues to be a need for constantly evolving methodology to investigate this pathway at each individual step. Accordingly, new assays to measure autophagic flux in a robust ... ...

Abstract	Macroautophagy/autophagy remains a rapidly advancing research topic, and there continues to be a need for constantly evolving methodology to investigate this pathway at each individual step. Accordingly, new assays to measure autophagic flux in a robust and reliable manner are essential to understand the mechanism and physiological roles of autophagy. Kaizuka et al. recently reported a new fluorescence probe, GFP-LC3-RFP-LC3ΔG to directly demonstrate autophagic flux without being combined with lysosomal inhibitors (see the Kaizuka et al. punctum in this issue of the journal). When expressed in cells, the probe is cleaved into a degradable/quenchable part, GFP-LC3, and stable/cytosolic part, RFP-LC3ΔG. The latter serves as an internal control and a decrease of the GFP:RFP ratio indicates the occurrence of autophagy. Since the key index of this probe is the degradation of GFP-LC3, it can be used to measure the cumulative effect of basal autophagy. The assay is applicable to high-throughput drug discovery as well as in vivo analysis.
Language	English
Publishing date	2017-04-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2017.1280646
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Article ; Online: An immune-based tool platform for in vivo cell clearance.

Zhang, Jieqiong / Tsukui, Tatsuya / Wu, Xiumin / Brito, Alyssa / Trumble, John Maxwell / Caraballo, Juan C / Allen, Greg M / Zavala-Solorio, José / Zhang, Chunlian / Paw, Jonathan / Lim, Wendell A / Geng, Jiefei / Kutskova, Yuliya / Freund, Adam / Kolumam, Ganesh / Sheppard, Dean / Cohen, Robert L

Life science alliance

2023 Volume 6, Issue 8

Abstract: Immunological targeting of pathological cells has been successful in oncology and is expanding to other pathobiological contexts. Here, we present a flexible platform that allows labeling cells of interest with the surface-expressed model antigen ... ...

Abstract	Immunological targeting of pathological cells has been successful in oncology and is expanding to other pathobiological contexts. Here, we present a flexible platform that allows labeling cells of interest with the surface-expressed model antigen ovalbumin (OVA), which can be eliminated via either antigen-specific T cells or newly developed OVA antibodies. We demonstrate that hepatocytes can be effectively targeted by either modality. In contrast, pro-fibrotic fibroblasts associated with pulmonary fibrosis are only eliminated by T cells in initial experiments, which reduced collagen deposition in a fibrosis model. This new experimental platform will facilitate development of immune-based approaches to clear potential pathological cell types in vivo.
MeSH term(s)	Humans ; Antibodies ; Fibroblasts ; Hepatocytes ; Kinetics ; Pulmonary Fibrosis
Chemical Substances	Antibodies
Language	English
Publishing date	2023-06-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202201869
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Article ; Online: The Golgi as a potential membrane source for autophagy.

Geng, Jiefei / Klionsky, Daniel J

Autophagy

2010 Volume 6, Issue 7, Page(s) 950–951

Abstract: In macroautophagy (hereafter autophagy), a morphological hallmark is the formation of double-membrane vesicles called autophagosomes that sequester and deliver cytoplasmic components to the lysosome/vacuole for degradation. This process begins with an ... ...

Abstract	In macroautophagy (hereafter autophagy), a morphological hallmark is the formation of double-membrane vesicles called autophagosomes that sequester and deliver cytoplasmic components to the lysosome/vacuole for degradation. This process begins with an initial sequestering compartment, the phagophore, which expands into the mature autophagosome. A tremendous amount of work has been carried out to elucidate the mechanism of how the autophagosome is formed. However, an important missing piece in this puzzle is where the membrane comes from. Independent lines of evidence have shown that preexisting organelles may continuously supply lipids to support autophagosome formation. In our analysis, we identified several components of the late stage secretory pathway that may redirect Golgi-derived membrane to autophagosome formation in response to starvation conditions.
MeSH term(s)	Autophagy/physiology ; Cell Membrane/metabolism ; Cell Membrane/ultrastructure ; Golgi Apparatus/metabolism ; Golgi Apparatus/ultrastructure ; Intracellular Membranes/metabolism ; Intracellular Membranes/ultrastructure ; Protein Transport ; Saccharomyces cerevisiae/cytology ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/metabolism ; Secretory Pathway/physiology
Chemical Substances	Saccharomyces cerevisiae Proteins
Language	English
Publishing date	2010-10-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.4161/auto.6.7.13009
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Article ; Online: Determining Atg protein stoichiometry at the phagophore assembly site by fluorescence microscopy.

Geng, Jiefei / Klionsky, Daniel J

Autophagy

2009 Volume 6, Issue 1, Page(s) 144–147

Abstract: In eukaryotic cells, autophagy is a lysosomal/ vacuolar degradative pathway necessary for the turnover of different macromolecules. Autophagy is under precise regulation, not only qualitatively but also quantitatively, and excess or reduced levels of ... ...

Abstract	In eukaryotic cells, autophagy is a lysosomal/ vacuolar degradative pathway necessary for the turnover of different macromolecules. Autophagy is under precise regulation, not only qualitatively but also quantitatively, and excess or reduced levels of autophagy may lead to various human diseases. In yeast, genetic screens led to the identification of more than 30 autophagy-related (ATG) genes, and most of the gene products reside at the phagophore assembly site (PAS). However, our attempt to understand the quantitative properties of autophagy is usually hampered, because traditional methods of analysis cannot provide stoichiometric information. We have recently used a fluorescence microscopy-based method to study the stoichiometry of Atg proteins at the PAS, trying to explain the mechanism of how the vesicle formation process is precisely regulated. This article describes a practical guide on this method. Its application and further analysis will improve our understanding of the quantitative properties of autophagy.
MeSH term(s)	Adaptor Proteins, Signal Transducing/analysis ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Autophagy/physiology ; Cells, Cultured ; Clinical Laboratory Techniques ; Humans ; Microscopy, Fluorescence/methods ; Phagosomes/chemistry ; Phagosomes/metabolism ; Protein Binding ; Protein Multimerization ; Small Ubiquitin-Related Modifier Proteins/analysis ; Small Ubiquitin-Related Modifier Proteins/metabolism ; Vesicular Transport Proteins/analysis ; Vesicular Transport Proteins/metabolism ; Yeasts
Chemical Substances	Adaptor Proteins, Signal Transducing ; Small Ubiquitin-Related Modifier Proteins ; Vesicular Transport Proteins
Language	English
Publishing date	2009-11-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.4161/auto.6.1.10249
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Article ; Online: The Atg8 and Atg12 ubiquitin-like conjugation systems in macroautophagy. 'Protein modifications: beyond the usual suspects' review series.

Geng, Jiefei / Klionsky, Daniel J

EMBO reports

2008 Volume 9, Issue 9, Page(s) 859–864

Abstract: As a lysosomal/vacuolar degradative pathway that is conserved in eukaryotic organisms, autophagy mediates the turnover of long-lived proteins and excess or aberrant organelles. The main characteristic of autophagy is the formation of a double-membrane ... ...

Abstract	As a lysosomal/vacuolar degradative pathway that is conserved in eukaryotic organisms, autophagy mediates the turnover of long-lived proteins and excess or aberrant organelles. The main characteristic of autophagy is the formation of a double-membrane vesicle, the autophagosome, which envelops part of the cytoplasm and delivers it to the lysosome/vacuole for breakdown and eventual recycling of the degradation products. Among the approximately 30 autophagy-related (Atg) genes identified so far, there are two ubiquitin-like proteins, Atg12 and Atg8. Analogous to ubiquitination, Atg12 is conjugated to Atg5 by Atg7--an E1-like protein--and Atg10--an E2-like protein. Similarly, Atg7 and Atg3 are the respective E1-like and E2-like proteins that mediate the conjugation of Atg8 to phosphatidylethanolamine. Both Atg12-Atg5 and Atg8 localize to the developing autophagosome. The Atg12-Atg5 conjugate facilitates the lipidation of Atg8 and directs its correct subcellular localization. Atg8-phosphatidylethanolamine is probably a scaffold protein that supports membrane expansion and the amount present correlates with the size of autophagosomes.
MeSH term(s)	Animals ; Autophagy/physiology ; Humans ; Models, Biological ; Models, Molecular ; Protein Isoforms/chemistry ; Protein Isoforms/metabolism ; Protein Isoforms/physiology ; Protein Processing, Post-Translational ; Protein Structure, Secondary ; Ubiquitin/chemistry ; Ubiquitin/metabolism ; Ubiquitin/physiology
Chemical Substances	Protein Isoforms ; Ubiquitin
Language	English
Publishing date	2008-08-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.1038/embor.2008.163
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Zs.A 5433: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Quantitative regulation of vesicle formation in yeast nonspecific autophagy.

Geng, Jiefei / Klionsky, Daniel J

Autophagy

2008 Volume 4, Issue 7, Page(s) 955–957

Abstract: In eukaryotic cells, autophagy is a degradative pathway necessary for the turnover of bulk cytoplasm. In yeast, this pathway also mediates the specific transport of a vacuolar hydrolase zymogen, precursor aminopeptidase (prApe1), from the cytoplasm to ... ...

Abstract	In eukaryotic cells, autophagy is a degradative pathway necessary for the turnover of bulk cytoplasm. In yeast, this pathway also mediates the specific transport of a vacuolar hydrolase zymogen, precursor aminopeptidase (prApe1), from the cytoplasm to the vacuole. Autophagy is under precise regulation, not only qualitatively but also quantitatively, especially in the steps involved in the vesicle formation process. We have recently used a fluorescence microscopy-based method to study the stoichiometry of autophagy-related (Atg) proteins during different conditions. This analysis shows that increased expression of Atg11 in the cytoplasm to vacuole targeting (Cvt) pathway increases the amount of this protein localized at the phagophore assembly site (PAS). In turn, under nutrient-rich conditions, the increased level of Atg11 causes the recruitment of higher than normal levels of Atg8 and Atg9 to the PAS, resulting in the formation of more Cvt vesicles, whereas the vesicle size is not affected. Combined with results from previous studies in starvation conditions, in this addendum we discuss the possible role of Atg8 and Atg9 in quantitatively regulating the vesicle formation process.
MeSH term(s)	Autophagy ; Autophagy-Related Protein 8 Family ; Autophagy-Related Proteins ; Cytoplasm/metabolism ; Cytoplasm/physiology ; Membrane Proteins/metabolism ; Microtubule-Associated Proteins/metabolism ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae/physiology ; Saccharomyces cerevisiae Proteins/metabolism ; Vacuoles/metabolism ; Vacuoles/physiology ; Vesicular Transport Proteins/metabolism
Chemical Substances	ATG8 protein, S cerevisiae ; ATG9 protein, S cerevisiae ; Atg11 protein, S cerevisiae ; Autophagy-Related Protein 8 Family ; Autophagy-Related Proteins ; Membrane Proteins ; Microtubule-Associated Proteins ; Saccharomyces cerevisiae Proteins ; Vesicular Transport Proteins
Language	English
Publishing date	2008-10-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.4161/auto.6791
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Article ; Online: Synergistic effect of a novel autophagy inhibitor and Quizartinib enhances cancer cell death.

Ouchida, Amanda Tomie / Li, Yingbo / Geng, Jiefei / Najafov, Ayaz / Ofengeim, Dimitry / Sun, Xiaoxiao / Yu, Qiang / Yuan, Junying

Cell death & disease

2018 Volume 9, Issue 2, Page(s) 138

Abstract: Drug combinations have been increasingly applied in chemotherapy as a strategy to enhance the efficacy of anti-cancer treatment. The appropriate drug combinations may achieve synergistic effects beyond monotherapies alone. AC220 (Quizartinib), an FLT3 ... ...

Abstract	Drug combinations have been increasingly applied in chemotherapy as a strategy to enhance the efficacy of anti-cancer treatment. The appropriate drug combinations may achieve synergistic effects beyond monotherapies alone. AC220 (Quizartinib), an FLT3 receptor tyrosine kinase inhibitor, developed for the treatment of AML, has been tested in phase II human clinical trials. However, AC220 as a monotherapy is not efficacious enough. In this study, we performed a small-molecule screening of 12 640 compounds in order to find a compound that increase the AC220 efficacy in chemotherapy. We identified that TAK-165, a HER2 inhibitor, even when used at low nanomolar doses in combination with AC220, was able to induce cell death in different cancer cells, but not in non-cancer cell lines. We showed that TAK-165 and AC220 act synergistically to downregulate key signaling pathways and potently induce cancer cell death. Furthermore, we demonstrated that TAK-165 inhibited autophagy in a HER2-independent manner. Finally, we showed that the combination of TAK-165 and AC220 induced cell death in cancer cells through the activation of chaperone-mediated autophagy. Overall, these findings support the strategy for using AC220 and an autophagy inhibitor such as TAK-165 in a combinatorial treatment to enhance the efficacy of cancer therapies.
MeSH term(s)	Apoptosis/drug effects ; Autophagy/drug effects ; Benzothiazoles/pharmacology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Drug Synergism ; Humans ; Neoplasms/pathology ; Oxazoles/chemistry ; Oxazoles/pharmacology ; Phenylurea Compounds/pharmacology ; Receptor, ErbB-2/metabolism ; Signal Transduction/drug effects ; Triazoles/chemistry ; Triazoles/pharmacology
Chemical Substances	Benzothiazoles ; Oxazoles ; Phenylurea Compounds ; TAK-165 ; Triazoles ; quizartinib (7LA4O6Q0D3) ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2018-01-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-017-0170-9
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Article ; Online: Post-Golgi Sec proteins are required for autophagy in Saccharomyces cerevisiae.

Geng, Jiefei / Nair, Usha / Yasumura-Yorimitsu, Kyoko / Klionsky, Daniel J

Molecular biology of the cell

2010 Volume 21, Issue 13, Page(s) 2257–2269

Abstract: In eukaryotic cells, autophagy mediates the degradation of cytosolic contents in response to environmental change. Genetic analyses in fungi have identified over 30 autophagy-related (ATG) genes and provide substantial insight into the molecular ... ...

Abstract	In eukaryotic cells, autophagy mediates the degradation of cytosolic contents in response to environmental change. Genetic analyses in fungi have identified over 30 autophagy-related (ATG) genes and provide substantial insight into the molecular mechanism of this process. However, one essential issue that has not been resolved is the origin of the lipids that form the autophagosome, the sequestering vesicle that is critical for autophagy. Here, we report that two post-Golgi proteins, Sec2 and Sec4, are required for autophagy. Sec4 is a Rab family GTPase, and Sec2 is its guanine nucleotide exchange factor. In sec2 and sec4 conditional mutant yeast, the anterograde movement of Atg9, a proposed membrane carrier, is impaired during starvation conditions. Similarly, in the sec2 mutant, Atg8 is inefficiently recruited to the phagophore assembly site, which is involved in autophagosome biogenesis, resulting in the generation of fewer autophagosomes. We propose that following autophagy induction the function of Sec2 and Sec4 are diverted to direct membrane flow to autophagosome formation.
MeSH term(s)	Autophagy/physiology ; Autophagy-Related Protein 8 Family ; Autophagy-Related Proteins ; Golgi Apparatus/metabolism ; Guanine Nucleotide Exchange Factors/genetics ; Guanine Nucleotide Exchange Factors/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Mutation ; Phagosomes/metabolism ; Phenotype ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/cytology ; Saccharomyces cerevisiae/physiology ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Signal Transduction/physiology ; rab GTP-Binding Proteins/genetics ; rab GTP-Binding Proteins/metabolism
Chemical Substances	ATG8 protein, S cerevisiae ; ATG9 protein, S cerevisiae ; Autophagy-Related Protein 8 Family ; Autophagy-Related Proteins ; Guanine Nucleotide Exchange Factors ; Membrane Proteins ; Microtubule-Associated Proteins ; Recombinant Fusion Proteins ; SEC2 protein, S cerevisiae ; Saccharomyces cerevisiae Proteins ; SEC4 protein, S cerevisiae (EC 3.6.1.-.) ; rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2010-05-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1098979-1
ISSN	1939-4586 ; 1059-1524
ISSN (online)	1939-4586
ISSN	1059-1524
DOI	10.1091/mbc.E09-11-0969
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Article ; Online: Regulation of a distinct activated RIPK1 intermediate bridging complex I and complex II in TNFα-mediated apoptosis.

Amin, Palak / Florez, Marcus / Najafov, Ayaz / Pan, Heling / Geng, Jiefei / Ofengeim, Dimitry / Dziedzic, Slawomir A / Wang, Huibing / Barrett, Vica Jean / Ito, Yasushi / LaVoie, Matthew J / Yuan, Junying

Proceedings of the National Academy of Sciences of the United States of America

2018 Volume 115, Issue 26, Page(s) E5944–E5953

Abstract: Stimulation of cells with TNFα can promote distinct cell death pathways, including RIPK1-independent apoptosis, necroptosis, and RIPK1-dependent apoptosis (RDA)-the latter of which we still know little about. Here we show that RDA involves the rapid ... ...

Abstract	Stimulation of cells with TNFα can promote distinct cell death pathways, including RIPK1-independent apoptosis, necroptosis, and RIPK1-dependent apoptosis (RDA)-the latter of which we still know little about. Here we show that RDA involves the rapid formation of a distinct detergent-insoluble, highly ubiquitinated, and activated RIPK1 pool, termed "iuRIPK1." iuRIPK1 forms after RIPK1 activation in TNF-receptor-associated complex I, and before cytosolic complex II formation and caspase activation. To identify regulators of iuRIPK1 formation and RIPK1 activation in RDA, we conducted a targeted siRNA screen of 1,288 genes. We found that NEK1, whose loss-of-function mutations have been identified in 3% of ALS patients, binds to activated RIPK1 and restricts RDA by negatively regulating formation of iuRIPK1, while LRRK2, a kinase implicated in Parkinson's disease, promotes RIPK1 activation and association with complex I in RDA. Further, the E3 ligases APC11 and c-Cbl promote RDA, and c-Cbl is recruited to complex I in RDA, where it promotes prodeath K63-ubiquitination of RIPK1 to lead to iuRIPK1 formation. Finally, we show that two different modes of necroptosis induction by TNFα exist which are differentially regulated by iuRIPK1 formation. Overall, this work reveals a distinct mechanism of RIPK1 activation that mediates the signaling mechanism of RDA as well as a type of necroptosis.
MeSH term(s)	Animals ; Apoptosis ; Cell Line ; Enzyme Activation ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/metabolism ; Mice ; Mice, Knockout ; Proto-Oncogene Proteins c-cbl/genetics ; Proto-Oncogene Proteins c-cbl/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism ; Ubiquitination
Chemical Substances	Tumor Necrosis Factor-alpha ; Proto-Oncogene Proteins c-cbl (EC 2.3.2.27) ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1) ; Lrrk2 protein, mouse (EC 2.7.11.1) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk1 protein, mouse (EC 2.7.11.1) ; Cbl protein, mouse (EC 6.3.2.-)
Language	English
Publishing date	2018-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1806973115
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Article ; Online: Modulating TRADD to restore cellular homeostasis and inhibit apoptosis.

Nature

2020 Volume 587, Issue 7832, Page(s) 133–138

Abstract: Cell death in human diseases is often a consequence of disrupted cellular homeostasis. If cell death is prevented without restoring cellular homeostasis, it may lead to a persistent dysfunctional and pathological state. Although mechanisms of cell death ... ...

Abstract	Cell death in human diseases is often a consequence of disrupted cellular homeostasis. If cell death is prevented without restoring cellular homeostasis, it may lead to a persistent dysfunctional and pathological state. Although mechanisms of cell death have been thoroughly investigated
MeSH term(s)	Animals ; Apoptosis/drug effects ; Autophagy/drug effects ; Baculoviral IAP Repeat-Containing 3 Protein/metabolism ; Beclin-1/chemistry ; Beclin-1/metabolism ; Bortezomib/antagonists & inhibitors ; Bortezomib/pharmacology ; Cell Line ; Homeostasis/drug effects ; Humans ; Huntingtin Protein/metabolism ; Inhibitor of Apoptosis Proteins/metabolism ; Male ; Mice ; Models, Molecular ; Neurofibrillary Tangles/metabolism ; Proteome/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/chemistry ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; TNF Receptor-Associated Death Domain Protein/antagonists & inhibitors ; TNF Receptor-Associated Death Domain Protein/chemistry ; TNF Receptor-Associated Death Domain Protein/deficiency ; TNF Receptor-Associated Death Domain Protein/metabolism ; TNF Receptor-Associated Factor 2/metabolism ; Ubiquitination ; alpha-Synuclein/metabolism ; tau Proteins/metabolism
Chemical Substances	Beclin-1 ; Huntingtin Protein ; Inhibitor of Apoptosis Proteins ; Proteome ; TNF Receptor-Associated Death Domain Protein ; TNF Receptor-Associated Factor 2 ; alpha-Synuclein ; tau Proteins ; Bortezomib (69G8BD63PP) ; Baculoviral IAP Repeat-Containing 3 Protein (EC 2.3.2.27) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2020-09-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-020-2757-z
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