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Nencki Institute of Experimental Biology
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About: Nencki Institute of Experimental Biology is a based out in . It is known for research contribution in the topics: Mitochondrion & Myosin. The organization has 2137 authors who have published 4094 publications receiving 108958 citations.
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TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Abstract: In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes.
For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure flux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy.
Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation, it is imperative to target by gene knockout or RNA interference more than one autophagy-related protein. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways implying that not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular assays, we hope to encourage technical innovation in the field.
5,187 citations
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TL;DR: It is demonstrated that VDAC1 is physically linked to the endoplasmic reticulum Ca2+-release channel inositol 1,4,5-trisphosphate receptor (IP3R) through the molecular chaperone glucose-regulated protein 75 (grp75) and functional interaction between the channels was shown by the recombinant expression of the ligand-binding domain of the IP3R on the ER or mitochondrial surface.
Abstract: The voltage-dependent anion channel (VDAC) of the outer mitochondrial membrane mediates metabolic flow, Ca2+, and cell death signaling between the endoplasmic reticulum (ER) and mitochondrial networks. We demonstrate that VDAC1 is physically linked to the endoplasmic reticulum Ca2+-release channel inositol 1,4,5-trisphosphate receptor (IP3R) through the molecular chaperone glucose-regulated protein 75 (grp75). Functional interaction between the channels was shown by the recombinant expression of the ligand-binding domain of the IP3R on the ER or mitochondrial surface, which directly enhanced Ca2+ accumulation in mitochondria. Knockdown of grp75 abolished the stimulatory effect, highlighting chaperone-mediated conformational coupling between the IP3R and the mitochondrial Ca2+ uptake machinery. Because organelle Ca2+ homeostasis influences fundamentally cellular functions and death signaling, the central location of grp75 may represent an important control point of cell fate and pathogenesis.
1,106 citations
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Henry Ford Health System1, Harvard University2, Stanford University3, University of Hasselt4, University of Texas MD Anderson Cancer Center5, Nencki Institute of Experimental Biology6, École Polytechnique Fédérale de Lausanne7, Sage Bionetworks8, Université libre de Bruxelles9, Poznan University of Medical Sciences10, George Washington University11, Cold Spring Harbor Laboratory12, University of Kansas13, University of California, Santa Cruz14, University of North Carolina at Chapel Hill15, Van Andel Institute16
TL;DR: Novel stemness indices for assessing the degree of oncogenic dedifferentiation are provided and it is found that the dedifferentiated oncogenic phenotype was generally most prominent in metastatic tumors.
1,099 citations
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TL;DR: Novel drugs modulate the activity of the p38 MAPK and JNK signalling cascades, and exhibit anti-inflammatory effects in preclinical disease models, primarily through the inhibition of the expression of inflammatory mediators.
1,091 citations
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TL;DR: It is demonstrated that branched and linear PEI can both induce membrane damage and initiate apoptosis in three clinically relevant human cell lines and have important implications for the design and execution of gene therapy protocols as well for controlling intracellular distribution of drugs with cationic-based polymer-delivery systems.
1,006 citations
Authors
Showing all 2146 results
Name | H-index | Papers | Citations |
---|---|---|---|
Gary Lynch | 117 | 532 | 46959 |
Jan Lubinski | 103 | 689 | 52120 |
John Patrick Aggleton | 97 | 331 | 32898 |
Richard M. Caprioli | 97 | 490 | 32749 |
Walter J. Chazin | 75 | 320 | 17561 |
Lars Ernster | 72 | 287 | 21608 |
Angelo Azzi | 68 | 319 | 17254 |
Leszek Kaczmarek | 67 | 302 | 15985 |
Yuji Goto | 64 | 290 | 14104 |
Elzbieta Jankowska | 64 | 204 | 14343 |
Mariusz R. Wieckowski | 57 | 151 | 11772 |
Bozena Kaminska | 47 | 184 | 7983 |
Marcin Golczak | 44 | 107 | 6174 |
George L. Gerstein | 44 | 91 | 11074 |
Lech Wojtczak | 43 | 132 | 5990 |