Bcl-xL inhibits tBid and Bax via distinct mechanisms

2020 ◽  
Author(s):  
Ana Garcia ◽  
Fabronia Murad

The proteins of the Bcl-2 family are key regulators of apoptosis. They form a complex interaction network in the cytosol and in the cellular membranes, whose outcome determines mitochondrial permeabilization...


2021 ◽  
Author(s):  
Hong Su

<div>In cross-chain scenarios, there are different blockchains, which need to cooperate. Cooperation among different blockchains is done by smart contracts that work together to complete cross-chain tasks. When numerous cooperative smart contracts are involved, smart contracts form a complex interaction network, which makes it difficult to evaluate the cooperation. It needs a common model to quantitatively analyze the cross-chain cooperation of associated smart contracts. In this paper, we model the cooperation among smart contracts as conditions and their corresponding actions, the condition-trigger model. Then we propose the method to calculate the cooperation probabilities by the graph weight. As the edge weight lacks the information of interaction probabilities, we introduce the dimension of the edge weight to calculate the probabilities. Finally, we verify the proposed condition-trigger model and its different types. It demonstrates that our proposed methods can effectively analyze the cross-chain cooperation among smart contracts.</div>



2021 ◽  
Author(s):  
Hong Su

<div>In cross-chain scenarios, there are different blockchains, which need to cooperate. Cooperation among different blockchains is done by smart contracts that work together to complete cross-chain tasks. When numerous cooperative smart contracts are involved, smart contracts form a complex interaction network, which makes it difficult to evaluate the cooperation. It needs a common model to quantitatively analyze the cross-chain cooperation of associated smart contracts. In this paper, we model the cooperation among smart contracts as conditions and their corresponding actions, the condition-trigger model. Then we propose the method to calculate the cooperation probabilities by the graph weight. As the edge weight lacks the information of interaction probabilities, we introduce the dimension of the edge weight to calculate the probabilities. Finally, we verify the proposed condition-trigger model and its different types. It demonstrates that our proposed methods can effectively analyze the cross-chain cooperation among smart contracts.</div>



2020 ◽  
Vol 315 ◽  
pp. e10
Author(s):  
K. Frey ◽  
S. Goetze ◽  
M. Mueller ◽  
L. Rohrer ◽  
A. Von Eckardstein ◽  
...  


2012 ◽  
Vol 15 (2) ◽  
pp. 429-445 ◽  
Author(s):  
Yotam Orchan ◽  
François Chiron ◽  
Assaf Shwartz ◽  
Salit Kark


Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3266
Author(s):  
Aleš Holoubek ◽  
Dita Strachotová ◽  
Petra Otevřelová ◽  
Pavla Röselová ◽  
Petr Heřman ◽  
...  

Nucleophosmin (NPM) interaction with tumor suppressor p53 is a part of a complex interaction network and considerably affects cellular stress response. The impact of NPM1 mutations on its interaction with p53 has not been investigated yet, although consequences of NPMmut-induced p53 export to the cytoplasm are important for understanding the oncogenic potential of these mutations. We investigated p53-NPM interaction in live HEK-293T cells by FLIM-FRET and in cell lysates by immunoprecipitation. eGFP lifetime-photoconversion was used to follow redistribution dynamics of NPMmut and p53 in Selinexor-treated cells. We confirmed the p53-NPMwt interaction in intact cells and newly documented that this interaction is not compromised by the NPM mutation causing displacement of p53 to the cytoplasm. Moreover, the interaction was not abolished for non-oligomerizing NPM variants with truncated oligomerization domain, suggesting that oligomerization is not essential for interaction of NPM forms with p53. Inhibition of the nuclear exporter XPO1 by Selinexor caused expected nuclear relocalization of both NPMmut and p53. However, significantly different return rates of these proteins indicate nontrivial mechanism of p53 and NPMmut cellular trafficking. The altered p53 regulation in cells expressing NPMmut offers improved understanding to help investigational strategies targeting these mutations.



Author(s):  
R.J. Barrnett

This subject, is like observing the panorama of a mountain range, magnificent towering peaks, but it doesn't take much duration of observation to recognize that they are still in the process of formation. The mountains consist of approaches, materials and methods and the rocky substance of information has accumulated to such a degree that I find myself concentrating on the foothills in the foreground in order to keep up with the advance; the edifices behind form a wonderous, substantive background. It's a short history for such an accumulation and much of it has been moved by the members of the societies that make up this International Federation. My panel of speakers are here to provide what we hope is an interesting scientific fare, based on the fact that there is a continuum of biological organization from biochemical molecules through macromolecular assemblies and cellular membranes to the cell itself. Indeed, this fact explains the whole range of towering peaks that have emerged progressively during the past 25 years.



2020 ◽  
Author(s):  
Jessica Mow ◽  
Arti Gandhi ◽  
Daniel Fulford

Decreased social functioning and high levels of loneliness and social isolation are common in schizophrenia spectrum disorders (SSD), contributing to reduced quality of life. One key contributor to social impairment is low social motivation, which may stem from aberrant neural processing of socially rewarding or punishing stimuli. To summarize research on the neurobiology of social motivation in SSD, we performed a systematic literature review of neuroimaging studies involving the presentation of social stimuli intended to elicit feelings of reward and/or punishment. Across 11 studies meeting criteria, people with SSD demonstrated weaker modulation of brain activity in regions within a proposed social interaction network, including prefrontal, cingulate, and striatal regions, as well as the amygdala and insula. Firm conclusions regarding neural differences in SSD in these regions, as well as connections within networks, are limited due to conceptual and methodological inconsistencies across the available studies. We conclude by making recommendations for the study of social reward and punishment processing in SSD in future research.



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