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71.
In this paper we consider networks of evolutionary processors with splicing rules and permitting context (NEPPS) as language generating and computational devices. Such a network consists of several processors placed on the nodes of a virtual graph and are able to perform splicing (which is a biologically motivated operation) on the words present in that node, according to the splicing rules present there. Before applying the splicing operation on words, we check for the presence of certain symbols (permitting context) in the strings on which the rule is applied. Each node is associated with an input and output filter. When the filters are based on random context conditions, one gets the computational power of Turing machines with networks of size two. We also show how these networks can be used to solve NP-complete problems in linear time. 相似文献
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Amod Ayush Pahal Sonu Choudhary Princy Gupta Ayushi Singh Sangeeta 《Biotechnology letters》2022,44(7):879-900
Biotechnology Letters - Hepatocellular carcinoma (HCC) is the uncontrolled growth of hepatocytes which results in nearly 5 million deaths worldwide. Specific strategies have been developed to treat... 相似文献
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Muthu Valliappan Dhaliwal Manpreet Sharma Arunima Nair Divya Kumar H. Mohan Rudramurthy Shivaprakash M. Sehgal Inderpaul Singh Choudhary Hansraj Panda Naresh Chakrabarti Arunaloke Agarwal Ritesh 《Mycopathologia》2022,187(4):355-362
Mycopathologia - In experimental models, the expression of glucose-regulated protein 78 (GRP78) in endothelial cells played a role in the pathogenesis of mucormycosis. However, the role of GRP78 in... 相似文献
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Analysis of acetylation stoichiometry suggests that SIRT3 repairs nonenzymatic acetylation lesions
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Brian T Weinert Tarek Moustafa Vytautas Iesmantavicius Rudolf Zechner Chunaram Choudhary 《The EMBO journal》2015,34(21):2620-2632
Acetylation is frequently detected on mitochondrial enzymes, and the sirtuin deacetylase SIRT3 is thought to regulate metabolism by deacetylating mitochondrial proteins. However, the stoichiometry of acetylation has not been studied and is important for understanding whether SIRT3 regulates or suppresses acetylation. Using quantitative mass spectrometry, we measured acetylation stoichiometry in mouse liver tissue and found that SIRT3 suppressed acetylation to a very low stoichiometry at its target sites. By examining acetylation changes in the liver, heart, brain, and brown adipose tissue of fasted mice, we found that SIRT3‐targeted sites were mostly unaffected by fasting, a dietary manipulation that is thought to regulate metabolism through SIRT3‐dependent deacetylation. Globally increased mitochondrial acetylation in fasted liver tissue, higher stoichiometry at mitochondrial acetylation sites, and greater sensitivity of SIRT3‐targeted sites to chemical acetylation in vitro and fasting‐induced acetylation in vivo, suggest a nonenzymatic mechanism of acetylation. Our data indicate that most mitochondrial acetylation occurs as a low‐level nonenzymatic protein lesion and that SIRT3 functions as a protein repair factor that removes acetylation lesions from lysine residues. 相似文献
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Initial analysis of copy number variations in cattle selected for resistance or susceptibility to intestinal nematodes 总被引:1,自引:0,他引:1
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