<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Roy, Rituparna Sinha</style></author><author><style face="normal" font="default" size="100%">Soni, Shivani</style></author><author><style face="normal" font="default" size="100%">Harfouche, Rania</style></author><author><style face="normal" font="default" size="100%">Vasudevan, Pooja R.</style></author><author><style face="normal" font="default" size="100%">Holmes, Oliver</style></author><author><style face="normal" font="default" size="100%">de Jonge, Hugo</style></author><author><style face="normal" font="default" size="100%">Rowe, Arthur</style></author><author><style face="normal" font="default" size="100%">Paraskar, Abhimanyu</style></author><author><style face="normal" font="default" size="100%">Hentschel, Dirk M.</style></author><author><style face="normal" font="default" size="100%">Chirgadze, Dimitri</style></author><author><style face="normal" font="default" size="100%">Blundell, Tom L.</style></author><author><style face="normal" font="default" size="100%">Gherardi, Ermanno</style></author><author><style face="normal" font="default" size="100%">Mashelkar, Raghunath Anant</style></author><author><style face="normal" font="default" size="100%">Sengupta, Shiladitya</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Coupling growth-factor engineering with nanotechnology for therapeutic angiogenesis</style></title><secondary-title><style face="normal" font="default" size="100%">Proceedings of the National Academy of Sciences of the United States of America</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">cardiovascular disease</style></keyword><keyword><style  face="normal" font="default" size="100%">HGF/SF</style></keyword><keyword><style  face="normal" font="default" size="100%">ischemic disease</style></keyword><keyword><style  face="normal" font="default" size="100%">nanoparticle</style></keyword><keyword><style  face="normal" font="default" size="100%">protein engineering</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">AUG</style></date></pub-dates></dates><number><style face="normal" font="default" size="100%">31</style></number><publisher><style face="normal" font="default" size="100%">NATL ACAD SCIENCES</style></publisher><pub-location><style face="normal" font="default" size="100%">2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA</style></pub-location><volume><style face="normal" font="default" size="100%">107</style></volume><pages><style face="normal" font="default" size="100%">13608-13613</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Therapeutic angiogenesis is an emerging paradigm for the management of ischemic pathologies. Proangiogenic Therapy is limited, however, by the current inability to deliver angiogenic factors in a sustained manner at the site of pathology. In this study, we investigated a unique nonglycosylated active fragment of hepatocyte growth factor/scatter factor, 1K1, which acts as a potent angiogenic agent in vitro and in a zebrafish embryo and a murine matrigel implant model. Furthermore, we demonstrate that nanoformulating 1K1 for sustained release temporally alters downstream signaling through the mitogen activated protein kinase pathway, and amplifies the angiogenic outcome. Merging protein engineering and nanotechnology offers exciting possibilities for the treatment of ischemic disease, and furthermore allows the selective targeting of downstream signaling pathways, which translates into discrete phenotypes.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">31</style></issue><custom3><style face="normal" font="default" size="100%">Foreign</style></custom3><custom4><style face="normal" font="default" size="100%">10.43
</style></custom4></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Mishra, Manasi</style></author><author><style face="normal" font="default" size="100%">Singh, Vigyasa</style></author><author><style face="normal" font="default" size="100%">Tellis, Meenakshi B.</style></author><author><style face="normal" font="default" size="100%">Joshi, Rakesh S.</style></author><author><style face="normal" font="default" size="100%">Singh, Shailja</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Repurposing the McoTI-II rigid molecular scaffold in to inhibitor of `papain superfamily' cysteine proteases</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmaceuticals</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Cathepsin</style></keyword><keyword><style  face="normal" font="default" size="100%">Clan CA cysteine proteases</style></keyword><keyword><style  face="normal" font="default" size="100%">cyclotide</style></keyword><keyword><style  face="normal" font="default" size="100%">cystatin</style></keyword><keyword><style  face="normal" font="default" size="100%">McoTI-II</style></keyword><keyword><style  face="normal" font="default" size="100%">papain</style></keyword><keyword><style  face="normal" font="default" size="100%">protein engineering</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2021</style></year><pub-dates><date><style  face="normal" font="default" size="100%">JAN</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">14</style></volume><pages><style face="normal" font="default" size="100%">7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Clan C1A or `papain superfamily' cysteine proteases are key players in many important physiological processes and diseases in most living systems. Novel approaches towards the development of their inhibitors can open new avenues in translational medicine. Here, we report a novel design of a re-engineered chimera inhibitor Mco-cysteine protease inhibitor (CPI) to inhibit the activity of C1A cysteine proteases. This was accomplished by grafting the cystatin first hairpin loop conserved motif (QVVAG) onto loop 1 of the ultrastable cyclic peptide scaffold McoTI-II. The recombinantly expressed Mco-CPI protein was able to bind with micromolar affinity to papain and showed remarkable thermostability owing to the formation of multi-disulphide bonds. Using an in silico approach based on homology modelling, protein-protein docking, the calculation of the free-energy of binding, the mechanism of inhibition of Mco-CPI against representative C1A cysteine proteases (papain and cathepsin L) was validated. Furthermore, molecular dynamics simulation of the Mco-CPI-papain complex validated the interaction as stable. To conclude, in this McoTI-II analogue, the specificity had been successfully redirected towards C1A cysteine proteases while retaining the moderate affinity. The outcomes of this study pave the way for further modifications of the Mco-CPI design for realizing its full potential in therapeutics. This study also demonstrates the relevance of ultrastable peptide-based scaffolds for the development of novel inhibitors via grafting.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><work-type><style face="normal" font="default" size="100%">Article</style></work-type><custom3><style face="normal" font="default" size="100%">&lt;p&gt;Foreign&lt;/p&gt;
</style></custom3><custom4><style face="normal" font="default" size="100%">&lt;p&gt;4.286&lt;/p&gt;
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