scholarly journals Fatal attraction or reluctance to part: Is oculomotor disengagement independent of the initial capture of the eyes?

2010 ◽  
Vol 10 (7) ◽  
pp. 137-137
Author(s):  
S. Born ◽  
D. Kerzel ◽  
J. Theeuwes
2020 ◽  
Author(s):  
Mitchell Begelman ◽  
Martin Rees
Keyword(s):  

2021 ◽  
Vol 22 (5) ◽  
pp. 2240
Author(s):  
Yu Wai Chen ◽  
Shah Kamranur Rahman

The frameshift mutants K192Sfs*7 and R153Sfs*41, of the polyglutamine tract-binding protein 1 (PQBP-1), are stable intrinsically disordered proteins (IDPs). They are each associated with the severe cognitive disorder known as the Renpenning syndrome, a form of X-linked intellectual disability (XLID). Relative to the monomeric wild-type protein, these mutants are dimeric, contain more folded contents, and have higher thermal stabilities. Comparisons can be drawn to the toxic oligomerisation in the “conformational diseases”, which collectively describe medical conditions involving a substantial protein structural transition in the pathogenic mechanism. At the molecular level, the end state of these diseases is often cytotoxic protein aggregation. The conformational disease proteins contain varying extents of intrinsic disorder, and the consensus pathogenesis includes an early oligomer formation. We reviewed the experimental characterisation of the toxic oligomers in representative cases. PQBP-1 mutant dimerisation was then compared to the oligomerisation of the conformational disease proteins. The PQBP-1 mutants are unique in behaving as stable soluble dimers, which do not further develop into higher oligomers or aggregates. The toxicity of the PQBP-1 mutant dimers lies in the native functions (in transcription regulation and possibly, RNA splicing) being compromised, rather than proceeding to aggregation. Other examples of stable IDP dimers were discussed and we speculated on the roles of IDP dimerisation in protein evolution.


10.1038/87842 ◽  
2001 ◽  
Vol 7 (5) ◽  
pp. 528-530 ◽  
Author(s):  
Alexander McCampbell ◽  
Kenneth H. Fischbeck
Keyword(s):  

2021 ◽  
Vol 75 (12) ◽  
Author(s):  
Stefânia P. R. Ventura ◽  
Conrado A. B. Galdino ◽  
Paulo Enrique C. Peixoto

2012 ◽  
Vol 12 (11) ◽  
pp. 735-735
Author(s):  
Catriona Rodwell
Keyword(s):  

2011 ◽  
Vol 89 (12) ◽  
pp. 1214-1222 ◽  
Author(s):  
Ashley A.D. McLaren ◽  
Lenore Fahrig ◽  
Nigel Waltho

Previous studies suggest the gap in forest cover generated by roads contributes to the barrier effect of roads on movement of forest-dwelling small mammals. However, it is not known if vegetated medians of divided highways affect movement of small mammals by reducing the effective highway width. The purpose of our study was to determine whether the type of vegetation cover in the median (treed or grassy) or median width affects small-mammal crossings of divided highways. At 11 study sites varying in median cover type and width, we live-trapped small mammals next to one side of the highway and translocated them to the opposite side of the highway using a standardized translocation distance. In total, 24% of translocated individuals were recaptured on the side of the highway of initial capture, i.e., they had moved across the entire highway. This was significantly lower than what would have been expected in the absence of the highway (58%). The overall probability of recapturing a translocated individual was not significantly related to median cover type or width. Our results suggest that efforts to mitigate the barrier effect of highways on small mammals cannot be accomplished by altering median vegetation type and width.


2021 ◽  
Vol 220 (8) ◽  
Author(s):  
Marta Bosch ◽  
Matthew J. Sweet ◽  
Robert G. Parton ◽  
Albert Pol

In the ongoing conflict between eukaryotic cells and pathogens, lipid droplets (LDs) emerge as a choke point in the battle for nutrients. While many pathogens seek the lipids stored in LDs to fuel an expensive lifestyle, innate immunity rewires lipid metabolism and weaponizes LDs to defend cells and animals. Viruses, bacteria, and parasites directly and remotely manipulate LDs to obtain substrates for metabolic energy, replication compartments, assembly platforms, membrane blocks, and tools for host colonization and/or evasion such as anti-inflammatory mediators, lipoviroparticles, and even exosomes. Host LDs counterattack such advances by synthesizing bioactive lipids and toxic nucleotides, organizing immune signaling platforms, and recruiting a plethora of antimicrobial proteins to provide a front-line defense against the invader. Here, we review the current state of this conflict. We will discuss why, when, and how LDs efficiently coordinate and precisely execute a plethora of immune defenses. In the age of antimicrobial resistance and viral pandemics, understanding innate immune strategies developed by eukaryotic cells to fight and defeat dangerous microorganisms may inform future anti-infective strategies.


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