A translational block

2012 ◽  
Vol 18 (10) ◽  
pp. 1472-1472
Author(s):  
Meera Swami
Keyword(s):  
2003 ◽  
Vol 278 (39) ◽  
pp. 37375-37385 ◽  
Author(s):  
Shengzhan Luo ◽  
Peter Baumeister ◽  
Shujie Yang ◽  
Steve F. Abcouwer ◽  
Amy S. Lee
Keyword(s):  

2010 ◽  
Vol 21 (15) ◽  
pp. 2624-2638 ◽  
Author(s):  
Cornelia Kilchert ◽  
Julie Weidner ◽  
Cristina Prescianotto-Baschong ◽  
Anne Spang

mRNA is sequestered and turned over in cytoplasmic processing bodies (PBs), which are induced by various cellular stresses. Unexpectedly, in Saccharomyces cerevisiae, mutants of the small GTPase Arf1 and various secretory pathway mutants induced a significant increase in PB number, compared with PB induction by starvation or oxidative stress. Exposure of wild-type cells to osmotic stress or high extracellular Ca2+ mimicked this increase in PB number. Conversely, intracellular Ca2+-depletion strongly reduced PB formation in the secretory mutants. In contrast to PB induction through starvation or osmotic stress, PB formation in secretory mutants and by Ca2+ required the PB components Pat1 and Scd6, and calmodulin, indicating that different stressors act through distinct pathways. Consistent with this hypothesis, when stresses were combined, PB number did not correlate with the strength of the translational block, but rather with the type of stress encountered. Interestingly, independent of the stressor, PBs appear as spheres of ∼40–100 nm connected to the endoplasmic reticulum (ER), consistent with the idea that translation and silencing/degradation occur in a spatially coordinated manner at the ER. We propose that PB assembly in response to stress occurs at the ER and depends on intracellular signals that regulate PB number.


2010 ◽  
Vol 33 (2) ◽  
pp. 236-243 ◽  
Author(s):  
Barbara Bettegazzi ◽  
Marija Mihailovich ◽  
Alessandra Di Cesare ◽  
Alessandra Consonni ◽  
Romina Macco ◽  
...  

Landslides ◽  
2019 ◽  
Vol 16 (9) ◽  
pp. 1709-1719 ◽  
Author(s):  
Sandra G. Catane ◽  
Nathan Azriel S. Veracruz ◽  
John Romel R. Flora ◽  
Chatty Mae M. Go ◽  
Rochelle E. Enrera ◽  
...  

Development ◽  
2008 ◽  
Vol 135 (6) ◽  
pp. 1039-1047 ◽  
Author(s):  
D. J. Bornemann ◽  
S. Park ◽  
S. Phin ◽  
R. Warrior

1986 ◽  
Vol 123 (1) ◽  
pp. 13-25 ◽  
Author(s):  
D. G. Bishop ◽  
R. J. Norris

AbstractThe East Abbotsford translational block landslide failed suddenly on 8 August, 1979, after months and probably years of slowly accelerating movement. A displacement of about 50 m occurred on a bedding plane dipping 7°, about 30 m below ground surface, at or very near the contact between two formations.The complex graben formed around the head of the landslide is a small scale example of extensional (rift) tectonics. A wedge and prism model is developed to fit the geometry, and meet the constraints of preserving the cross-sectional area and stratal length of the beds involved and also to account for the sequential retrogressive failures of the trailing edge of the sliding block.Reconstruction of the failure sequence at the toe shows the compressional zone to be dominated by overthrusting on upward sloping surfaces or ramps, with subsidiary backthrusting and buckling.The energy expended in overthrusting, coupled with the decrease in mass (and hence driving force) resulting from the retrogressive spalling of the trailing edge of the slide block, indicates that the phase of rapid movement was accompanied by a sudden decrease in resistance on the failure surface for a movement of 50 m to have occurred.Both the rift and thrust structures associated with the landslide have large scale tectonic analogues.


2021 ◽  
Vol 15 ◽  
Author(s):  
Athanasios Lourbopoulos ◽  
Iordanis Mourouzis ◽  
Christodoulos Xinaris ◽  
Nefeli Zerva ◽  
Konstantinos Filippakis ◽  
...  

Why can we still not translate preclinical research to clinical treatments for acute strokes? Despite > 1000 successful preclinical studies, drugs, and concepts for acute stroke, only two have reached clinical translation. This is the translational block. Yet, we continue to routinely model strokes using almost the same concepts we have used for over 30 years. Methodological improvements and criteria from the last decade have shed some light but have not solved the problem. In this conceptual analysis, we review the current status and reappraise it by thinking “out-of-the-box” and over the edges. As such, we query why other scientific fields have also faced the same translational failures, to find common denominators. In parallel, we query how migraine, multiple sclerosis, and hypothermia in hypoxic encephalopathy have achieved significant translation successes. Should we view ischemic stroke as a “chronic, relapsing, vascular” disease, then secondary prevention strategies are also a successful translation. Finally, based on the lessons learned, we propose how stroke should be modeled, and how preclinical and clinical scientists, editors, grant reviewers, and industry should reconsider their routine way of conducting research. Translational success for stroke treatments may eventually require a bold change with solutions that are outside of the box.


Virology ◽  
1996 ◽  
Vol 219 (1) ◽  
pp. 321-323 ◽  
Author(s):  
SATHYAMANGALAM SWAMINATHAN ◽  
PRITHI RAJAN ◽  
OLGA SAVINOVA ◽  
ROSEMARY JAGUS ◽  
BAYAR THIMMAPAYA

1979 ◽  
Vol 180 (3) ◽  
pp. 545-549 ◽  
Author(s):  
G C T Yeoh ◽  
T Arbuckle ◽  
I T Oliver

1. The administration of dexamethasone to foetal rats in utero does not result in the appearance of specific tyrosine aminotransferase activity even after 24 h. 2. When foetal hepatocytes are cultured in vitro from animals treated in utero with dexamethasone, significantly higher activities of specific tyrosine aminotransferase are found than in untreated controls. 3. Dexamethasone in vitro induces specific tyrosine aminotransferase in cells cultured from control animals and the effect is maximal at 10 nM in the culture medium. 4. Actinomycin D at 0.2 microgram/ml in the culture medium completely prevents the induction of activity in vitro. 5. In cultures established from animals treated with dexamethasone in utero, the increase in specific tyrosine aminotransferase activity over the control cultures is only marginally decreased in the presence of actinomycin D. 6. The results can be interpreted to mean that dexamethasone in utero stimulates the transcription of enzyme-specific mRNA, which is not rranslated until a translational block in the foetal liver is removed by the conditions of culture in vitro.


2009 ◽  
Vol 8 (4) ◽  
pp. 665-675 ◽  
Author(s):  
Harm J. Mulder ◽  
Igor Nikolaev

ABSTRACTActivation of the unfolded protein response (UPR) in eukaryotes involves the splicing of an unconventional intron from the mRNA encoding the transcriptional activator of the pathway. InSaccharomyces cerevisiaea 252-nucleotide (nt) unconventional intron is spliced out of the transcript ofHAC1, changing the 3′ end of theHAC1open reading frame and relieving the transcript from a translational block in a single step. The translational block is caused by the base pairing of part of the unconventional intron with the 5′-untranslated region (5′UTR). InAspergillus nigerand other aspergilli, the unconventional intron inhacAmRNA is only 20 nt long. Since this intron is part of a stable stem-loop structure, base pairing with the 5′UTR, in contrast to the case with yeastHAC1, is not possible. However, analysis of thehacAmRNA revealed a GC-rich inverted repeat (18 base pairings). Upon the activation of the UPR, the 5′UTR ofhacAmRNA is truncated by 230 nt, removing the left part of this inverted repeat. This implies a similar release of a translational block as in the case ofS. cerevisiae HAC1but in two steps. The mechanism behind the 5′ truncation, which does not take place in either yeastHAC1or mammalianxbp1mRNA, has been hitherto unknown. Here we show that during secretion stress inA. niger,hacAtranscription starts from a new start site closer to the ATG, relieving the transcript from translational attenuation. This transcriptional switch is mediated by HacA itself and the unfolded protein response element 2 (UPRE2) in thehacApromoter.


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