排序方式: 共有7条查询结果,搜索用时 15 毫秒
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Plenderleith Fiona A. Irrazabal Valentina A. Burslem David F. R. P. Travis Justin M. J. Powell Priscila Ana 《Biological invasions》2022,24(7):2201-2216
Biological Invasions - Understanding the drivers of invasive species spread is key to designing optimal management programmes for controlling them. Population models, parameterized from demographic... 相似文献
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K Castillo V Valenzuela S Matus M Nassif M O?ate Y Fuentealba G Encina T Irrazabal G Parsons F A Court B L Schneider D Armentano C Hetz 《Cell death & disease》2013,4(11):e917
Accurate methods to measure autophagic activity in vivo in neurons are not available, and most of the studies are based on correlative and static measurements of autophagy markers, leading to conflicting interpretations. Autophagy is an essential homeostatic process involved in the degradation of diverse cellular components including organelles and protein aggregates. Autophagy impairment is emerging as a relevant factor driving neurodegeneration in many diseases. Moreover, strategies to modulate autophagy have been shown to provide protection against neurodegeneration. Here we describe a novel and simple strategy to express an autophagy flux reporter in the nervous system of adult animals by the intraventricular delivery of adeno-associated viruses (AAV) into newborn mice. Using this approach we efficiently expressed a monomeric tandem mCherry-GFP-LC3 construct in neurons of the peripheral and central nervous system, allowing the measurement of autophagy activity in pharmacological and disease settings. 相似文献
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Diego A Rodriguez Sebastian Zamorano Fernanda Lisbona Diego RojasRivera Hery Urra Juan R CubillosRuiz Ricardo Armisen Daniel R Henriquez Emily H Cheng Michal Letek Tomas Vaisar Thergiory Irrazabal Christian GonzalezBillault Anthony Letai Felipe X PimentelMuios Guido Kroemer Claudio Hetz 《The EMBO journal》2021,40(18)
Correction to: The EMBO Journal (2012) 31: 2322–2335. DOI 10.1038/emboj.2012.84 ¦ Published online 17 April 2012 Figure 4A. Original.Source data are available online for this figure. Figure 4A. Corrected. Source data are available online for this figure. The journal was alerted to the claim that the IRE input panels are identical in Figure 1G. Since the IRE input panels show a high degree of similarity, the source data for both panels are published with this notice for the avoidance of doubt.The HSP90 blot looks very similar in Fig 3F and Fig S4A. The authors confirmed that they had stripped and re‐probed the original HSP90 blot in Fig 3F and Fig S4A. Specifically, the membrane was probed with antibodies to IRE1, and HSP90, and then re‐probed with anti‐PERK antibodies. For that reason, HSP90 was presented in both figures because it is the same experiment. In the source data published with this correction, the authors have marked the original data with contrast boxes and arrows to indicate which blots were presented in the figure. The legends have been updated to state that a control originating from one blot is displayed in both figures.The authors acknowledge that they had removed one set of experimental conditions with wild‐type parental DKO cells when preparing Fig 4A and state that this does not change the conclusions of the figure. The figure is herewith updated with a demarcating line and source data for the full experiment is published with this notice.All authors agree with this corrigendum. The authors apologize for any confusion caused by these errors. 相似文献
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Ute Woehlbier Alicia Colombo Mirva J Saaranen Viviana Pérez Jorge Ojeda Fernando J Bustos Catherine I Andreu Mauricio Torres Vicente Valenzuela Danilo B Medinas Pablo Rozas Rene L Vidal Rodrigo Lopez‐Gonzalez Johnny Salameh Sara Fernandez‐Collemann Natalia Muñoz Soledad Matus Ricardo Armisen Alfredo Sagredo Karina Palma Thergiory Irrazabal Sandra Almeida Paloma Gonzalez‐Perez Mario Campero Fen‐Biao Gao Pablo Henny Brigitte van Zundert Lloyd W Ruddock Miguel L Concha Juan P Henriquez Robert H Brown Claudio Hetz 《The EMBO journal》2016,35(8):845-865
Disturbance of endoplasmic reticulum (ER) proteostasis is a common feature of amyotrophic lateral sclerosis (ALS). Protein disulfide isomerases (PDIs) are ER foldases identified as possible ALS biomarkers, as well as neuroprotective factors. However, no functional studies have addressed their impact on the disease process. Here, we functionally characterized four ALS‐linked mutations recently identified in two major PDI genes, PDIA1 and PDIA3/ERp57. Phenotypic screening in zebrafish revealed that the expression of these PDI variants induce motor defects associated with a disruption of motoneuron connectivity. Similarly, the expression of mutant PDIs impaired dendritic outgrowth in motoneuron cell culture models. Cellular and biochemical studies identified distinct molecular defects underlying the pathogenicity of these PDI mutants. Finally, targeting ERp57 in the nervous system led to severe motor dysfunction in mice associated with a loss of neuromuscular synapses. This study identifies ER proteostasis imbalance as a risk factor for ALS, driving initial stages of the disease. 相似文献
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Antoaneta Belcheva Thergiory Irrazabal Susan J. Robertson Catherine Streutker Heather Maughan Stephen Rubino Eduardo H. Moriyama Julia K. Copeland Anu Surendra Sachin Kumar Blerta Green Kaoru Geddes Rossanna C. Pezo William W. Navarre Michael Milosevic Brian C. Wilson Stephen E. Girardin Thomas M.S. Wolever Winfried Edelmann David S. Guttman Dana J. Philpott Alberto Martin 《Cell》2014
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