In: The journal of biological chemistry, 2015, vol. 290, no. 39, p. 23631-23645
Although the accumulation of a misfolded and protease-resistant form of the prion protein (PrP) is a key event in Prion pathogenesis, the cellular factors involved in its folding and quality control are poorly understood. PrP is a glycosylated and disulfide-bonded protein synthesized at the endoplasmic reticulum (ER). The ER foldase ERp57 (also known as Grp58) is highly expressed in the brain...
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In: Holz als Roh- und Werkstoff, 2006, vol. 64, no. 6, p. 491-496
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In: Contributions to Mineralogy and Petrology, 2007, vol. 153, no. 6, p. 647-667
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In: Insectes Sociaux, 2009, vol. 56, no. 1, p. 44-48
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In: Molecular Plant-Microbe Interactions, 2017, vol. 31, no. 3, p. 344–355
We isolated previously several Arabidopsis thaliana mutants with constitutive expression of the early microbe-associated molecular pattern–induced gene ATL2, named eca (expresión constitutiva de ATL2). Here, we further explored the interaction of eca mutants with pest and pathogens. Of all eca mutants, eca2 was more resistant to a fungal pathogen (Botrytis cinerea) and a bacterial pathogen...
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In: Cell Discovery, 2017, vol. 3, p. 17012
Eukaryotic cell cycle progression through G1–S is driven by hormonal and growth- related signals that are transmitted by the target of rapamycin complex 1 (TORC1) pathway. In yeast, inactivation of TORC1 restricts G1–S transition due to the rapid clearance of G1 cyclins (Cln) and the stabilization of the B-type cyclin (Clb) cyclin- dependent kinase (CDK) inhibitor Sic1. The latter mechanism...
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In: Monthly Notices of the Royal Astronomical Society, 2015, vol. 453, no. 1, p. 214-221
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In: Monthly Notices of the Royal Astronomical Society, 2015, vol. 452, no. 1, p. 1060-1067
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In: International Immunology, 2000, vol. 12, no. 9, p. 1275-1284
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In: Nature Communications, 2015, vol. 6, p. 8256
The target of rapamycin complex 1 (TORC1) pathway couples nutrient, energy and hormonal signals with eukaryotic cell growth and division. In yeast, TORC1 coordinates growth with G₁–S cell cycle progression, also coined as START, by favouring the expression of G₁ cyclins that activate cyclin-dependent protein kinases (CDKs) and by destabilizing the CDK inhibitor Sic1. Following TORC1...
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