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Your search keyword '"Egaña I"' showing total 2 results
Start Over Author "Egaña I" Topic apoptosis
2 results on '"Egaña I"'

1. Female mice lacking Pald1 exhibit endothelial cell apoptosis and emphysema.

Author

Egaña I, Kaito H, Nitzsche A, Becker L, Ballester-Lopez C, Niaudet C, Petkova M, Liu W, Vanlandewijck M, Vernaleken A, Klopstock T, Fuchs H, Gailus-Durner V, Hrabe de Angelis M, Rask-Andersen H, Johansson HJ, Lehtiö J, He L, Yildirim AÖ, and Hellström M

Subjects
Animals, Disease Models, Animal, Embryo, Mammalian, Emphysema genetics, Female, Heterozygote, Humans, Lung blood supply, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Phosphoprotein Phosphatases genetics, Sex Factors, Apoptosis physiology, Emphysema pathology, Endothelial Cells pathology, Endothelium, Vascular growth & development, Phosphoprotein Phosphatases metabolism
Abstract

Paladin (Pald1, mKIAA1274 or x99384) was identified in screens for vascular-specific genes and is a putative phosphatase. Paladin has also been proposed to be involved in various biological processes such as insulin signaling, innate immunity and neural crest migration. To determine the role of paladin we have now characterized the Pald1 knock-out mouse in a broad array of behavioral, physiological and biochemical tests. Here, we show that female, but not male, Pald1 heterozygous and homozygous knock-out mice display an emphysema-like histology with increased alveolar air spaces and impaired lung function with an obstructive phenotype. In contrast to many other tissues where Pald1 is restricted to the vascular compartment, Pald1 is expressed in both the epithelial and mesenchymal compartments of the postnatal lung. However, in Pald1 knock-out females, there is a specific increase in apoptosis and proliferation of endothelial cells, but not in non-endothelial cells. This results in a transient reduction of endothelial cells in the maturing lung. Our data suggests that Pald1 is required during lung vascular development and for normal function of the developing and adult lung in a sex-specific manner. To our knowledge, this is the first report of a sex-specific effect on endothelial cell apoptosis.

Published
2017
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2. The RING ubiquitin E3 RNF114 interacts with A20 and modulates NF-κB activity and T-cell activation

Author

Lobato-Gil S, Lopez-Mato Mp, Egaña I, Manuel S. Rodriguez, Akaitz Dorronsoro, César Trigueros, James D. Sutherland, Fabienne Aillet, Fernando Lopitz-Otsoa, Rosa Barrio, and Lang

Subjects
Cancer Research, Transcription, Genetic, T-Lymphocytes, Ubiquitin-Protein Ligases, T cell, Immunology, Apoptosis, Biology, Jurkat cells, Jurkat Cells, Cellular and Molecular Neuroscience, chemistry.chemical_compound, NF-KappaB Inhibitor alpha, immune system diseases, hemic and lymphatic diseases, medicine, Humans, RNA, Small Interfering, Nuclear protein, Tumor Necrosis Factor alpha-Induced Protein 3, Tumor Necrosis Factor-alpha, Intracellular Signaling Peptides and Proteins, NF-kappa B, Ubiquitination, Nuclear Proteins, NF-κB, Cell Biology, NFKB1, Molecular biology, Cell biology, DNA-Binding Proteins, IκBα, HEK293 Cells, medicine.anatomical_structure, chemistry, Original Article, I-kappa B Proteins, RNA Interference, Signal transduction, Corrigendum, Carrier Proteins, Protein Binding
Abstract

Accurate regulation of nuclear factor-κB (NF-κB) activity is crucial to prevent a variety of disorders including immune and inflammatory diseases. Active NF-κB promotes IκBα and A20 expression, important negative regulatory molecules that control the NF-κB response. In this study, using two-hybrid screening we identify the RING-type zinc-finger protein 114 (RNF114) as an A20-interacting factor. RNF114 interacts with A20 in T cells and modulates A20 ubiquitylation. RNF114 acts as negative regulator of NF-κB-dependent transcription, not only by stabilizing the A20 protein but also IκBα. Importantly, we demonstrate that in T cells, the effect of RNF114 is linked to the modulation of T-cell activation and apoptosis but is independent of cell cycle regulation. Altogether, our data indicate that RNF114 is a new partner of A2O involved in the regulation of NF-κB activity that contributes to the control of signaling pathways modulating T cell-mediated immune response.

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