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18 results on '"Louvi A"'

1. Interferon-γ resistance and immune evasion in glioma develop via Notch-regulated co-evolution of malignant and immune cells

Author

Parmigiani, Elena, primary, Ivanek, Robert, additional, Rolando, Chiara, additional, Hafen, Katrin, additional, Turchinovich, Gleb, additional, Lehmann, Frank Michael, additional, Gerber, Alexandra, additional, Brkic, Sime, additional, Frank, Stephan, additional, Meyer, Sara C., additional, Wakimoto, Hiroaki, additional, Günel, Murat, additional, Louvi, Angeliki, additional, Mariani, Luigi, additional, Finke, Daniela, additional, Holländer, Georg, additional, Hutter, Gregor, additional, Tussiwand, Roxane, additional, Taylor, Verdon, additional, and Giachino, Claudio, additional

Published
2022
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4. Interferon-γ Resistance and Immune Evasion in Glioma Develop via Notch-Regulated Co-Evolution of Malignant and Immune Cells

Author

Elena Parmigiani, Robert Ivanek, Chiara Rolando, Katrin Hafen, Alexandra Gerber, Frank Michael Lehmann, Sime Brkic, Stephan Frank, Sara C. Meyer, Hiroaki Wakimoto, Murat Günel, Angeliki Louvi, Luigi Mariani, Daniela Finke, Georg Holländer, Gregor Hutter, Roxane Tussiwand, Verdon Taylor, and Claudio Giachino

Subjects
History, Polymers and Plastics, Business and International Management, Industrial and Manufacturing Engineering
Published
2021
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5. Interferon-γ Resistance and Immune Evasion in Glioma Develop via Notch-Regulated Co-Evolution of Malignant and Immune Cells

Author

Parmigiani, Elena, primary, Ivanek, Robert, additional, Rolando, Chiara, additional, Hafen, Katrin, additional, Gerber, Alexandra, additional, Lehmann, Frank Michael, additional, Brkic, Sime, additional, Frank, Stephan, additional, Meyer, Sara C., additional, Wakimoto, Hiroaki, additional, Günel, Murat, additional, Louvi, Angeliki, additional, Mariani, Luigi, additional, Finke, Daniela, additional, Holländer, Georg, additional, Hutter, Gregor, additional, Tussiwand, Roxane, additional, Taylor, Verdon, additional, and Giachino, Claudio, additional

Published
2021
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7. Cilia in the CNS: The Quiet Organelle Claims Center Stage

Author

Elizabeth A. Grove and Angeliki Louvi

Subjects
Central Nervous System, biology, Neurogenesis, General Neuroscience, Cilium, Neuroscience(all), Article, Cell biology, Neuronal signaling, Human disease, Organelle, biology.protein, Animals, Humans, Hedgehog Proteins, Cilia, Sonic hedgehog, Signal transduction, Protein trafficking, Signal Transduction
Abstract

The primary cilium is a cellular organelle that is almost ubiquitous in eukaryotes, yet its functions in vertebrates have been slow to emerge. The last fifteen years have been marked by accelerating insight into the biology of primary cilia, arising from the synergy of three major lines of research. These research programs describe a specialized mode of protein trafficking in cilia, reveal that genetic disruptions of primary cilia cause complex human disease syndromes, and establish that Sonic hedgehog (Shh) signal transduction requires the primary cilium. New lines of research have branched off to investigate the role of primary cilia in neuronal signaling, adult neurogenesis, and brain tumor formation. We review a fast expanding literature to determine what we now know about the primary cilium in the developing and adult CNS, and what new directions should lead to further clarity.

Published
2011
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10. Growth-Promoting Interaction of IGF-II with the Insulin Receptor during Mouse Embryonic Development

Author

Argiris Efstratiadis, Angeliki Louvi, and Domenico Accili

Subjects
medicine.medical_specialty, Mutant, medicine.disease_cause, Receptor, IGF Type 1, Embryonic and Fetal Development, Mice, Insulin-Like Growth Factor II, Pregnancy, Internal medicine, medicine, Animals, Humans, Receptor, Molecular Biology, Crosses, Genetic, Insulin-like growth factor 1 receptor, Mutation, Fetal Growth Retardation, biology, Embryogenesis, Embryo, Cell Biology, Phenotype, Receptor, Insulin, body regions, Insulin receptor, Endocrinology, biology.protein, Female, Developmental Biology
Abstract

Genetic analyses of dwarfing phenotypes resulting from targeted mutagenesis of the genes encoding the insulin-like growth factors (IGF-I and IGF-II) and their cognate type 1 IGF receptor (IGF1R) have demonstrated that this signaling system is a major determinant of mouse embryonic growth. Of the two IGF ligands, IGF-I interacts exclusively with IGF1R, whereas IGF-II recognizes an additional receptor (XR), because the growth retardation of embryos lacking both IGR1R and IGF-II (30% of normal birthweight) is more severe than that manifested in either class of single Igf1r or Igf2 null mutants (45 and 60% of normal, respectively). To determine whether XR is the insulin receptor (IR), we examined embryos nullizygous for both Igf1r and Insr. While the growth of embryos lacking solely IR is affected very mildly and only at the end of gestation, concomitant absence of IGF1R results in a severe growth-deficiency phenotype (30% of normal size at birth) that is first detected at Embryonic Day 13.5 and is also characterized by transient edema, curly tail, generalized organ hypoplasia, including the muscles, developmental delays in ossification, and thin epidermis. The Igf1r/Insr double nullizygotes are phenotypically indistinguishable from double mutants lacking IGF1R and IGF-II and from other double and triple mutants in which all of the IGF ligand/receptor interactions have been eliminated. Therefore, these results provide genetic evidence that the growth-promoting function of IGF-II during mouse embryogenesis is mediated in part by signaling through the insulin receptor.

Published
1997
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11. Mutations in KATNB1 Cause Complex Cerebral Malformations by Disrupting Asymmetrically Dividing Neural Progenitors

Author

Mishra-Gorur, Ketu, primary, Çağlayan, Ahmet Okay, additional, Schaffer, Ashleigh E., additional, Chabu, Chiswili, additional, Henegariu, Octavian, additional, Vonhoff, Fernando, additional, Akgümüş, Gözde Tuğce, additional, Nishimura, Sayoko, additional, Han, Wenqi, additional, Tu, Shu, additional, Baran, Burçin, additional, Gümüş, Hakan, additional, Dilber, Cengiz, additional, Zaki, Maha S., additional, Hossni, Heba A.A., additional, Rivière, Jean-Baptiste, additional, Kayserili, Hülya, additional, Spencer, Emily G., additional, Rosti, Rasim Ö., additional, Schroth, Jana, additional, Per, Hüseyin, additional, Çağlar, Caner, additional, Çağlar, Çağri, additional, Dölen, Duygu, additional, Baranoski, Jacob F., additional, Kumandaş, Sefer, additional, Minja, Frank J., additional, Erson-Omay, E. Zeynep, additional, Mane, Shrikant M., additional, Lifton, Richard P., additional, Xu, Tian, additional, Keshishian, Haig, additional, Dobyns, William B., additional, Chi, Neil C., additional, Šestan, Nenad, additional, Louvi, Angeliki, additional, Bilgüvar, Kaya, additional, Yasuno, Katsuhito, additional, Gleeson, Joseph G., additional, and Günel, Murat, additional

Published
2015
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12. Mutations in KATNB1 Cause Complex Cerebral Malformations by Disrupting Asymmetrically Dividing Neural Progenitors

Author

Mishra-Gorur, Ketu, primary, Çağlayan, Ahmet Okay, additional, Schaffer, Ashleigh E., additional, Chabu, Chiswili, additional, Henegariu, Octavian, additional, Vonhoff, Fernando, additional, Akgümüş, Gözde Tuğce, additional, Nishimura, Sayoko, additional, Han, Wenqi, additional, Tu, Shu, additional, Baran, Burçin, additional, Gümüş, Hakan, additional, Dilber, Cengiz, additional, Zaki, Maha S., additional, Hossni, Heba A.A., additional, Rivière, Jean-Baptiste, additional, Kayserili, Hülya, additional, Spencer, Emily G., additional, Rosti, Rasim Ö., additional, Schroth, Jana, additional, Per, Hüseyin, additional, Çağlar, Caner, additional, Çağlar, Çağri, additional, Dölen, Duygu, additional, Baranoski, Jacob F., additional, Kumandaş, Sefer, additional, Minja, Frank J., additional, Erson-Omay, E. Zeynep, additional, Mane, Shrikant M., additional, Lifton, Richard P., additional, Xu, Tian, additional, Keshishian, Haig, additional, Dobyns, William B., additional, Chi, Neil C., additional, Šestan, Nenad, additional, Louvi, Angeliki, additional, Bilgüvar, Kaya, additional, Yasuno, Katsuhito, additional, Gleeson, Joseph G., additional, and Günel, Murat, additional

Published
2014
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17. Molecular Cytogenetic Analysis and Resequencing of Contactin Associated Protein-Like 2 in Autism Spectrum Disorders

Author

Bakkaloglu, Betul, primary, O'Roak, Brian J., additional, Louvi, Angeliki, additional, Gupta, Abha R., additional, Abelson, Jesse F., additional, Morgan, Thomas M., additional, Chawarska, Katarzyna, additional, Klin, Ami, additional, Ercan-Sencicek, A. Gulhan, additional, Stillman, Althea A., additional, Tanriover, Gamze, additional, Abrahams, Brett S., additional, Duvall, Jackie A., additional, Robbins, Elissa M., additional, Geschwind, Daniel H., additional, Biederer, Thomas, additional, Gunel, Murat, additional, Lifton, Richard P., additional, and State, Matthew W., additional

Published
2008
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