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20 results on '"Alikashani, Azadeh"'

2. Angiopoietin-like 2 is essential to aortic valve development in mice

Author

Labbé, Pauline, Munoz Goyette, Victoria, Thorin-Trescases, Nathalie, Villeneuve, Louis, Desanlis, Ines, Delwarde, Constance, Shi, Yan-Fen, Martel, Cécile, Yu, Carol, Alikashani, Azadeh, Mamarbachi, Maya, Lesage, Frédéric, Mathieu, Samuel, Tardif, Jean-Claude, Mathieu, Patrick, Kmita, Marie, and Thorin, Éric

Published
2022
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4. TECRL, a new life‐threatening inherited arrhythmia gene associated with overlapping clinical features of both LQTS and CPVT

Author

Devalla, Harsha D, Gélinas, Roselle, Aburawi, Elhadi H, Beqqali, Abdelaziz, Goyette, Philippe, Freund, Christian, Chaix, Marie‐A, Tadros, Rafik, Jiang, Hui, Le Béchec, Antony, Monshouwer‐Kloots, Jantine J, Zwetsloot, Tom, Kosmidis, Georgios, Latour, Frédéric, Alikashani, Azadeh, Hoekstra, Maaike, Schlaepfer, Jurg, Mummery, Christine L, Stevenson, Brian, Kutalik, Zoltan, de Vries, Antoine AF, Rivard, Léna, Wilde, Arthur AM, Talajic, Mario, Verkerk, Arie O, Al‐Gazali, Lihadh, Rioux, John D, Bhuiyan, Zahurul A, and Passier, Robert

Published
2016
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5. Characterization of a Human Induced Pluripotent Stem Cell–Derived Cardiomyocyte Model for the Study of Variant Pathogenicity: Validation of a KCNJ2 Mutation

Author

Gélinas, Roselle, El Khoury, Nabil, Chaix, Marie-A., Beauchamp, Claudine, Alikashani, Azadeh, Ethier, Nathalie, Boucher, Gabrielle, Villeneuve, Louis, Robb, Laura, Latour, Frédéric, Mondesert, Blandine, Rivard, Lena, Goyette, Philippe, Talajic, Mario, Fiset, Céline, and Rioux, John David

Published
2017
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6. Downregulation of low-density lipoprotein receptor mRNA in lymphatic endothelial cells impairs lymphatic function through changes in intracellular lipids

Author

Vachon, Laurent, primary, Smaani, Ali, additional, Tessier, Nolwenn, additional, Jean, Gabriel, additional, Demers, Annie, additional, Milasan, Andreea, additional, Ardo, Nadine, additional, Jarry, Stéphanie, additional, Villeneuve, Louis, additional, Alikashani, Azadeh, additional, Finherty, Vincent, additional, Ruiz, Matthieu, additional, Sorci-Thomas, Mary G., additional, Mayer, Gaétan, additional, and Martel, Catherine, additional

Published
2022
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8. Additional file 2 of Functional screen of inflammatory bowel disease genes reveals key epithelial functions

Author

Ntunzwenimana, Jessy Carol, Boucher, Gabrielle, Paquette, Jean, Gosselin, Hugues, Alikashani, Azadeh, Morin, Nicolas, Beauchamp, Claudine, Thauvette, Louise, Rivard, Marie-��ve, Dupuis, Fr��d��rique, Desch��nes, Sonia, Foisy, Sylvain, Latour, Fr��d��ric, Lavall��e, Genevi��ve, Daly, Mark J., Xavier, Ramnik J., Charron, Guy, Goyette, Philippe, and Rioux, John D.

Abstract

Additional file 2: Supplementary Figures S1-S12., Box 1 & Box 2

Published
2021
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11. Functional screen of inflammatory bowel disease genes reveals key epithelial functions.

Author

Ntunzwenimana, Jessy Carol, Boucher, Gabrielle, Paquette, Jean, Gosselin, Hugues, Alikashani, Azadeh, Morin, Nicolas, Beauchamp, Claudine, Thauvette, Louise, Rivard, Marie-Ève, Dupuis, Frédérique, Deschênes, Sonia, Foisy, Sylvain, Latour, Frédéric, Lavallée, Geneviève, Daly, Mark J., Xavier, Ramnik J., the iGenoMed Consortium, Bitton, Alain, Charron, Guy, and Rosiers, Christine Des

Subjects
INFLAMMATORY bowel diseases, INTESTINAL mucosa, LOCUS (Genetics), IMMUNOGLOBULIN receptors, GENES, PHENOTYPES, TYPE I interferons
Abstract

Background: Genetic studies have been tremendously successful in identifying genomic regions associated with a wide variety of phenotypes, although the success of these studies in identifying causal genes, their variants, and their functional impacts has been more limited. Methods: We identified 145 genes from IBD-associated genomic loci having endogenous expression within the intestinal epithelial cell compartment. We evaluated the impact of lentiviral transfer of the open reading frame (ORF) of these IBD genes into the HT-29 intestinal epithelial cell line via transcriptomic analyses. By comparing the genes in which expression was modulated by each ORF, as well as the functions enriched within these gene lists, we identified ORFs with shared impacts and their putative disease-relevant biological functions. Results: Analysis of the transcriptomic data for cell lines expressing the ORFs for known causal genes such as HNF4a, IFIH1, and SMAD3 identified functions consistent with what is already known for these genes. These analyses also identified two major clusters of genes: Cluster 1 contained the known IBD causal genes IFIH1, SBNO2, NFKB1, and NOD2, as well as genes from other IBD loci (ZFP36L1, IRF1, GIGYF1, OTUD3, AIRE and PITX1), whereas Cluster 2 contained the known causal gene KSR1 and implicated DUSP16 from another IBD locus. Our analyses highlight how multiple IBD gene candidates can impact on epithelial structure and function, including the protection of the mucosa from intestinal microbiota, and demonstrate that DUSP16 acts a regulator of MAPK activity and contributes to mucosal defense, in part via its regulation of the polymeric immunoglobulin receptor, involved in the protection of the intestinal mucosa from enteric microbiota. Conclusions: This functional screen, based on expressing IBD genes within an appropriate cellular context, in this instance intestinal epithelial cells, resulted in changes to the cell's transcriptome that are relevant to their endogenous biological function(s). This not only helped in identifying likely causal genes within genetic loci but also provided insight into their biological functions. Furthermore, this work has highlighted the central role of intestinal epithelial cells in IBD pathophysiology, providing a scientific rationale for a drug development strategy that targets epithelial functions in addition to the current therapies targeting immune functions. [ABSTRACT FROM AUTHOR]

Published
2021
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12. Lrrk2 alleles modulate inflammation during microbial infection of mice in a sex-dependent manner

Author

Shutinoski, Bojan, primary, Hakimi, Mansoureh, additional, Harmsen, Irene E., additional, Lunn, Michaela, additional, Rocha, Juliana, additional, Lengacher, Nathalie, additional, Zhou, Yi Yuan, additional, Khan, Jasmine, additional, Nguyen, Angela, additional, Hake-Volling, Quinton, additional, El-Kodsi, Daniel, additional, Li, Juan, additional, Alikashani, Azadeh, additional, Beauchamp, Claudine, additional, Majithia, Jay, additional, Coombs, Kevin, additional, Shimshek, Derya, additional, Marcogliese, Paul C., additional, Park, David S., additional, Rioux, John D., additional, Philpott, Dana J., additional, Woulfe, John M., additional, Hayley, Shawn, additional, Sad, Subash, additional, Tomlinson, Julianna J., additional, Brown, Earl G., additional, and Schlossmacher, Michael G., additional

Published
2019
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15. Deep resequencing of GWAS loci identifies rare variants in CARD9, IL23R and RNF186 that are associated with ulcerative colitis

Author

Beaudoin, Melissa, Goyette, Philippe, Goel, Gautam, Louis, E., Mansfield, J. C., Mathew, C. G., McGovern, D. P., Mitrovic, M., Montgomery, G. W., Mowat, C., Newman, W., Palmieri, O., Panés, J., Lagace, Caroline, Parkes, M., Phillips, A., Ponsioen, C. Y., Potocnik, U., Prescott, N. J., Proctor, D. D., Radford-Smith, G. L., Regueiro, M., Rioux, J. D., Roberts, R., Annese, Vito, Rotter, J. I., Rutgeerts, P., Sanderson, J., Sans, M., Satsangi, J., Schreiber, S., Schumm, P., Seibold, F., Sharma, Y., Silverberg, M. S., Bitton, Alain, Simms, L. A., Steinhart, A., Targan, S. R., Taylor, K. D., Torkvist, L., Vermeire, S., Halfvarson, J., Verspaget, H. W., De Vos, M., Walters, T., Begun, Jakob, Wang, K., Weersma, R. K., Whiteman, D., Wijmenga, C., Brant, Steven R., Bresso, Francesca, Cho, Judy H., Duerr, Richard H., Halfvarson, Jonas, Boucher, Gabrielle, McGovern, Dermot P. B., Radford-Smith, Graham, Schreiber, Stefan, Schumm, Philip L., Sharma, Yashoda, Silverberg, Mark S., Weersma, Rinse K., Quebec IBD Genetics Consortium, NIDDK IBD Genetics Consortium, International IBD Genetics Consortium (IIBDGC), Lo, Ken Sin, D'Amato, Mauro, Vermeire, Severine, Franke, Andre, Lettre, Guillaume, Xavier, Ramnik J., Daly, Mark J., Rioux, John D., Aumais, G., Bernard, E. J., Bitton, A., Rivas, Manuel A., Cohen, A., Deslandres, C., Lahaie, R., Paré, P., Brant, S. R., Cho, J. H., Duerr, R. H., Stevens, Christine, Ahmad, T., Anderson, C. A., Annese, V., Baldassano, R. N., Balschun, T., Barclay, M., Barrett, J. C., Bayless, T. M., Bis, J. C., Alikashani, Azadeh, Brand, S., Bumpstead, S., Buning, C., Colombel, J. F., Cottone, M., D'Amato, M., D'Inca, R., Ladouceur, Martin, Daly, M. J., Denson, T., Dubinsky, M., Edwards, C., Ellinghaus, D., Florin, T., Franchimont, D., Franke, A., Gearry, R., Ellinghaus, David, Georges, M., Glas, J., Van Gossum, A., Griffiths, A. M., Guthery, S. L., Hakonarson, H., Haritunians, T., Hugot, J. P., de Jong, D. J., Jostins, L., Torkvist, Leif, Kugathasan, S., Kullak-Ublick, G., Latiano, A., Laukens, D., Lawrance, I., Lee, J., Lees, C. W., Lemann, M., Levine, A., Libioulle, C., and Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI)

Subjects
Cancer Research, Génétique clinique, LIVER, Genome-wide association study, Inflammatory bowel disease, 0302 clinical medicine, Crohn Disease, GENETIC-VARIANTS, Medicine and Health Sciences, Ethnicity, UBIQUITIN LIGASES, Genetics(clinical), Genetics (clinical), Genetics, 0303 health sciences, Ecology, High-Throughput Nucleotide Sequencing, CROHN-DISEASE, CROHNS-DISEASE, 3. Good health, 030220 oncology & carcinogenesis, Medical genetics, Biologie, Research Article, EXPRESSION, medicine.medical_specialty, Canada, lcsh:QH426-470, SUSCEPTIBILITY LOCI, Evolution, Ubiquitin-Protein Ligases, Ethnic Groups, Evolution des espèces, Biology, Molecular gastro-enterology and hepatology Pathogenesis and modulation of inflammation [IGMD 2], Polymorphism, Single Nucleotide, 03 medical and health sciences, Behavior and Systematics, medicine, Humans, Genetic Predisposition to Disease, Ligase activity, MODULATION, Allele, GENOME-WIDE ASSOCIATION, Molecular Biology, Genotyping, Ecology, Evolution, Behavior and Systematics, 030304 developmental biology, Genetic association, Ecologie, Biologie moléculaire, Receptors, Interleukin, medicine.disease, NUCLEAR FACTOR 4-ALPHA, Genetic architecture, Cancérologie, CARD Signaling Adaptor Proteins, lcsh:Genetics, CELLS, Colitis, Ulcerative, INTESTINAL EPITHELIAL-CELLS, Genome-Wide Association Study, INFLAMMATORY-BOWEL-DISEASE
Abstract

Genome-wide association studies and follow-up meta-analyses in Crohn's disease (CD) and ulcerative colitis (UC) have recently identified 163 disease-associated loci that meet genome-wide significance for these two inflammatory bowel diseases (IBD). These discoveries have already had a tremendous impact on our understanding of the genetic architecture of these diseases and have directed functional studies that have revealed some of the biological functions that are important to IBD (e.g. autophagy). Nonetheless, these loci can only explain a small proportion of disease variance (~14% in CD and 7.5% in UC), suggesting that not only are additional loci to be found but that the known loci may contain high effect rare risk variants that have gone undetected by GWAS. To test this, we have used a targeted sequencing approach in 200 UC cases and 150 healthy controls (HC), all of French Canadian descent, to study 55 genes in regions associated with UC. We performed follow-up genotyping of 42 rare non-synonymous variants in independent case-control cohorts (totaling 14,435 UC cases and 20,204 HC). Our results confirmed significant association to rare non-synonymous coding variants in both IL23R and CARD9, previously identified from sequencing of CD loci, as well as identified a novel association in RNF186. With the exception of CARD9 (OR = 0.39), the rare non-synonymous variants identified were of moderate effect (OR = 1.49 for RNF186 and OR = 0.79 for IL23R). RNF186 encodes a protein with a RING domain having predicted E3 ubiquitin-protein ligase activity and two transmembrane domains. Importantly, the disease-coding variant is located in the ubiquitin ligase domain. Finally, our results suggest that rare variants in genes identified by genome-wide association in UC are unlikely to contribute significantly to the overall variance for the disease. Rather, these are expected to help focus functional studies of the corresponding disease loci. © 2013 Beaudoin et al., 0, SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2013
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16. Genome-wide expression profiling implicates a MAST3-regulated gene set in colonic mucosal inflammation of ulcerative colitis patients

Author

Labbé, Catherine, primary, Boucher, Gabrielle, additional, Foisy, Sylvain, additional, Alikashani, Azadeh, additional, Nkwimi, Herbert, additional, David, Geneviève, additional, Beaudoin, Mélissa, additional, Goyette, Philippe, additional, Charron, Guy, additional, Xavier, Ramnik J., additional, and Rioux, John D., additional

Published
2012
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17. Deep Resequencing of GWAS Loci Identifies Rare Variants in CARD9, IL23R and RNF186 That Are Associated with Ulcerative Colitis.

Author

Beaudoin, Mélissa, Goyette, Philippe, Boucher, Gabrielle, Lo, Ken Sin, Rivas, Manuel A., Stevens, Christine, Alikashani, Azadeh, Ladouceur, Martin, Ellinghaus, David, Törkvist, Leif, Goel, Gautam, Lagacé, Caroline, Annese, Vito, Bitton, Alain, Begun, Jakob, Brant, Steve R., Bresso, Francesca, Cho, Judy H., Duerr, Richard H., and Halfvarson, Jonas

Subjects
GENOMES, META-analysis, CROHN'S disease, ULCERATIVE colitis, INFLAMMATORY bowel diseases
Abstract

Genome-wide association studies and follow-up meta-analyses in Crohn's disease (CD) and ulcerative colitis (UC) have recently identified 163 disease-associated loci that meet genome-wide significance for these two inflammatory bowel diseases (IBD). These discoveries have already had a tremendous impact on our understanding of the genetic architecture of these diseases and have directed functional studies that have revealed some of the biological functions that are important to IBD (e.g. autophagy). Nonetheless, these loci can only explain a small proportion of disease variance (∼14% in CD and 7.5% in UC), suggesting that not only are additional loci to be found but that the known loci may contain high effect rare risk variants that have gone undetected by GWAS. To test this, we have used a targeted sequencing approach in 200 UC cases and 150 healthy controls (HC), all of French Canadian descent, to study 55 genes in regions associated with UC. We performed follow-up genotyping of 42 rare non-synonymous variants in independent case-control cohorts (totaling 14,435 UC cases and 20,204 HC). Our results confirmed significant association to rare non-synonymous coding variants in both IL23R and CARD9, previously identified from sequencing of CD loci, as well as identified a novel association in RNF186. With the exception of CARD9 (OR = 0.39), the rare non-synonymous variants identified were of moderate effect (OR = 1.49 for RNF186 and OR = 0.79 for IL23R). RNF186 encodes a protein with a RING domain having predicted E3 ubiquitin-protein ligase activity and two transmembrane domains. Importantly, the disease-coding variant is located in the ubiquitin ligase domain. Finally, our results suggest that rare variants in genes identified by genome-wide association in UC are unlikely to contribute significantly to the overall variance for the disease. Rather, these are expected to help focus functional studies of the corresponding disease loci. [ABSTRACT FROM AUTHOR]

Published
2013
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19. Deep resequencing of GWAS loci identifies rare variants in CARD9, IL23R and RNF186 that are associated with ulcerative colitis

Author

Beaudoin, Melissa, Goyette, Philippe, Boucher, Gabrielle, Lo, Ken Sin, Rivas, Manuel A., Stevens, Christine, Alikashani, Azadeh, Ladouceur, Martin, Ellinghaus, David, Torkvist, Leif, Goel, Gautam, Lagace, Caroline, Annese, Vito, Bitton, Alain, Begun, Jakob, Brant, Steven R., Bresso, Francesca, Cho, Judy H., Duerr, Richard H., Halfvarson, Jonas, McGovern, Dermot P. B., Radford-Smith, Graham, Schreiber, Stefan, Schumm, Philip L., Sharma, Yashoda, Silverberg, Mark S., Weersma, Rinse K., Quebec IBD Genetics Consortium, NIDDK IBD Genetics Consortium, International IBD Genetics Consortium (IIBDGC), D'Amato, Mauro, Vermeire, Severine, Franke, Andre, Lettre, Guillaume, Xavier, Ramnik J., Daly, Mark J., Rioux, John D., Aumais, G., Bernard, E. J., Bitton, A., Cohen, A., Deslandres, C., Lahaie, R., Paré, P., Rioux, J. D., Brant, S. R., Cho, J. H., Duerr, R. H., McGovern, D. P., Silverberg, M. S., Ahmad, T., Anderson, C. A., Annese, V., Baldassano, R. N., Balschun, T., Barclay, M., Barrett, J. C., Bayless, T. M., Bis, J. C., Brand, S., Bumpstead, S., Buning, C., Colombel, J. F., Cottone, M., D'Amato, M., D'Inca, R., Daly, M. J., Denson, T., Dubinsky, M., Edwards, C., Ellinghaus, D., Florin, T., Franchimont, D., Franke, A., Gearry, R., Georges, M., Glas, J., Van Gossum, A., Griffiths, A. M., Guthery, S. L., Hakonarson, H., Haritunians, T., Hugot, J. P., De Jong, D. J., Jostins, L., Kugathasan, S., Kullak-Ublick, G., Latiano, A., Laukens, D., Lawrance, I., Lee, J., Lees, C. W., Lemann, M., Levine, A., Libioulle, C., Louis, E., Mansfield, J. C., Mathew, C. G., Mitrovic, M., Montgomery, G. W., Mowat, C., Newman, W., Palmieri, O., Panés, J., Parkes, M., Phillips, A., Ponsioen, C. Y., Potocnik, U., Prescott, N. J., Proctor, D. D., Radford-Smith, G. L., Regueiro, M., Roberts, R., Rotter, J. I., Rutgeerts, P., Sanderson, J., Sans, M., Satsangi, J., Schreiber, S., Schumm, P., Seibold, F., Sharma, Y., Simms, L. A., Steinhart, A., Targan, S. R., Taylor, K. D., Torkvist, L., Vermeire, S., Halfvarson, J., Verspaget, H. W., De Vos, M., Walters, T., Wang, K., Weersma, R. K., Whiteman, D., and Wijmenga, C.

Subjects
3. Good health
Abstract

PLoS genetics 9(9), e1003723 (2013). doi:10.1371/journal.pgen.1003723, Published by Public Library of Science, San Francisco, Calif.

20. Lrrk2alleles modulate inflammation during microbial infection of mice in a sex-dependent manner

Author

Shutinoski, Bojan, Hakimi, Mansoureh, Harmsen, Irene E., Lunn, Michaela, Rocha, Juliana, Lengacher, Nathalie, Zhou, Yi Yuan, Khan, Jasmine, Nguyen, Angela, Hake-Volling, Quinton, El-Kodsi, Daniel, Li, Juan, Alikashani, Azadeh, Beauchamp, Claudine, Majithia, Jay, Coombs, Kevin, Shimshek, Derya, Marcogliese, Paul C., Park, David S., Rioux, John D., Philpott, Dana J., Woulfe, John M., Hayley, Shawn, Sad, Subash, Tomlinson, Julianna J., Brown, Earl G., and Schlossmacher, Michael G.

Abstract

The Lrrk2gene modulates the course of infections in mice in a sex-dependent manner.

Published
2019
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