Articles by Irati Romero-Garmendia in JoVE
Subcellular Fractionation from Fresh and Frozen Gastrointestinal Specimens Irati Romero-Garmendia*1, Amaia Jauregi-Miguel*1, Izortze Santin2, Jose Ramón Bilbao1, Ainara Castellanos-Rubio1 1Department of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country (UPV-EHU), Biocruces Health Research Institute, 2Endocrinology and Diabetes Research Group, Biocruces Health Research Institute, UPV-EHU, CIBERDEM Here, we present a protocol to perform a simple cellular fractionation for the subcellular separation of cytoplasmic and nuclear proteins in human fresh and frozen intestinal biopsies.
Other articles by Irati Romero-Garmendia on PubMed
Ancestry-based Stratified Analysis of Immunochip Data Identifies Novel Associations with Celiac Disease European Journal of Human Genetics : EJHG. 12, 2016 | Pubmed ID: 27650971 To identify candidate genes in celiac disease (CD), we reanalyzed the whole Immunochip CD cohort using a different approach that clusters individuals based on immunoancestry prior to disease association analysis, rather than by geographical origin. We detected 636 new associated SNPs (P
A Celiac Diasease Associated LncRNA Named HCG14 Regulates NOD1 Expression in Intestinal Cells Journal of Pediatric Gastroenterology and Nutrition. Mar, 2018 | Pubmed ID: 29601440 To identify additional celiac disease associated loci in the Major Histocompatibility Complex independent from classical HLA risk alleles (HLA-DR3-DQ2) and to characterize their potential functional impact in celiac disease pathogenesis at the intestinal level.
Transcription Factor Binding Site Enrichment Analysis in Co-Expression Modules in Celiac Disease Genes. May, 2018 | Pubmed ID: 29748492 The aim of this study was to construct celiac co-expression patterns at a whole genome level and to identify transcription factors (TFs) that could drive the gliadin-related changes in coordination of gene expression observed in celiac disease (CD). Differential co-expression modules were identified in the acute and chronic responses to gliadin using expression data from a previous microarray study in duodenal biopsies. Transcription factor binding site (TFBS) and Gene Ontology (GO) annotation enrichment analyses were performed in differentially co-expressed genes (DCGs) and selection of candidate regulators was performed. Expression of candidates was measured in clinical samples and the activation of the TFs was further characterized in C2BBe1 cells upon gliadin challenge. Enrichment analyses of the DCGs identified 10 TFs and five were selected for further investigation. Expression changes related to active CD were detected in four TFs, as well as in several of their in silico predicted targets. The activation of TFs was further characterized in C2BBe1 cells upon gliadin challenge, and an increase in nuclear translocation of CAMP Responsive Element Binding Protein 1 (CREB1) and IFN regulatory factor-1 (IRF1) in response to gliadin was observed. Using transcriptome-wide co-expression analyses we are able to propose novel genes involved in CD pathogenesis that respond upon gliadin stimulation, also in non-celiac models.