Gene expression profile in Lmna knockout mouse embryonic fibroblast
Ontology highlight
ABSTRACT: Alteration of gene expression profile due to Lmna knockout was studied in MEF. Total RNA obtained from Lmna +/+ MEF and Lmna -/- MEF were compared.
Project description:A distinct highly invasive subpopulation was identified in breast cancer cell lines. The molecular characteristics of these cells was investigated, revealing a set of genes whose high expression confers the ability to invade. Total RNA isolated from the invasive subpopulation from 2 cells lines was compared to total RNA isolated from 2 noninvasive populations.
Project description:Through analysis of a high-content screen we discovered that mir-203 can impair cell migration by suppressing p63 expression. We further determined that p63 promotes motility by inducing the expression of multiple target genes. Total RNA isolated from cell lines with different rated of motility was compared.
Project description:Analysis of gene expression change due to knockdown of Slug expression in a basal-subtype breast cancer cell line, MCFDCIS. Total RNA isolated from MCFDCIS cells transfected with control or Slug specific siRNA.
Project description:Using ATAC seq analysis, we showed that the MEFs with a knockout of Lmna gene (i.e., missing the lamin A/C nuclear scaffolding protein) (Lmna-/- MEFs) display a striking change in chromatin accessibility landscape (peak signals that are both up and down), both within and outside lamina-associated domains (LADs); moreover, there was a clear overrepresentation of peaks with a gain in chromatin accessibility (within and outside LADs) in the Lmna-/- MEFs, and within LADs compared to outside LADs.
Project description:Over 180 LMNA gene mutations have been identified in human diseases including cardiac and skeletal myopathies, lipodystrophies, and premature aging syndromes. Postulated mechanisms by which these mutations result in different phenotypes include perturbation of normal nuclear structure and chromosome organization, and gene activity. We investigated whether a cardiomyopathic LMNA mutation, E161K, displayed abnormal gene expression. We compared the gene expression profile in the E161K LMNA-mutant heart to that of an end stage LMNA-normal heart. We compared the gene expression levels between two end-stage cardiomyopathic hearts in order to detect the gene expression differences more likely to reflect the LMNA mutation state. A region of left ventricle tissue that was grossly less fibrotic and contained cardiomyocytes of the LMNA-mutant heart was selected for RNA isolation. A region of a male heart that was also end-stage dilated cardiomyopathy, but LMNA-normal and also devoid of obvious fibrosis was selected for RNA isolation. Two technical replicates were performed for each sample, and data were analyzed using two different normalization strategies (Mas5 and RMA).
Project description:LMNA mutations cause laminopathies, a group of rare genetic diseases with no known cure, only symptomatic treatment and supportive care. In this study, we characterized five LMNA mutations (LMNA(L35P), LMNA(A539V), LMNA(W520G), LMNA(E358K), and LMNA(R453W)) identified from patients diagnosed with muscular laminopathy in the zebrafish model.
Project description:Over 180 LMNA gene mutations have been identified in human diseases including cardiac and skeletal myopathies, lipodystrophies, and premature aging syndromes. Postulated mechanisms by which these mutations result in different phenotypes include perturbation of normal nuclear structure and chromosome organization, and gene activity. We investigated whether a cardiomyopathic LMNA mutation, E161K, displayed abnormal gene expression. We compared the gene expression profile in the E161K LMNA-mutant heart to that of an end stage LMNA-normal heart.