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Alpha1-Antitrypsin Deficiency Registry (AADR-BioLINCC)

ABSTRACT: Alpha1-Antitrypsin Deficiency Registry (AADR-BioLINCC)

PROVIDER: PRJNA1296685 | ENA |

REPOSITORIES: ENA

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Alpha1-Antitrypsin Deficiency Registry (AADR-BioLINCC)

Project description:Alpha1-Antitrypsin Deficiency Registry (AADR-BioLINCC)

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Curative and beta cell regenerative effects of alpha1 antitrypsin treatment in autoimmune diabetic NOD mice

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Candida albicans: control vs. alpha1-antitrypsin (AAT) treatment

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Expression data from transgenic mice (3 mo) inducibly expressing human alpha1-antitrypsin in the liver

Project description:In the classical form of α1antitrypsin deficiency a mutant protein accumulates in a polymerized form in the ER of liver cells causing liver damage and carcinogenesis by a gain-of-toxic function mechanism. Recent studies have indicated that the accumulation of mutant α1antitrypsin Z in the ER specifically activates the autophagic response but not the unfolded protein response and that autophagy plays a critical role in disposal of insoluble α1antitrypsin Z. In this study, we used genomic analysis of the liver in a novel transgenic mouse model with inducible expression to screen for changes in gene expression that would potentially define how the liver responds to accumulation of this mutant protein. Keywords: genomic analysis, alpha1-antitrypsin deficiency, comparative study, adult animals, inducible expression, liver specific

2007-07-26 | GSE8599 | GEO

Transcription profiling of mouse transgenics (3 mo) inducibly expresssing human alpha1-antitrypsin in the liver

Project description:In the classical form of Î±1antitrypsin deficiency a mutant protein accumulates in a polymerized form in the ER of liver cells causing liver damage and carcinogenesis by a gain-of-toxic function mechanism. Recent studies have indicated that the accumulation of mutant Î±1antitrypsin Z in the ER specifically activates the autophagic response but not the unfolded protein response and that autophagy plays a critical role in disposal of insoluble Î±1antitrypsin Z. In this study, we used genomic analysis of the liver in a novel transgenic mouse model with inducible expression to screen for changes in gene expression that would potentially define how the liver responds to accumulation of this mutant protein. Experiment Overall Design: Liver RNA from adult (3 mo old) male mice inducibly expressing human alpha1-antitrypsin wild type (M) or mutant (Z) form exclusively in the liver was subjected to genomic analysis. Groups: mutant AAT (Z), wild type AAT (M), expressing (4), non-expressing (1), wild type littermates (WT); 3 biological replicates/each group

2008-06-16 | E-GEOD-8599 | biostudies-arrayexpress

Transcription profiling of mouse (6 wk) inducibly expresssing human alpha1-antitrypsin in the liver

Project description:In the classical form of Î±1antitrypsin deficiency a mutant protein accumulates in a polymerized form in the ER of liver cells causing liver damage and carcinogenesis by a gain-of-toxic function mechanism. Recent studies have indicated that the accumulation of mutant Î±1antitrypsin Z in the ER specifically activates the autophagic response but not the unfolded protein response and that autophagy plays a critical role in disposal of insoluble Î±1antitrypsin Z. In this study, we used genomic analysis of the liver in a novel transgenic mouse model with inducible expression to screen for changes in gene expression that would potentially define how the liver responds to accumulation of this mutant protein. Experiment Overall Design: Liver RNA from juvenile (6 wk old) male mice inducibly expressing human alpha1-antitrypsin wild type (M) or mutant (Z) form exclusively in the liver was subjected to genomic analysis. Groups: mutant AAT (Z), wild type AAT (M), expressing (4), non-expressing (1); 3 biological replicates/each group. Experiment Overall Design: Groups: mutant AAT (Z), wild type AAT (M), expressing (4), non-expressing (1); 3 biological replicates/each group, all males, 6 weeks of age

2008-06-16 | E-GEOD-8600 | biostudies-arrayexpress

The Genomic Research in Alpha-1 Antitrypsin Deficiency and Sarcoidosis Study (GRADS) Alpha-1 study [A1AT]

Project description:Whole genome mRNA and microRNA profiling of bronchoalveolar lavage (BAL) and peripheral blood mononuclear cell (PBMC) in Alpha-1 Antitrypsin Deficiency patients with PiZZ or PiMZ alpha-1 antitrypsin genotypes

2020-11-03 | GSE109515 | GEO

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